Search

Your search keyword '"Hechtman H"' showing total 414 results
Start Over Author "Hechtman H"
414 results on '"Hechtman H"'

1. Mediators of Remote Lung Injury

Author

Lindsay, T., Hill, J., Valeri, C. R., Shepro, D., Hechtman, H. B., Faist, Eugen, editor, Meakins, Jonathan L., editor, and Schildberg, Friedrich W., editor

Published
1993
Full Text
View/download PDF

18. Continuous cardiac output measurement - Aspects of Doppler frequency analysis

Author

Mackay, R. S and Hechtman, H. B

Subjects
Man/System Technology And Life Support
Abstract

From the suprasternal notch blood flow velocity in the aorta can be measured non-invasively by a Doppler probe. Integration over systole after frequency analysis gives a measure of stroke volume if a separate diameter observation is incorporated. Frequency analysis by a zero crossing counter or by a set of parallel phaselock loops was less effective than a set of bandpass filters. Observations on dogs, baboons and humans before and after exercise or surgery suggest the indications to be useful. Application to judging heart failure by the effect of introducing a volume load is indicated. Changes in output also are measured in freely moving subjects.

Published
1975

19. In Vivo Tracking of Platelets: Circulating Degranulated Platelets Rapidly Lose Surface P-Selectin but Continue to Circulate and Function

Author

NAVAL BLOOD RESEARCH LAB BOSTON MA, Michelson, A. D., Barnard, M. R., Hechtman, H. B., Macgregor, H., Connolly, R. J., NAVAL BLOOD RESEARCH LAB BOSTON MA, Michelson, A. D., Barnard, M. R., Hechtman, H. B., Macgregor, H., and Connolly, R. J.

Abstract

To examine the hypothesis that surface P-selectin-positive (degranulated) platelets are rapidly cleared from the circulation, we developed novel methods for tracking of platelets and measurement of platelet function in vivo. Washed platelets prepared from non-human primates (baboons) were labeled with PKH2 (a lipophilic fluorescent dye), thrombin-activated, washed, and re-infused into the same baboons. Three color whole blood flow cytometry was used to simultaneously: (1) identify platelets with a monoclonal antibody directed against GPIIb-IIIa (integrin alpha sub IIb Beta sub 3), (2) distinguish infused platelets by their PKH2 fluorescence, and (3) analyze platelet function with monoclonal antibodies. Two hours after infusion of autologous thrombin-activated platelets (P-selectin-positive, PKH2-labeled), 95 +/- 1% (mean +/- SEM, n = 5) of the circulating PKH2-labeled platelets had become P-selectin-negative. Compared with platelets not activated with thrombin pre-infusion, the recovery of these circulating PKH2-labeled, P-selectin-negative platelets was similar 24 hours after infusion and only slightly less 48 hours after infusion. The loss of platelet surface P-selectin was fully accounted for by a 67.1 +/- 16.7 ng/mL increase in the plasma concentration of soluble P selectin. The circulating PKH2-labeled, P-selectin-negative platelets were still able to function in vivo, as determined by their: (a) participation in platelet aggregates emerging from a bleeding time wound, (b) binding to Dacron in an arteriovenous shunt, (c) binding of monoclonal antibody PAC1 (directed against the fibrinogen binding site on GPIIb-IIIa), and (d) generation of procoagulant platelet-derived microparticles.

Published
1995

20. Ischaemia-Reperfusion Injury: Pathophysiology and Treatment

Author

BOSTON UNIV MA SCHOOL OF MEDICINE, Welbourn, R., Goldman, G., Paterson, I. S., Valeri, C. R., Shepro, D., Hechtman, H. B., BOSTON UNIV MA SCHOOL OF MEDICINE, Welbourn, R., Goldman, G., Paterson, I. S., Valeri, C. R., Shepro, D., and Hechtman, H. B.

Abstract

Ischaemia is a common clinical event leading to local and remote injury. Evidence indicates that tissue damage is largely caused by activated neutrophils which accumulate when the tissue is perfused. If the area of ischaemic tissue is large, neutrophils also sequester in the lungs, inducing non-cardiogenic pulmonary oedema. Ischaemia-reperfusion injury is initiated by production of reactive oxygen species which initially appear responsible for the generation of chemotactic activity for neutrophils. Later, once adherent to endothelium, neutrophils mediate damage by secretion of additional reactive oxygen species as well as proteolytic enzymes, in particular elastase. Therapeutic options for limiting ischaemia-reperfusion injury include inhibition of oxygen radical formation, pharmacological prevention of neutrophil activation and chemotaxis, and also use of monoclonal antibodies which prevent neutrophil-endothelial adhesion, a prerequisite for injury.

Published
1991

28. Thromboxane Modulates Endothelial Permeability

Author

Klausner, J. M., primary, Abu-Abid, S., additional, Alexander, J. S., additional, Hanshke-Mineau, R., additional, Goldman, G., additional, Morel, N., additional, Valeri, C. R., additional, Shepro, D., additional, and Hechtman, H. B., additional

Published
1994
Full Text
View/download PDF

42. Survival and function of baboon RBCs released from clotted blood and washed before autologous transfusion.

Author

Valeri, C. Robert, Ragno, Gina, Pivacek, Linda E., Dennis, Richard C., Hechtman, Herbert B., Khuri, Shukri F., Valeri, C R, Ragno, G, Pivacek, L E, Dennis, R C, Hechtman, H B, and Khuri, S F

Subjects
ERYTHROCYTES, BLOOD coagulation, BABOONS, FIBRINOLYTIC agents, ANIMAL experimentation, BLOOD, AUTOTRANSFUSION of blood, CELL physiology, COMPARATIVE studies, IRRIGATION (Medicine), RESEARCH methodology, MEDICAL cooperation, OXYGEN, PRIMATES, REFERENCE values, RESEARCH, TIME, EVALUATION research, PHARMACODYNAMICS
Abstract

Background: One alternative to an allogeneic transfusion is the salvaging of the patient's own shed blood. In this study, baboon blood was allowed to clot and the RBCs that were released from the clotted blood lysed with and without urokinase were washed before autologous transfusion.Study Design and Methods: Forty-four studies were done in 13 baboons (Papio cynocephalus or Papio anubis) over a 3-year period. In 24 studies, a 50-mL volume of blood was collected without an anticoagulant and stored at 22 degrees C for as long as 72 hours before washing and autologous transfusion. In 20 other studies, a 50-mL volume of blood was collected without an anticoagulant and allowed to clot for 30 to 60 minutes. Urokinase, ranging from 2,500 to 10,000 units per mL, was added, and the blood was stored at 22 degrees C for 24 hours before washing and autologous transfusion.Results: RBCs that were stored at 22 degrees C without urokinase for 24 hours exhibited an in vitro recovery value of 45 percent, a (51)Cr 24-hour posttransfusion survival of 86 percent, and an index of therapeutic effectiveness of 39 percent. The (51)Cr T(50) value was normal at 14 days, and RBC oxygen-transport function was slightly reduced. RBCs that were stored at 22 degrees C for 24 hours with 10,000 units per mL of urokinase exhibited an in vitro recovery value of 89 percent, a (51)Cr 24-hour posttransfusion survival value of 86 percent, and an index of therapeutic effectiveness of 76 percent. The (51)Cr T(50) value was normal at 14 days, and the RBC oxygen-transport function was only slightly reduced.Conclusion: Autologous baboon RBCs isolated from clotted blood treated or not treated with urokinase and washed before transfusion have excellent survival and normal or only slightly reduced oxygen-transport function. [ABSTRACT FROM AUTHOR]

Published
2001
Full Text
View/download PDF

46. Reperfusion pulmonary edema.

Author

Klausner, J M, Paterson, I S, Mannick, J A, Valeri, R, Shepro, D, and Hechtman, H B

Subjects
ABDOMINAL aorta surgery, AORTIC aneurysms, ANIMAL experimentation, COMPARATIVE studies, FREE radicals, ISCHEMIA, LEUKOTRIENES, LUNGS, RESEARCH methodology, MEDICAL cooperation, PULMONARY edema, REPERFUSION injury, RESEARCH, THROMBOXANES, EVALUATION research, SURGERY
Abstract

Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B4 and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. We conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and, third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability. [ABSTRACT FROM AUTHOR]

Published
1989
Full Text
View/download PDF

48. Modulation of phospholipase A2 lytic activity by actin and myosin

Author

Dubose, D. A., Shepro, D., and Hechtman, H. B.

Abstract

Prostacyclin (PGI2) production is closely coupled with endothelial cell shape and F-actin distribution in vitro. These findings may implicate cytoskeletal constituents in a mechanism regulating eicosanoid metabolism. To determine the potential for such a regulatory mechanism, cytoskeletal protein effects on the ratelimiting eicosanoid cascade enzyme (phospholipase A2; PLA2) were studied. Membrane phospholipid degradation was indirectly determined by spectrophotometric measurement of PLA2-induced rat red blood cell ghost (RBC-G) hemolysis. PLA2 was incubated with actin (skeletal, smooth, or nonmuscle cell) at a nonmuscle cell concentration (100µM) and then exposed to the RBC-G. Comparisons in the presence or absence of actin revealed that F-actin stimulated whereas G-actin suppressed PLA2 lytic behavior significantly (P<0.05). When a 10: or 100:1 F-actin to myosin ratio was used, the F-actin stimulatory effect was significantly (P<0.05) reduced. These findings suggest that the in vitro correlation between PGI2 production and endothelial cell shape may be the result of PLA2 regulation by cytoskeletal elements that impart cellular form.

Published
1989
Full Text
View/download PDF

49. Microvascular pericyte contractility in vitro: comparison with other cells of the vascular wall.

Author

Kelley, C, D'Amore, P, Hechtman, H B, and Shepro, D

Abstract

Collagen lattices containing bovine retinal pericytes (RPs), vascular smooth muscle cells (VSMCs), pulmonary microvessel endothelial cells (PMECs), or aortic endothelial cells (AECs) were prepared and contraction was quantitated by measuring the resulting change in lattice area. VSMCs were the most efficient at lattice contraction followed by RPs and then PMECs. AECs did not contract the lattices. To document further that these observations represent contraction, cells were grown on inert silicone rubber sheets. Substratum wrinkling was indicative of tension development and quantitated as percent of cells contracted. RPs were more contractile than PMECs, and AECs were incapable of developing tension. VSMCs were less contractile than RPs, unlike the comparative contractility observed with the lattice system. Alteration of actin-containing filaments by cytochalasin B significantly reduced RP contraction of silicone rubber and inhibited their contraction of collagen lattices in a dose-dependent manner. Rhodamine-phalloidin staining of contracting RPs revealed microfilament bundle orientations that suggested their association in the force applied for contraction. RP, VSMC and PMEC contraction of collagen lattices was directly proportional to the concentration of fetal calf serum. Also, RP contraction was greater in calf serum than calf plasma-derived serum, an indication that RPs respond to substances that appear continuously and episodically in blood. These in vitro findings support the theory that pericytes in vivo are contractile but that endothelial cells may also contribute to microvascular tonus.

Published
1987
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results