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1. Efficacy and safety of tenecteplase in combination with enoxaparin, abciximab, or unfractionated heparin: the ASSENT-3 randomised trial in acute myocardial infarction

Author

Van de Werf, F., Armstrong, P. W., Granger, C., Wallentin, L., Adgey, A. A. J., Aylward, P., Binbrek, A. S., Califf, R., Cassim, S., Diaz, R., Fanebust, R., Fioretti, P. M., Huber, K., Husted, S., Lindahl, B., Lopez-Sendon, J. L., Makijarvi, M., Meyer, J., Navarro Robles, J., Pfisterer, M., Seabra-Gomes, R., Soares-Piegas, L., Sugrue, D., Tendera, M., Theroux, P., Toutouzas, P., Vahanian, A., Verheugt, F., Sarelin, H., Goetz, G., Bluhmki, E., Daclin, V., Danays, T., Houbracken, K., Kaye, J., Reilly, P., Hacke, W., von Kummer, R., Lesaffre, E., Bogaerts, K., Peeters, C., Fox, K. A. A., Brower, R., Hirsh, J., Maggioni, A., Tijssen, J., Weaver, D., Beernaert, A., Beysen, N., Broos, K., De Prins, E., D'Hollander, K., Dupon, L., Fomyna, N., Fransen, A., Genesse, D., Goffin, L., Hendrickx, R., Jansen, B., Jorissen, F., Luys, C., Luyten, A., Marschal, C., Moreira, M., Munsters, K., Salerno, R., Schoovaerts, C., Sinnaeve, P., Schildermans, C., Vandenberghe, K., Vandeschoot, K., Van Gucht, H., Van Rompaey, P., Vlassak, S., Watzeels, M., Wittockx, H., Galan, K., Humeniuk, L., Seidel, A., Molina, M., Hafley, G., Alexander, J., Pascual, A., Bestilny, S., Temple, T., Ahuad Guerrero, R., Albisu, J. P., Bassani Arrieta, C. A., Bono, J., Caccavo, A., Cagnolatti, A., Cartasegna, L. R., Castellanos, R., Chekerdemian, S., Covelli, G., Cuello, J. L., Cuneo, C. A., Fernandez, A., Ferrara, C., Ferro-Queirel, E., Gambarte, A., Garcia-Duran, R., Hasbani, E., Hrabar, A., Keller, L., Lobo Marquez, L. L., Luciardi, H., Macin, S. M., Marinig, A., Marzetti, E., Muntaner, J., Nordaby, R., Orlandini, A. D., Piombo, A. C., Pomposiello, J. C., Quijano, R. A., Amerena, J., Aroney, G., Buckmaster, N., Carroll, P., Fitzpatrick, M., Newman, R., Rowe, M., Singh, B., Thomson, A., Winter, C., Eber, B., Gaul, G. B., Klein, W., Leisch, F., Mayr, H., Mlczoch, J., Niessner, H., Pachinger, O., Pall, H., Pichler, M., Roggla, G., Schaflinger, E., Schreiber, W., Slany, J., Traindl, O., Zenker, G., Beckers, J., Bekaert, I., Berthe, C., Bodur, G., Carlier, B., Carlier, M., Carpentier, J., Celen, H., Charlier, F., Clement, A., Coenen, A., Crochelet, L., De Keyser, F., De Man, F., de Meester, A., Dendale, P., Dhondt, E., Dhooghe, G., El Allaf, D., Elshot, S., Emmerechts, C., Foret, F., Gatera, E., Geraedts, J., Gerardy, A. C., Gysbrechts, M., Hallemans, R., Hellemans, S., Herssens, H., Huygens, L., Janssens, L., Lalmand, J., Maamar, R., Marechal, P., Mertens, D., Michel, P., Morandini, E., Nannan, M., Nguyen, D., Odeurs, W., Peerenboom, P., Pirenne, B., Quinonez, M., Raymenants, E., Renard, M., Silance, P. G., Standaert, A. M., Striekwold, H., Thiels, H., Valadi, D., van Brabandt, H., Van Dormael, M., Van Iseghem, P., Van Walleghem, U., Vanden Bosch, H., Vandenbossche, J. L., Vermylen, J., Verstraete, S., Vo Ngoc, P., Willems, P., Zenner, R., Campos de Albuquerque, D., Coutinho, M., de Camargo Carvalho, A. C., Fernandes Manenti, E. R., Ferreira Azevedo, A., Golin, V., Gun, C., Marin Neto, J. A., Marino, R. L., Miranda Abrantes, J. A., Nicolau, J. C., Porto Alegre Dancini, E. M., Rabelo, A., Ramos, R. F., Rizzi Coelho, O., Alexander, D., Bata, I. R., Bhargava, R. K., Bogaty, P., D'Amours, G., Darcel, I., Finnie, K. J. C., Fowlis, R., Gupta, M. K., Henderson, M., Howlett, M. K., Javier, J. J., Kieu, C. V., Kumar, G., Lebouthillier, P., Leduc, F., Lepage, S., Mcavinue, T., Mcgillen, J. E., Mcmeekin, J. D., Morse, J. W., Pistawka, K., Raimondo, E. F., Sandrin, F., Smith, H., Smylie, P. C., Tran, K., Turabian, M., Wagner, K. R., Winkler, L. H., Woo, K. S., Falstie-Jensen, N., Lind Rasmussen, S., Lomholt, P., Markenvard, J., Nielsen, H., Petersen, J., Romer, F., Ahonen, J., Huttunen, M., Kokkonen, L., Luukkonen, J., Mantyla, P., Melin, J., Mustonen, J., Valli, J., Voutilainen, S., Agraou, B., Allam, S., Baradat, G., Battistella, P., Bazin, P., Bouvier, J. -M., Destrac, S., Fouche, R., Fournier, P. -Y., Funck, F., Garnier, H., Grall, J. -Y., Gully, C., Lallement, P. -Y., Loiselet, P., Mycinsky, C., Page, A., Parisot, M., Range, G., Rocher, R., Tafani, C., Thisse, J. -Y., Tibi, T., Tissot, M., Wahl, P., Backenkohler, U., Bavastro, P., Beckmann-Hiss, H., Behnke, M., Bermes, M., Bernsmeier, R., Bethge, K. P., Bethge, H., Block, M., Burkhardt, W., Cieslinski, G., Claus, G., Deetjen, A., Diefenbach, A., Diehm, C., Dietz, A., Dippold, W. G., Eichner, A., Erckenbrecht, J. F., Gawlick, L., Gerber, V., Goppel, L., Gottwik, M., Grosch, B., Hammer, B., Hanheide, M., Hanrath, P., Haspel, J., Hennersdorf, F., Hermanns, M., Hoffmeister, H. M., Holzapfel, P., Hubner, H., Jansen, W., Jung, S., Kaddatz, J., Kienbock, H., Klein, H. H., Konz, K. H., Kulschbach, M., Leschke, M., Liebau, G., Linnartz, M., Lockert, G., Loesbrock, R., Lollgen, H., Ludwig, N., Mudra, H., Munzer, K., Nebel, B., Nellessen, U., Neu, C., Olbrich, H. G., Pfeffer, A., Pfeiffer, P., Plate, V., Pollock, B., Rapp, H., Rommele, U., Sauer, K., Scheffler, N., Schlotterbeck, K., Schmidt-Salzmann, A., Schnitzler, G., Schumann, H., Schuster, C. J., Schuster, P., Schweizer, P., Seitz, K., Simon, R., Spes, C., Szabo, S., Terhardt-Kasten, E., Theuerkauf, B., Tigges, R., Tinnappel, J., Topp, H., Trockel, P., Unland, N., Veth, V., Vom Dahl, J., Vossbeck, G., Weindel, K., Weib, D., Wiewel, D., Wirtz, P., Zipp, C., Apostolou, T., Chalkidis, C., Exadaktylos, N., Foussas, S., Hatseras, D., Karas, S., Karydis, K., Lambrou, S., Louridas, G., Manolis, A., Nanas, J., Novas, I., Panagiotidou, T., Papadopoulos, C., Papakonstantinou, D., Papasteriadis, E., Pavlidis, P., Pyrgakis, V., Skoufas, P., Stavrati, A., Tyrologos, A., Vardas, P., Vrouchos, G., Zacharoulis, A., Zarifis, J., Brown, A., Daly, K., Fennell, W., Horgan, J., Mccann, H., Mcdonald, K., O'Reilly, M., Sullivan, P., Altamura, G., Ambrosio, G., Auteri, A., Aveta, P., Azzarito, M., Badano, L. P., Barbiero, M., Barletta, C., Biscosi, C., Boccanelli, A., Bottero, M., Brizio, E., Brunazzi, M. C., Brunelli, C., Bugatti, U., Capozi, A., Capucci, A., Carfora, A., Caronna, A., Carrone, M., Casazza, F., Cauticci, A., Ceci, V., Ciconte, V., Circo, A., Ciricugno, S., Comito, F., Cornacchia, D., Corsini, G., D'Andrea, F., De Rosa, P., De Simone, M., Del Citerna, F., Del Pinto, M., Dell'Ali, C., Della Casa, S., Della Monica, R., Delogu, G., Di Biase, M., Di Chiara, A., Di Guardo, G., Di Marco, S., Di Mario, F., Di Napoli, T., Di Palma, F., Fadin, B. M., Fazzari, M., Ferraiuolo, G., Fiaschetti, R., Fontanelli, A., Fresco, C., Gambelli, G., Gasbarri, F., Gemelli, M., Giani, P., Gigantino, A., Giomi, A., Giorgi, G., Greco, C., Gregorio, G., Guagnozzi, G., Guiducci, U., Guzzardi, G., Izzo, A., La Rosa, A., Leone, F., Leone, G., Lo Bianco, F., Locuratolo, N., Maggiolini, S., Malinconico, M., Mancone, C., Mangiameli, S., Marchi, S. M., Maresta, A., Mauri, F., Mazzini, C. A., Michisanti, M., Miracapillo, G., Modena, M. G., Morgagni, G. L., Mossuti, E., Nascimbeni, F., Negrelli, M., Notaristefano, A., Pardi, S., Peci, P., Pettinati, G., Pietropaolo, F., Pirelli, S., Pretolani, M., Prinzi, D., Proietti, F., Raganelli, L., Rapino, S., Re, F., Ricci, R., Rinaldi, G., Rusticali, G., Severi, S., Spallarossa, P., Tartagni, F., Terrosu, P., Tortorella, G., Tota, F., Tritto, I., Tuccilo, B., Turco, V., Uscio, G., Valagussa, F., Vergoni, W., Verzuri, M. S., Vetrano, A., Villani, R., Zanini, R., Boisante, L., Niclou, R., Alcocer, L., Castro, A., Fragoso, J., Gonzalez, V., Gonzalez-Pacheco, H., Hernandez-Santamaria, I., Huerta, R., Huerta, D., Martinez, A., Mendoza, M., Moguel, R., Navarro, J., Portos, J. M., Rodriguez, I., Sierra, L., Valencia, S., Vazquez, A., Arnold, A. E. R., Boehmer, A. G., de Graaf, J. J., Funke Kupper, A. J., Gobel, E. J. A. M., Janus, C. L., Linssen, G. C. M., Sedney, M. I., Slegers, L. C., Spierenburg, H. A. M., Strikwerda, S., Tans, J. G. M., Twisk, S. P. M., van der Heijden, R., van Kalmthout, P. M., Verheugt, F. W. A., Holt, E., Skogsholm, A., Thorshaug, R., Thybo, N. K., Wang, H., Maciejewicz, J., Piotrowski, W., Pluta, W., Ruminski, W., Skura, M., Smielak-Korombel, W., Carranca, J., Carvalho, M., Catarino, C., Cunha, D., Ferreira, D., Ferreira, J., Ferreira da Costa, A. F., Lopes de Carvalho, J., Martins, L., Mourao, L., Oliveira Carrageta, M., Prazeres de Sa, E., Puig, J., Ramalho Dos Santos, M. J. J., Resende, M., Seabra Gomes, R., Baig, M. M. E., Bayat, J., Benjamin, J. D., Ranjith, N., Routier, R., Wittmer, H., Abizanda Campos, R., Alonso Garcia, M. A., Amaro Cendon, A., Arboleda Sanchez, J. A., Blanco Varela, J., Bruguera I Cortada, J., Carpintero Avellaneda, J. L., Caturla Such, J., Civeira Murillo, E., Fernandez Aviles, F., Fernandez Fernandez, R., Figueras Bellot, J., Fiol Sala, M., Froufe Sanchez, J., Garcia Calabozo, R., Garcia Palacios, J. L., Gonzalez Maqueda, I., Kallmeyer Martin, C., Lopez Sendon, J. L., Manzano Ramirez, A., Marine Rebull, J., Monton Rodriguez, A., Pique Gilart, M., Reina Toral, A., Rodriguez Llorian, A., Ruano Marco, M., Sanchez Miralles, A., Sanjose Garagarza, J. M., Santalo Bel, M., Torres Ruiz, J. M., Valentin Segura, V., Ahlstrom, P., Ahremark, U., Bandh, S., Bellinetto, A., Dahlberg, A., Hansen, O., Hurtig, U., Jonasson, L., Karlsson, J. E., Larsson, L. E., Moller, B., Ohlin, H., Persson, H., Sandstedt, L., Soderberg, S., Svennberg, L., Swahn, E., Tygesen, H., Broccard, A. F., Estlinbaum, W., Follath, F., Frutiger, A., Hess, N., Maggiorini, M., Marti, D., Muller, P., Rickenbacher, P., Schaller, M. D., Weinbacher, M., Abdulali, S., Ahmad, G., George, S., Ghazi, A., Rao, K. N., Bishop, A., Bridges, A., Canepa-Anson, R., Cave, M., Clarck, R., Cooper, I., de Belder, A., Farrer, M., Kendall, J. M., Ludman, P., Mattu, R., Mcglinchey, P., Moriarty, A. J., Muthusamy, S., Nee, P. A., Nolan, J., Papouchado, M., Rose, E. L., Shahi, M., Stephens, J., Trevelyan, J., Abdul-Karim, A., Adler, L., Arunasalam, S., Avington, D., Baron, S., Beel, T., Bellamy, B., Bennett, J., Berndt, T., Berrick, A., Bersin, R. M., Bethala, V., Bharath, S., Bouchard, A., Boulet, J. E., Bowerman, R., Boyek, T., Brar, R. S., Brodell, G., Bryant, B., Buckner, J. K., Cage, J., Cannon, J. D., Carducci, B., Carr, K., Chang, M., Chelliah, N., Chin, W. L., Chin, J., Church, D. H., Clark, R., Coulis, L., Dadkhah, S., Dearing, B., Defranco, A., Dharawat, M., Dharawat, R., Dhruva, N., Dicola, J., Dykstra, G., Eisenberg, S., El-Bialy, A., Fera, S., Ford, K., Foreman, R. D., Friedman, S., Friedman, V., Garibian, G., Gelormini, J., Geninatti, M. R., Genovese, R., Ghazi, F., Gilchrist, I., Gitler, B., Glover, R., Gonzalez, J., Goulah, R., Graham, B., Gray, R., Grodman, R., Habib, G. B., Hack, T., Hamroff, G., Hanna, G., Hart, M., Haught, H., Hawkins, J., Hempel, R., Hiremath, Y., Hiser, W., Holland, E., Jaffe, N., Jamal, N., James, K. F., Kalla, S., Kates, M., Kemper, A. J., Kennedy, J. J., Kerut, E. K., Killpack, M., King, J., T. Y., Ko, Kollar, K., Kontos, M., Kugelmassluu, A., Kumar, A., Kutscher, A. H., Lambrecht, C., Lancaster, L., Layden, J., Lazar, A., Lebow, M., Lee, C., Lee, A. B., Lehr, J., Levin, F. L., Levitt, R., Levy, R. M., Lieberman, A., Litman, G. I., Lui, H., Luu, M. Q., Macdonald, G., Madyoon, H., Mancherje, C., Marmulstein, M., Mclaurin, B. T., Mcnellis, M., Mendelson, R., Micale, P. J., Miller, M. J., Miller, M. S., Miller, J., Millman, A., Millsaps, R., Minor, S., Modica, J., Morse, H., Moskovits, N., Nester, B. A., Newton, A. S., Niazi, I., Niederman, A., Oatfield, R., Painter, J. A., Pamfilis, S. M., Pamulapati, K. M., Patel, N., Payne, R., Pearson, C., Peizner, D. S., Petrovich, L., Piriz, J., Pollack, M., Pollock, S., Popkave, A., Puma, J. A., Quesada, R., Quigley-Malcolm, D., Raby, K., Ravindran, K., Rees, A. P., Reiner, J., Rivera, E., Rogers, F., Rosenthal, A., Rowe, W. W., Ryan, P. F., Ryman, K., Salacata, A., Santolin, C., Saucedo, J., Savage, R., Savage, W., Schumacher, R., Segarra, S., Sharkey, S., Shonkoff, D., Silver, M., Silver, S. L., Singh, G., Sinyard, R. D., Sporn, D., Srivastava, N. K., Stomel, R., Suresh, D. P., Tallman, M., Togioka, T., Varma, S., Verant, R. P., Wallach, R., Weinberg, M., Weinberg, D., Weinstein, J. M., Wesley, G., Westerman, J. H., Wheeling, J., Whitaker, J., Widmer, M., Yasin, M., and Zakrzewski, M. J.

Subjects
Male, medicine.medical_specialty, Abciximab, Ischemia, Myocardial Infarction, Tenecteplase, Injections, Immunoglobulin Fab Fragments, Reperfusion therapy, Fibrinolytic Agents, Recurrence, Internal medicine, medicine, Humans, Myocardial infarction, Enoxaparin, Aged, Intention-to-treat analysis, Chi-Square Distribution, business.industry, Heparin, Antibodies, Monoclonal, General Medicine, Middle Aged, medicine.disease, Survival Analysis, Regimen, Treatment Outcome, Anesthesia, Tissue Plasminogen Activator, Cardiology, Drug Therapy, Combination, Female, business, Platelet Aggregation Inhibitors, medicine.drug
Abstract

BACKGROUND: Current fibrinolytic therapies fail to achieve optimum reperfusion in many patients. Low-molecular-weight heparins and platelet glycoprotein IIb/IIIa inhibitors have shown the potential to improve pharmacological reperfusion therapy. We did a randomised, open-label trial to compare the efficacy and safety of tenecteplase plus enoxaparin or abciximab, with that of tenecteplase plus weight-adjusted unfractionated heparin in patients with acute myocardial infarction. METHODS: 6095 patients with acute myocardial infarction of less than 6 h were randomly assigned one of three regimens: full-dose tenecteplase and enoxaparin for a maximum of 7 days (enoxaparin group; n=2040), half-dose tenecteplase with weight-adjusted low-dose unfractionated heparin and a 12-h infusion of abciximab (abciximab group; n=2017), or full-dose tenecteplase with weight-adjusted unfractionated heparin for 48 h (unfractionated heparin group; n=2038). The primary endpoints were the composites of 30-day mortality, in-hospital reinfarction, or in-hospital refractory ischaemia (efficacy endpoint), and the above endpoint plus in-hospital intracranial haemorrhage or in-hospital major bleeding complications (efficacy plus safety endpoint). Analysis was by intention to treat. FINDINGS: There were significantly fewer efficacy endpoints in the enoxaparin and abciximab groups than in the unfractionated heparin group: 233/2037 (11.4%) versus 315/2038 (15.4%; relative risk 0.74 [95% CI 0.63-0.87], p=0.0002) for enoxaparin, and 223/2017 (11.1%) versus 315/2038 (15.4%; 0.72 [0.61-0.84], p

Published
2001

3. Influence of immunosuppression on cadaver kidney graft survival

Author

Melot, Christian, Naeije, Robert, Mols, Pierre, Hallemans, R, Lejeune, Philippe, Jaspar, Nadine, Melot, Christian, Naeije, Robert, Mols, Pierre, Hallemans, R, Lejeune, Philippe, and Jaspar, Nadine

Abstract

SCOPUS: cp.j, info:eu-repo/semantics/published

Published
1994

11. Eicosanoids and hypoxic pulmonary vasoconstriction in normal man

Author

Naeije R, Hallemans R, Christian MELOT, Jm, Boeynaems, Mols P, Lejeune P, and Ma, Rie

Subjects
Adult, Male, Prostaglandins E, Imidazoles, Capillary Resistance, Ibuprofen, Oxygen, Eicosanoic Acids, Vasoconstriction, Humans, Female, Thromboxane-A Synthase, Hypoxia, Lung
Abstract

Pulmonary haemodynamics and blood gas tensions were investigated in eight healthy volunteers, breathing room air and at the 15th min of an acute inspiratory hypoxia (fraction of inspired oxygen, (FIO2), 0.125) before and after administration of ibuprofen, a cyclooxygenase inhibitor, and of dazoxiben, a thromboxane A2 (TxA2) synthetase inhibitor; both drugs either with or without an infusion of prostaglandin E1. Hypoxia decreased arterial oxygen tension (PaO2) to below 50 mmHg in every subject and increased pulmonary vascular resistance by an average of 100-150% from baseline values. Acute and chronic dazoxiben or ibuprofen administration markedly reduced serum thromboxane B2 (TxB2), the stable metabolite of TxA2, but had no effect on pulmonary haemodynamics and blood gas tensions in both normoxic and hypoxic conditions. Prostaglandin E1 given in addition to ibuprofen or to dazoxiben did not inhibit hypoxia-induced increases in pulmonary vascular resistance. The stability of this hypoxic pressor response on repetition of an acute hypoxic exposure was established in six additional healthy subjects. Although obtained on a small number of subjects, these results do not suggest that products of the cyclooxygenase pathway of arachidonic acid metabolism play an important role in modulating normoxic or hypoxic pulmonary vascular tone in man.

Published
1987

14. Beneficial effects of almitrine bismesylate on pulmonary gas exchange in COPD

Author

Christian MELOT, Naeije R, Hallemans R, Mols P, and Lejeune P

Subjects
Male, Pulmonary Gas Exchange, Ventilation-Perfusion Ratio, Humans, Female, Lung Diseases, Obstructive, Middle Aged, Almitrine, Piperazines, Aged
Abstract

Almitrine bismesylate 100 mg orally was given to eight patients with severe chronic obstructive pulmonary disease (COPD). In five patients, gasometric, haemodynamic and lung mechanics parameters, and almitrine plasma levels were measured at baseline and every hour up to five hours after almitrine bismesylate intake. Maximal almitrine plasma levels were reached after 2 hours (89 +/- 41 ng/ml, mean +/- SEM) and persisted up to the fifth hour (68 +/- 25 ng/ml). Pulmonary vascular resistance increased significantly from baseline 433 +/- 120 dynes.s.cm-5 to 503 +/- 124, p less than 0.05 at the second hour and to 509 +/- 119, p less than 0.05 at the fifth hour. Arterial oxygen saturation increased significantly from baseline 81.7 +/- 4.9% to 84.5 +/- 5.0, p less than 0.05 at the second hour and to 84.5 +/- 4.6, p less than 0.05 at the fifth hour. Venous admixture decreased significantly from baseline 35 +/- 9% to 30 +/- 9, p less than 0.05 at the second hour and to 28 +/- 9, p less than 0.01 at the fifth hour. Pulmonary artery mean pressure, cardiac output and minute ventilation did not change. The continuous distributions of ventilation-perfusion ratios (VA/Q), using the multiple inert gas elimination technique, were determined in six patients, at baseline and two hours after almitrine bismesylate intake. An improvement in VA/Q matching was observed after almitrine with a diversion of an average of 15 per cent of total blood flow from hypoxic units (VA/Q between 0.08 and 0.4) to normoxic units (VA/Q between 0.5 and 1.8).(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1983

15. Effects of almitrine in decompensated chronic respiratory insufficiency

Author

Naeije R, Mélot C, Mols P, Hallemans R, Naeije N, Cornil A, and Sergysels R

Subjects
Male, Clinical Trials as Topic, Hypertension, Pulmonary, Respiration, Hemodynamics, Middle Aged, Almitrine, Piperazines, Chronic Disease, Ventilation-Perfusion Ratio, Humans, Female, Infusions, Parenteral, Lung Diseases, Obstructive, Aged
Published
1981

23. Stimulus-response curves for hypoxic pulmonary vasoconstriction in piglets.

Author

De Canniere D, Stefanidis C, Hallemans R, Delcroix M, Brimioulle S, and Naeije R

Subjects
Animals, Aspirin pharmacology, Blood Pressure drug effects, Doxapram pharmacology, Stimulation, Chemical, Swine, Vasoconstriction drug effects, Hypoxia physiopathology, Pulmonary Artery physiopathology, Vasoconstriction physiology
Abstract

Objective: The aim was to characterise stimulus-response curves for hypoxic pulmonary vasoconstriction and to observe the effects of drugs reputed to enhance it: aspirin (a cyclo-oxygenase inhibitor), and doxapram (a peripheral chemoreceptor agonist)., Methods: Mean pulmonary artery pressure (Ppa) versus fraction of inspired O2 (FIO2) relationships were studied in 18 intact anaesthetised piglets, before and after the intravenous administration, in random order, of either physiological saline, 1 g aspirin, or 20 mg.kg-1 doxapram. Cardiac output (Q) was kept constant, to avoid passive Q dependent changes in Ppa., Results: A progressive decrease in FIO2 from 100% to 12% was associated with an average increase in Ppa from 19 to 38 mm Hg (p < 0.001). When FIO2 was further decreased to 8%, Ppa decreased to 32 mm Hg (p < 0.01). This stimulus-response curve was unaffected by saline, but displaced in a non-PO2-dependent manner to higher Ppa by doxapram and by aspirin., Conclusions: The pulmonary vascular response to inspiratory hypoxia in intact anaesthetised piglets is biphasic, with a maximum at an FIO2 of 12%. Neither aspirin nor doxapram affect the shape of this stimulus-response curve, and in particular do not prevent low FIO2 associated inhibition of hypoxic pulmonary vasoconstriction.

Published
1992
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24. Restored hypoxic pulmonary vasoconstriction by peripheral chemoreceptor agonists in dogs.

Author

Naeije R, Lejeune P, Vachiéry JL, Leeman M, Mélot C, Hallemans R, Delcroix M, and Brimioulle S

Subjects
Almitrine administration & dosage, Animals, Blood Pressure drug effects, Carbon Dioxide blood, Chemoreceptor Cells drug effects, Dogs, Doxapram administration & dosage, Doxapram pharmacology, Hemodynamics drug effects, Hypoxia blood, Oxygen blood, Almitrine pharmacology, Chemoreceptor Cells physiology, Hypoxia physiopathology, Pulmonary Circulation drug effects, Vasoconstriction drug effects
Abstract

Hypoxic stimulation of the peripheral chemoreceptors inhibits hypoxic pulmonary vasoconstriction (HPV). On the other hand, almitrine, a peripheral chemoreceptor agonist, has been reported in some studies to enhance HPV. To further explore this apparent contradiction, we investigated the effects of two different low intravenous doses of almitrine on pulmonary arterial pressure (Ppa) versus cardiac index (Q) plots in 32 pentobarbital-anesthetized dogs ventilated alternatively in hyperoxia (FIO2, 0.4) and in hypoxia (FIO2 0.1). HPV, defined as a hypoxia-induced increase in Ppa over the entire range of Q studied, from 2 to 5 L/min/m2, was elicited in 16 dogs. In the first eight of these "responders," almitrine 2 micrograms/kg/min had no vascular effect, and in the other eight, almitrine 4 micrograms/kg/min inhibited HPV. In 16 other dogs, hypoxia did not affect Ppa over the entire range of Q. In these "nonresponders," almitrine 2 micrograms/kg/min (n = 8) as well as 4 micrograms/kg/min (n = 8) restored HPV. To answer the question whether the ability to restore HPV would be specific to almitrine, we administered intravenously the structurally unrelated chemoreceptor agonist doxapram at the dose of 20 micrograms/kg/min to an additional group of eight "nonresponders," and this treatment also restored HPV. Intravenous infusion of the malic acid solution solvent of almitrine had no effect on Ppa/Q plots in a final group of eight "nonresponders". We conclude that low dose almitrine and doxapram restore HPV in dogs with a naturally absent hypoxic pulmonary pressor response, probably by a direct effect at the pulmonary vessels.

Published
1990
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25. Enhancement of hypoxic pulmonary vasoconstriction by metabolic acidosis in dogs.

Author

Lejeune P, Brimioulle S, Leeman M, Hallemans R, Melot C, and Naeije R

Subjects
Animals, Aspirin pharmacology, Bicarbonates administration & dosage, Blood Pressure drug effects, Blood Pressure physiology, Carbon Dioxide blood, Cardiac Output drug effects, Cardiac Output physiology, Dogs, Heart Rate drug effects, Hydrochloric Acid administration & dosage, Hydrochloric Acid pharmacology, Hydrogen-Ion Concentration, Oxygen blood, Pulmonary Artery, Pulmonary Circulation physiology, Pulmonary Wedge Pressure drug effects, Pulmonary Wedge Pressure physiology, Sodium administration & dosage, Sodium Bicarbonate, Acidosis physiopathology, Hypoxia physiopathology, Lung blood supply, Vasoconstriction physiology
Abstract

The effects of HCl infusion on multipoint mean pulmonary arterial pressure (PAP)/cardiac index (CI) plots in pentobarbital-anesthetized dogs whose lungs were ventilated alternately in hyperoxia (fraction of inspired O2 [FIO2], 0.4) and hypoxia (FIO2, 0.1) were investigated. Over the range of CI studied (1 to 5 l.min-1.m-2), hypoxia increased PAP in 22 dogs (responders) and did not affect PAP in 16 other dogs (nonresponders). In eight nonresponders, two repetitions of alternated 0.4 and 0.1 FIO2 exposures did not restore hypoxic pulmonary vasoconstriction (HPV), defined as a hypoxia-induced increase in PAP at a given flow. Intravenous infusion of 2 M HCl (2 mmol.kg-1.h-1) decreased arterial pH from normal to around 7.20 in eight responders and eight nonresponders. This metabolic acidosis increased PAP at all levels of CI in hyperoxia and in hypoxia in all the dogs, enhanced HPV in the responders, and restored HPV in the nonresponders. In eight responders, 2 M HCl infusion (2 mmol.kg-1.h-1) together with a 7% sodium bicarbonate infusion (adjusted to maintain arterial pH unchanged) did not affect hyperoxic or hypoxic PAP/CI plots. Pretreatment with 1 g acetylsalicylic acid iv (6 dogs) did not affect the pulmonary vasoreactivity to HCl-induced (2 M HCl, 2 mmol.kg-1.h-1) metabolic acidosis. It was concluded that in intact dogs: 1) metabolic acidosis enhances HPV; 2) at the given dose, HCl does not produce pulmonary vascular effects unrelated to the circulating blood pH; and 3) it is unlikely that the pulmonary vasoreactivity to metabolic acidosis is mediated by products of the cyclooxygenase pathway.

Published
1990
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26. Pulmonary vascular tone improves pulmonary gas exchange in the adult respiratory distress syndrome.

Author

Melot C, Naeije R, Mols P, Hallemans R, Lejeune P, and Jaspar N

Subjects
Adult, Aged, Diltiazem pharmacology, Female, Humans, Hypertension, Pulmonary etiology, Lung drug effects, Male, Middle Aged, Oxygen blood, Respiratory Distress Syndrome complications, Hypertension, Pulmonary physiopathology, Lung blood supply, Respiratory Distress Syndrome physiopathology, Vascular Resistance drug effects, Ventilation-Perfusion Ratio drug effects
Abstract

Hemodynamics, blood gases, lung mechanics, and the distributions of ventilation-perfusion ratios (VA/Q) were studied before and after iv diltiazem, 0.5 mg/kg over 30 min, in 6 patients with pulmonary hypertension secondary to the adult respiratory distress syndrome (ARDS) ventilated with 7 to 20 cm H2O positive end-expiratory pressure (PEEP). Diltiazem decreased systemic and pulmonary arterial pressures without changes in cardiac output and in filling pressures of the heart, and with a slowing of heart rate. Pulmonary vascular resistances decreased from 401 +/- 59 to 329 +/- 58 dyne.s.cm-5.m2 (mean +/- SEM), p less than 0.01. Arterial Po2 decreased from 87 +/- 10 to 80 +/- 11 mm Hg (p less than 0.02) without changes in arterial PCO2, mixed venous PO2, and O2 consumption. Lung compliance and airway resistances did not change. Diltiazem increased true shunt from 23 +/- 5 to 30 +/- 7% of total blood flow (p less than 0.02) without other modification in the pattern of VA/Q distribution as measured by the multiple inert gas elimination technique. These results suggest that pulmonary vascular tone contributes to the maintenance of VA/Q matching in patients with ARDS.

Published
1987
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27. Hypoxic pulmonary vasoconstriction in liver cirrhosis.

Author

Naeije R, Hallemans R, Mols P, and Melot C

Subjects
Adult, Aged, Female, Humans, Male, Middle Aged, Vascular Resistance, Hypoxia physiopathology, Liver Cirrhosis physiopathology, Pulmonary Circulation, Vasoconstriction
Abstract

Impairment of hypoxic pulmonary vasoconstriction (HPV) is frequently cited as an explanation for the hypoxemia of liver cirrhosis. We investigated the pulmonary and systemic hemodynamic responses to acute inspiratory hypoxia, 12.5 percent oxygen in nitrogen during 10 minutes, in 24 patients with mildly to moderately decompensated liver cirrhosis and arterial hypoxemia. A mean increase of 50 percent in pulmonary vascular resistance (PVR) was observed, which is comparable to reported responses of normal subjects to a similar degree of hypoxia. Seven of the 24 patients showed an increase in PVR of less than 20 percent. Compared with the other patients, no difference could be found between both groups in baseline blood gas and hemodynamic determinations, physical examination, liver function tests, and laboratory tests that may be disturbed by circulating endotoxin. Five of the 24 patients had a hyperkinetic circulatory state, but only one of them failed to increase PVR in response to hypoxia. Considering the whole group of 24 patients, there was no correlation between PaO2, PVR, and PVR response to hypoxia. Impairment of HPV is probably not the right explanation for most cirrhotic patients with arterial hypoxemia.

Published
1981
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29. Enhancement of hypoxic pulmonary vasoconstriction by low dose almitrine bismesylate in normal humans.

Author

Mélot C, Dechamps P, Hallemans R, Decroly P, and Mols P

Subjects
Adult, Almitrine, Blood Pressure drug effects, Double-Blind Method, Female, Humans, Male, Oxygen blood, Piperazines administration & dosage, Random Allocation, Vascular Resistance drug effects, Ventilation-Perfusion Ratio drug effects, Hypoxia physiopathology, Piperazines pharmacology, Pulmonary Circulation drug effects, Vasoconstriction drug effects
Abstract

The effect of almitrine bismesylate on hypoxic pulmonary vasoconstriction (HPV) remains controversial. We therefore investigated in a double-blind, placebo-controlled, randomized design the effects of low dose of almitrine bismesylate (4 micrograms/kg/min given intravenously) on blood gases, pulmonary hemodynamics, and ventilation-perfusion (VA/Q) distributions in normal subjects breathing a hypoxic mixture (FIO2, 0.125), room air (FIO2, 0.21), and oxygen (FIO2, 1.0) in a random sequence. In the placebo group (7 subjects), no change was recorded. In the almitrine group (10 subjects), arterial PO2 improved during hypoxia (from 42 +/- 2 to 47 +/- 1 mm Hg, p less than 0.05, mean +/- SEM) and normoxia (from 99 +/- 3 to 104 +/- 2, p less than 0.05). Pulmonary arterial mean pressure and pulmonary vascular resistance index increased with almitrine during hypoxia, respectively, from 20 +/- 1 to 23 +/- 1 mm Hg (p less than 0.01) and from 207 +/- 22 to 283 +/- 35 dyne.s.cm-5.m2 (p less than 0.01), and during normoxia, respectively, from 12 +/- 1 to 14 +/- 1 mm Hg (p less than 0.05) and from 90 +/- 11 to 137 +/- 13 dyne.s.cm-5.m2 (p less than 0.05). The VA/Q distribution improved during hypoxia, with a shift of the blood flow distribution to better oxygenated lung units with higher VA/Q ratios. We conclude that in normal humans low dose of almitrine improves gas exchange by an enhancement of HPV.

Published
1989
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30. Hemodynamic effects of vasopressin, alone and in combination with nitroprusside, in patients with liver cirrhosis and portal hypertension.

Author

Mols P, Hallemans R, Van Kuyk M, Melot C, Lejeune P, Ham H, Vertongen F, and Naeije R

Subjects
Adult, Coronary Circulation drug effects, Drug Therapy, Combination, Female, Humans, Hypertension, Portal physiopathology, Liver Circulation drug effects, Liver Cirrhosis physiopathology, Male, Middle Aged, Nitroprusside pharmacology, Pulmonary Circulation drug effects, Renal Circulation drug effects, Vasopressins pharmacology, Ferricyanides administration & dosage, Hemodynamics drug effects, Hypertension, Portal drug therapy, Liver Cirrhosis drug therapy, Nitroprusside administration & dosage, Vasopressins administration & dosage
Abstract

We have investigated the effects on systemic, pulmonary, hepatic, and renal hemodynamics, and on blood gases of vasopressin, 0.4 U/min I.V. first alone, then in combination with nitroprusside 1-5 micrograms/kg/min I.V., in 12 patients with liver cirrhosis and portal hypertension. Portal pressures were estimated by the gradient between occluded and free hepatic vein pressures, hepatic blood flow was measured by indocyanine green infusion, renal blood flow by an isotopic method, and cardiac output by thermodilution. Vasopressin alone reduced cardiac output (-23%) and O2 delivery to the tissues (-25%), increased mean arterial pressure (+20%) and filling pressures of the heart (+136%), reduced portal pressures (-36%) (from 19 +/- 1 to 12 +/- 1 mmHg, mean +/- SEM), hepatic blood flow (-35%) (1.33 +/- 0.2 to 0.87 +/- 0.1 l/min), and renal blood flow (-16%) (0.77 +/- 0.07 to 0.65 +/- 0.05 l/min). Adding nitroprusside restored cardiac output, preload and afterload, and renal blood flow to pretreatment values. Oxygen delivery remained depressed (-12%) because of a negative effect on pulmonary gas exchange (physiologic shunt increased from 16 +/- 2 to 28 +/- 4%). Portal pressures remained reduced by 31% and hepatic blood flow by 25%. These results suggest that small doses of I.V. nitroprusside minimize the deleterious hemodynamic effects of vasopressin while maintaining the therapeutic benefit of portal pressure reduction in cirrhotic patients.

Published
1984
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31. Effect of vasopressin and somatostatin on hemodynamics and blood gases in patients with liver cirrhosis.

Author

Naeije R, Hallemans R, Mols P, Mélot C, and Reding P

Subjects
Adult, Aged, Blood Gas Analysis, Female, Humans, Male, Middle Aged, Somatostatin therapeutic use, Vasopressins therapeutic use, Hemodynamics drug effects, Liver Cirrhosis drug therapy, Somatostatin pharmacology, Vasopressins pharmacology
Abstract

The effects of somatostatin and vasopressin on blood gases, pulmonary and systemic hemodynamics, and portal pressure assessed by the gradient between occluded and free hepatic vein pressures, were investigated in 18 patients with liver cirrhosis. In the first 10 patients, an iv bolus of 250 microgram somatostatin, followed by an infusion of 125 microgram somatostatin over 30 min, caused a sudden rise in pulmonary and systemic vascular pressures lasting 2 to 5 min and accompanied by bradycardia. There was a slight and transient increase in venous admixture (Qsp/Qt) and alveolar-arterial oxygen tension gradients (P(A-a)O2), and a transient reduction in O2 delivery (O2 del) (-11% of the baseline values) and portal pressures (-14%). In the next 8 patients, vasopressin, 0.4 U/min infused over 30 min, caused a more persistent pulmonary and systemic hypertension and bradycardia, a slight increase in P(A.a)O2 and Qsp/Qt, a reduction in O2 del (-27%) and a decrease in portal pressures (-32%). These effects were marked during the entire vasopressin infusion period. Both somatostatin and vasopressin had vasoconstrictive properties and exerted negative effects on hemodynamics and blood gases. Vasopressin appeared to be a more potent drug than somatostatin.

Published
1982
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33. Beneficial effects of almitrine bismesylate on pulmonary gas exchange in COPD.

Author

Melot C, Naeije R, Hallemans R, Mols P, and Lejeune P

Subjects
Aged, Almitrine, Female, Humans, Male, Middle Aged, Ventilation-Perfusion Ratio drug effects, Lung Diseases, Obstructive drug therapy, Piperazines therapeutic use, Pulmonary Gas Exchange drug effects
Abstract

Almitrine bismesylate 100 mg orally was given to eight patients with severe chronic obstructive pulmonary disease (COPD). In five patients, gasometric, haemodynamic and lung mechanics parameters, and almitrine plasma levels were measured at baseline and every hour up to five hours after almitrine bismesylate intake. Maximal almitrine plasma levels were reached after 2 hours (89 +/- 41 ng/ml, mean +/- SEM) and persisted up to the fifth hour (68 +/- 25 ng/ml). Pulmonary vascular resistance increased significantly from baseline 433 +/- 120 dynes.s.cm-5 to 503 +/- 124, p less than 0.05 at the second hour and to 509 +/- 119, p less than 0.05 at the fifth hour. Arterial oxygen saturation increased significantly from baseline 81.7 +/- 4.9% to 84.5 +/- 5.0, p less than 0.05 at the second hour and to 84.5 +/- 4.6, p less than 0.05 at the fifth hour. Venous admixture decreased significantly from baseline 35 +/- 9% to 30 +/- 9, p less than 0.05 at the second hour and to 28 +/- 9, p less than 0.01 at the fifth hour. Pulmonary artery mean pressure, cardiac output and minute ventilation did not change. The continuous distributions of ventilation-perfusion ratios (VA/Q), using the multiple inert gas elimination technique, were determined in six patients, at baseline and two hours after almitrine bismesylate intake. An improvement in VA/Q matching was observed after almitrine with a diversion of an average of 15 per cent of total blood flow from hypoxic units (VA/Q between 0.08 and 0.4) to normoxic units (VA/Q between 0.5 and 1.8).(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1983

34. Effects of vasodilators on hypoxic pulmonary vasoconstriction in normal man.

Author

Naeije R, Mélot C, Mols P, and Hallemans R

Subjects
Adult, Female, Hemodynamics drug effects, Humans, Male, Nifedipine pharmacology, Nitroglycerin pharmacology, Nitroprusside pharmacology, Oxygen blood, Ventilation-Perfusion Ratio drug effects, Hypoxia physiopathology, Pulmonary Circulation drug effects, Vasoconstriction drug effects, Vasodilator Agents pharmacology
Abstract

A reduction of arterial PO2 is generally observed when vasodilators are given to patients with cardiac or pulmonary disease. This has been attributed to a release of preexisting hypoxic pulmonary vasoconstriction (HPV). We investigated the effects of hemodynamics and blood gases of IV nitroglycerin, IV nitroprusside and sublingual nifedipine, at dosages currently used in clinical practice, in 23 healthy volunteers at normoxic conditions (fraction of inspired O2, FIO2 0.21) and at acute inspiratory hypoxia (FIO2 0.125 during 10 min). Breathing FIO2 0.125 elicited pulmonary vasoconstriction in all the subjects. At FIO2 0.21, nitroglycerin reduced preload, nifedipine reduced afterload, nitroprusside had balanced effects, but none of the drugs induced pulmonary vasodilation and only nitroglycerin deteriorated arterial oxygenation. At FIO2 0.125, nitroglycerin did not at all affect the pulmonary pressor response, while both nitroprusside and nifedipine decreased it. An inhibition of HPV was obtained with certainty in only one subject who received nitroprusside. In all the subjects in whom HPV was partially inhibited by vasodilator administration, the alveolar-arterial PO2 gradients remained significantly lowered, suggesting that the pulmonary vascular tone adaptation to alveolar hypoxia still was effective in improving ventilation/perfusion relationships. The role of impaired HPV in the reduction of arterial PO2 in patients under vasodilator therapy may have to be reevaluated.

Published
1982
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35. Reduction in pulmonary hypertension by prostaglandin E1 in decompensated chronic obstructive pulmonary disease.

Author

Naeije R, Mélot C, Mols P, and Hallemans R

Subjects
Aged, Alprostadil, Carbon Dioxide blood, Female, Hemodynamics drug effects, Humans, Hypertension, Pulmonary etiology, Injections, Intravenous, Lung blood supply, Lung Diseases, Obstructive therapy, Male, Middle Aged, Oxygen blood, Partial Pressure, Respiration, Artificial, Vasoconstriction drug effects, Hypertension, Pulmonary drug therapy, Lung Diseases, Obstructive complications, Prostaglandins E pharmacology
Abstract

Prostaglandin E1 (PgE1) was administered intravenously to 26 patients with decompensated chronic obstructive pulmonary disease (COPD) in order to investigate the effects on hemodynamics and blood gases of a reduction in pulmonary hypertension in this condition. In the first 10 patients, PgE1 at 0.02 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 20 and 7%, increased cardiac index (CI) and oxygen delivery to the tissues (TO2), and did not affect blood gases. In the next 9 patients, PgE1 at 0.04 microgram/kg/min decreased pulmonary and systemic pressures, respectively, by 24 and 14%, increased CI and TO2, slightly decreased arterial oxygenation, and did not affect mixed venous blood gases. Side effects, consisting in facial flush, headache, and malaise occurred in 4 of these patients. In the last 7 patients who were artificially ventilated, PgE1 at 0.02 microgram/kg/min increased CI and TO2 but had no effect on vascular pressures and blood gases. Prostaglandin E1 was also given intravenously to 7 healthy subjects breathing 12.5% O2 in N2 for 10 min. Hypoxic pulmonary vasoconstriction was not inhibited by PgE1, even at the highest dosage of 0.04 microgram/kg/min, which caused a flush of the skin, headache, and malaise in all the subjects. Infusion of PgE1 reduces the pulmonary hypertension secondary to decompensated COPD. At adequate dosage, this effect can be obtained with minimal systemic vasodilation and no alteration in the gas exchange function of the lungs, which may be due to preservation of pulmonary vascular tone adaptation to hypoxia. The vasodilating activity fo PgE1 appears to be blunted during artificial ventilation.

Published
1982
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36. Central and regional hemodynamic effects of nitrendipine in normotensive patients with chronic obstructive lung disease.

Author

Mols P, Naeije R, Hallemans R, Mélot C, Lejeune P, and Englert M

Subjects
Adult, Aged, Blood Pressure drug effects, Calcium Channel Blockers pharmacology, Cardiac Output drug effects, Drug Evaluation, Humans, Liver Circulation drug effects, Lung Diseases, Obstructive physiopathology, Male, Middle Aged, Nifedipine pharmacology, Nitrendipine, Pulmonary Gas Exchange drug effects, Renal Circulation drug effects, Vasodilation drug effects, Hemodynamics drug effects, Nifedipine analogs & derivatives
Abstract

Central and regional hemodynamic studies were performed before and after administration of nitrendipine, a recently introduced calcium-channel blocker, in 10 normotensive patients with chronic obstructive pulmonary disease. None of them had a mean pulmonary artery pressure higher than 20 mm Hg. Ninety minutes after oral intake of 20 mg nitrendipine, cardiac output increased by 22%, heart rate increased by 12%, mean arterial pressure decreased by 7%, and pulmonary artery pressures as well as filling pressures of the heart did not change. Venous admixture and alveolar to arterial PO2 gradients increased by 54% and 22%, respectively. Hepatic blood flow increased by 33%. Renal blood flow remained unchanged and glomerular filtration rate decreased by 11%. Thus, in normotensive patients, nitrendipine administration induces systemic vasodilatation with an apparently reflex increase in cardiac output. These effects are accompanied by a deterioration in pulmonary gas exchange, increase in hepatic perfusion, no change in renal perfusion, and possibly a slight deterioration in renal function.

Published
1986
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37. Deleterious effect of nifedipine on pulmonary gas exchange in chronic obstructive pulmonary disease.

Author

Melot C, Hallemans R, Naeije R, Mols P, and Lejeune P

Subjects
Aged, Arteries, Biomechanical Phenomena, Female, Hemodynamics drug effects, Humans, Lung physiopathology, Lung Diseases, Obstructive physiopathology, Male, Middle Aged, Noble Gases, Oxygen blood, Partial Pressure, Ventilation-Perfusion Ratio drug effects, Lung Diseases, Obstructive drug therapy, Nifedipine adverse effects, Pulmonary Gas Exchange drug effects
Abstract

Nifedipine was given, 20 mg sublingually, to 6 patients with pulmonary hypertension secondary to advanced chronic obstructive pulmonary disease, and its effects on hemodynamics, blood gases, lung mechanics, and the distribution of ventilation-perfusion ratios (VA/Q) were investigated. Systemic vasodilation was obtained, with a reduction in mean systemic arterial pressure and in systemic vascular resistance by 16 and 36%, respectively. Cardiac index increased by 29%. Pulmonary vascular resistance decreased by 28%, without changes in pulmonary arterial mean pressure. Arterial PO2 decreased from 52 +/- 4 to 47 +/- 3 mmHg (p less than 0.001). A deterioration in VA/Q matching could be demonstrated, with a redistribution of blood flow into the lungs by a diversion of 20% of total blood flow from units with normal VA/Q, between 0.23 to 3.0, to hypoxic units with low VA/Q between 0.19 to 0.009. These changes might be explained by a partial inhibition of hypoxic pulmonary vasoconstriction.

Published
1984
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38. Pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis.

Author

Mélot C, Naeije R, Dechamps P, Hallemans R, and Lejeune P

Subjects
Adult, Aged, Alkalosis, Respiratory etiology, Alkalosis, Respiratory physiopathology, Blood Gas Analysis, Female, Hemodynamics, Humans, Hypoxia blood, Hypoxia physiopathology, Liver Cirrhosis physiopathology, Male, Middle Aged, Ventilation-Perfusion Ratio, Hypoxia etiology, Liver Cirrhosis complications, Lung physiopathology
Abstract

To determine and to quantify the pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis, we measured in 10 cirrhotics blood gases, P50, hemodynamics, ventilation, and the distribution of ventilation-perfusion ratios (VA/Q) using the multiple inert gas elimination technique. Seven patients had an arterial hypoxemia (PaO2 = 69 +/- 6 mm Hg, mean +/- SD), and three patients were normoxemic (PaO2 = 89 +/- 6 mm Hg). In each hypoxemic patient, the VA/Q distributions were characterized by the presence of low VA/Q units. A negative logarithmic correlation was found between the dispersion of the blood flow distribution and the arterial PO2. An acute inspiratory hypoxia (FIO2, 0.125) elicited an increase in pulmonary vascular resistance by 58.5% in the hypoxemic group and by 81.6% in the normoxemic one (p = NS between the two groups). The percent change in pulmonary vascular resistance induced by hypoxia was not correlated with the percent change in the dispersion of the blood flow distribution. A theoretical analysis showed that the mean arterial PO2 of 69 mm Hg of the hypoxemic group differed from a normal reference value of 96 mm Hg as a result of the combined effects of reduced hemoglobin (-4 mm Hg), increased P50 (+4 mm Hg), increased ventilation (+10 mm Hg), low VA/Q (-35 mm Hg), and true shunt (-2 mm Hg). These results show that the "hypoxemia of liver cirrhosis" is essentially caused by VA/Q mismatching, which is not explained by an abnormal hypoxic pulmonary vasoconstriction.

Published
1989
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39. Hypoxic pulmonary vasoconstriction and pulmonary gas exchange in normal man.

Author

Mélot C, Naeije R, Hallemans R, Lejeune P, and Mols P

Subjects
Adult, Blood Pressure, Cardiac Output, Female, Humans, Male, Middle Aged, Nifedipine pharmacology, Vascular Resistance, Hypoxia physiopathology, Pulmonary Circulation drug effects, Pulmonary Gas Exchange, Vasoconstriction drug effects
Abstract

Blood gases, hemodynamics and ventilation were measured in 7 healthy volunteers at baseline while breathing room air (FIO2 0.21), during hypoxia (FIO2 0.125, 15 min) and after nifedipine 20 mg sublingually at FIO2 0.21 (45 min) and at FIO2 0.125 (15 min). Distributions of ventilation-perfusion ratios (VA/Q) were determined, using the multiple inert gas elimination technique, at baseline, during hypoxia, and again during hypoxia after nifedipine intake. Hypoxia was associated with an average increase in pulmonary vascular resistances by 104%, which was partially inhibited by nifedipine. The inert gas data showed a mild deterioration in the distribution of VA/Q ratios during hypoxia. However, when blood flow and ventilation were constrained to the baseline normoxic values in the distributions recovered during hypoxia ('normalization procedure') a slight improvement in VA/Q matching could be evidenced, which was blunted during hypoxia after nifedipine. This was interpreted as the functional effect of hypoxic pulmonary vasoconstriction (HPV). Using the 'normalized' distributions, we computed the relationship between the decrease in compartmental blood flow that occurred during hypoxia and the corresponding alveolar PO2, and calculated the gain due to HPV feedback using equations of the control theory. The contribution of HPV to the stability of compartmental VA/Q was greatest for alveolar PO2 values around 60 mm Hg, but at best the feedback had only a moderate efficiency.

Published
1987
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41. Systemic and regional hemodynamic effects of isosorbide dinitrate in patients with liver cirrhosis and portal hypertension.

Author

Mols P, Hallemans R, Melot C, Lejeune P, and Naeije R

Subjects
Adult, Aged, Blood Gas Analysis, Female, Humans, Hypertension, Portal complications, Hypertension, Portal physiopathology, Indocyanine Green, Isosorbide Dinitrate therapeutic use, Kidney blood supply, Liver Circulation drug effects, Liver Cirrhosis physiopathology, Male, Middle Aged, Hemodynamics drug effects, Hypertension, Portal drug therapy, Isosorbide Dinitrate pharmacology, Liver Cirrhosis complications
Abstract

In a group of 17 cirrhotic patients with portal hypertension, we have investigated the effects of 5 mg sublingual administration of isosorbide dinitrate (IDN) on central hemodynamics, on regional (hepatic and renal) hemodynamics and on blood gases. Fifteen min after drug administration, we observed a decrease in the right atrial mean pressure from 4 +/- 1 to 3 +/- 1 mmHg (mean +/- S.E.M., P less than 0.02) and of pulmonary arterial wedge pressure from 7 +/- 1 to 4 +/- 1 mmHg (P less than 0.001) with decreases of the cardiac index from 4.2 +/- 0.2 to 3.7 +/- 0.2 l/min/m2 (P less than 0.001) and the mean arterial pressure from 89 +/- 4 to 72 +/- 3 mmHg (P less than 0.001) and an increase in heart rate from 86 +/- 4 to 94 +/- 5 beats/min (P less than 0.001). Arterial PO2 decreased from 73 +/- 2 to 66 +/- 2 mmHg (P less than 0.001). As a consequence of both cardiac index and arterial PO2 reductions, O2 transport to the tissues was reduced from 602 +/- 32 to 518 +/- 26 ml/min.m2 (P less than 0.001). The hepatic venous pressure gradient decreased from 17 +/- 1 to 14 +/- 1 mmHg (P less than 0.001) and hepatic vein PO2 did not change. The hepatic blood flow (HBF) determined in 7 patients remained unchanged. Renal blood flow (RBF) determined in 5 patients decreased from 0.76 +/- 0.11 to 0.68 +/- 0.11 l/min (P less than 0.001). In conclusion, isosorbide dinitrate reduces portal hypertension in patients with liver cirrhosis without compromising hepatic perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Published
1989
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42. Acute hemodynamic effects of controlled oxygen therapy in decompensated chronic obstructive pulmonary disease.

Author

Lejeune P, Mols P, Naeije R, Hallemans R, and Melot C

Subjects
Adult, Aged, Blood Gas Analysis, Female, Humans, Male, Middle Aged, Hemodynamics, Lung Diseases, Obstructive therapy, Oxygen Inhalation Therapy methods
Abstract

The acute effects of controlled O2 therapy on hemodynamics and blood gases were investigated in 22 patients with decompensated chronic obstructive pulmonary disease (COPD). An inspired O2 fraction (FIO2) of 0.24 and 0.28 given to the first 12 patients markedly improved arterial and mixed-venous blood oxygenation with no (FIO2 0.24) or slight (FIO2 0.28) aggravation of hypercapnia, but did not change O2 delivery to the tissues. Higher FIO2 values of 0.35 and 0.40 in the next ten patients improved blood oxygenation even more, together with an increase in O2 delivery to the tissues and a significant aggravation of hypercapnia. All four FIO2 values reduced cardiac output without changing pulmonary vascular resistance. These results suggest that in patients with decompensated COPD, low-flow O2 improves oxygenation by diffusion rather than convection. On the other hand, controlled O2 therapy does not appear to be an immediately effective pulmonary vasodilating treatment in these patients.

Published
1984
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43. Absence of parasympathetic control of pulmonary vascular pressure-flow plots in hyperoxic and hypoxic dogs.

Author

Lejeune P, Vachiery JL, Leeman M, Brimioulle S, Hallemans R, Melot C, and Naeije R

Subjects
Animals, Dogs, Hemodynamics, Pulmonary Circulation drug effects, Atropine pharmacology, Hypoxia physiopathology, Oxygen pharmacology, Parasympathetic Nervous System physiology, Pulmonary Circulation physiology, Vagotomy
Abstract

Hypoxic stimulation of the peripheral chemoreceptors has been reported to inhibit hypoxic pulmonary vasoconstriction (HPV). This has been explained by a reflex vagal (Chapleau et al., 1988) or sympathetic (Naeije et al., 1989) pulmonary vasodilation. We therefore investigated the effects of bilateral cervical vagotomy and of muscarinic block (atropine sulfate 0.1 mg.kg-1 i.v.) on multipoint pulmonary arterial pressure (Ppa)-cardiac index (Q) plots in 16 sodium pentobarbital-anesthetized dogs ventilated alternately in hyperoxia (fraction of inspired O2, FIO2, 0.4) and in hypoxia (FIO2 0.1). Over the range of Q studied, 2 to 5 L.min-1.m-2, hypoxia increased Ppa and did not change pulmonary capillary wedge pressure (Ppw). After bilateral cervical vagotomy or after atropine, Ppa and Ppw at all levels of Q were not modified either during hyperoxia or during hypoxia. These results show that the parasympathetic system does not affect the global hypoxia-induced pulmonary vasopressor response and thus suggest that the depressor effect of chemoreceptor stimulation on HPV is not vagally mediated.

Published
1989
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44. Improvement in ventilation-perfusion matching by almitrine in COPD.

Author

Mélot C, Naeije R, Rothschild T, Mertens P, Mols P, and Hallemans R

Subjects
Administration, Oral, Aged, Almitrine, Carbon Dioxide blood, Hemodynamics drug effects, Humans, Lung physiopathology, Lung Diseases, Obstructive physiopathology, Male, Middle Aged, Oxygen blood, Piperazines pharmacology, Pulmonary Circulation drug effects, Central Nervous System Stimulants therapeutic use, Lung Diseases, Obstructive drug therapy, Piperazines therapeutic use, Ventilation-Perfusion Ratio drug effects
Abstract

Almitrine, a peripheral chemoreceptor stimulating drug, was given 100 mg orally to six patients with advanced chronic obstructive pulmonary disease (COPD), and its effects on hemodynamics, blood gases, lung mechanics, and the distribution of ventilation/perfusion ratios (VA/Q), determined by the inert gas elimination technique, were investigated. Arterial Po2 increased from 52 +/- 4 to 59 +/- 3 mm Hg, mean +/- SEM, p less than 0.01, arterial Pco2 decreased from 46 +/- 3 to 43 +/- 3 mm Hg, p less than 0.05, and venous admixture from 30 +/- 6 to 19 +/- 3 percent, p less than 0.02. No change occurred in ventilation, variables of lung mechanics, systemic and pulmonary hemodynamics, except an increase in pulmonary vascular resistance (from 364 +/- 103 to 438 +/- 99 dyne.s.cm-5, p less than 0.05). A reduction in VA/Q inequality could be demonstrated with a redistribution of blood flow into the lungs by a diversion of 15 percent of total blood flow from units with low VA/Q (between 0.08 and 0.4) to units with normal VA/Q (between 0.5 and 1.8). These changes might be explained by an enhancement of hypoxic pulmonary vasoconstriction. Pharmacologic peripheral chemoreceptor stimulation, at an infra-ventilatory analeptic dosage, might be of therapeutic interest to patients with respiratory insufficiency due to VA/Q inequality.

Published
1983
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