35 results on '"Skovgaard, Nini"'
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2. Low cost of pulmonary ventilation in American alligators (Alligator mississippiensis) stimulated with doxapram
- Author
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Skovgaard, Nini, primary, Crossley, Dane A., additional, and Wang, Tobias, additional
- Published
- 2016
- Full Text
- View/download PDF
3. Protection against high intravascular pressure in giraffe legs
- Author
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Petersen, Karin K., primary, Hørlyck, Arne, additional, Østergaard, Kristine H., additional, Andresen, Joergen, additional, Broegger, Torbjoern, additional, Skovgaard, Nini, additional, Telinius, Niklas, additional, Laher, Ismael, additional, Bertelsen, Mads F., additional, Grøndahl, Carsten, additional, Smerup, Morten, additional, Secher, Niels H., additional, Brøndum, Emil, additional, Hasenkam, John M., additional, Wang, Tobias, additional, Baandrup, Ulrik, additional, and Aalkjaer, Christian, additional
- Published
- 2013
- Full Text
- View/download PDF
4. Hydrogen sulfide mediates hypoxic vasoconstriction through a production of mitochondrial ROS in trout gills
- Author
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Skovgaard, Nini, primary and Olson, Kenneth R., additional
- Published
- 2012
- Full Text
- View/download PDF
5. Circulating nitric oxide metabolites and cardiovascular changes in the turtle Trachemys scripta during normoxia, anoxia and reoxygenation
- Author
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Jacobsen, Søren B., primary, Hansen, Marie N., additional, Jensen, Frank B., additional, Skovgaard, Nini, additional, Wang, Tobias, additional, and Fago, Angela, additional
- Published
- 2012
- Full Text
- View/download PDF
6. Humoral regulation of heart rate during digestion in pythons (Python molurusandPython regius)
- Author
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Enok, Sanne, primary, Simonsen, Lasse Stærdal, additional, Pedersen, Signe Vesterskov, additional, Wang, Tobias, additional, and Skovgaard, Nini, additional
- Published
- 2012
- Full Text
- View/download PDF
7. Vasoactivity of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta)
- Author
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Stecyk, Jonathan A. W., primary, Skovgaard, Nini, additional, Nilsson, Göran E., additional, and Wang, Tobias, additional
- Published
- 2010
- Full Text
- View/download PDF
8. Histamine induces postprandial tachycardia through a direct effect on cardiac H2-receptors in pythons
- Author
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Skovgaard, Nini, primary, Møller, Kate, additional, Gesser, Hans, additional, and Wang, Tobias, additional
- Published
- 2009
- Full Text
- View/download PDF
9. Hydrogen sulfide as an oxygen sensor in trout gill chemoreceptors
- Author
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Olson, Kenneth R., primary, Healy, Michael J., additional, Qin, Zhaohong, additional, Skovgaard, Nini, additional, Vulesevic, Branka, additional, Duff, Douglas W., additional, Whitfield, Nathan L., additional, Yang, Guangdong, additional, Wang, Rui, additional, and Perry, Steve F., additional
- Published
- 2008
- Full Text
- View/download PDF
10. Reappraisal of H2S/sulfide concentration in vertebrate blood and its potential significance in ischemic preconditioning and vascular signaling
- Author
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Whitfield, Nathan L., primary, Kreimier, Edward L., additional, Verdial, Francys C., additional, Skovgaard, Nini, additional, and Olson, Kenneth R., additional
- Published
- 2008
- Full Text
- View/download PDF
11. Hypoxia-induced vasoconstriction in alligator (Alligator mississippiensis) intrapulmonary arteries: a role for endothelin-1?
- Author
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Skovgaard, Nini, primary, Zibrandtsen, Helle, additional, Laursen, Britt Elmedal, additional, Simonsen, Ulf, additional, and Wang, Tobias, additional
- Published
- 2008
- Full Text
- View/download PDF
12. Evidence that neurotensin mediates postprandial intestinal hyperemia in the python, Python regius
- Author
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Skovgaard, Nini, primary, Conlon, J. Michael, additional, and Wang, Tobias, additional
- Published
- 2007
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- View/download PDF
13. Cardiovascular changes under normoxic and hypoxic conditions in the air-breathing teleostSynbranchus marmoratus: importance of the venous system
- Author
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Skals, Marianne, primary, Skovgaard, Nini, additional, Taylor, Edwin W., additional, Leite, Cleo A. C., additional, Abe, Augusto S., additional, and Wang, Tobias, additional
- Published
- 2006
- Full Text
- View/download PDF
14. Hypoxic pulmonary vasoconstriction in reptiles: a comparative study of four species with different lung structures and pulmonary blood pressures
- Author
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Skovgaard, Nini, primary, Abe, Augusto S., additional, Andrade, Denis V., additional, and Wang, Tobias, additional
- Published
- 2005
- Full Text
- View/download PDF
15. Venous tone and cardiac function in the South American rattlesnakeCrotalus durissus: mean circulatory filling pressure during adrenergic stimulation in anaesthetised and fully recovered animals
- Author
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Skals, Marianne, primary, Skovgaard, Nini, additional, Abe, Augusto S., additional, and Wang, Tobias, additional
- Published
- 2005
- Full Text
- View/download PDF
16. Endothelin-1 causes systemic vasodilatation in anaesthetised turtles(Trachemys scripta) through activation of ETB-receptors
- Author
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Skovgaard, Nini, primary, Warren, Daniel E., additional, Jackson, Donald C., additional, and Wang, Tobias, additional
- Published
- 2005
- Full Text
- View/download PDF
17. Cardiovascular actions of rattlesnake bradykinin ([Val1,Thr6]bradykinin) in the anesthetized South American rattlesnakeCrotalus durissus terrificus
- Author
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Galli, Gina L. J., primary, Skovgaard, Nini, additional, Abe, Augusto S., additional, Taylor, Edwin W., additional, Conlon, J. Michael, additional, and Wang, Tobias, additional
- Published
- 2005
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- View/download PDF
18. Humoral regulation of heart rate during digestion in pythons (Python molurus and Python regius).
- Author
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Enok, Sanne, Simonsen, Lasse Stærdal, Pedersen, Signe Vesterskov, Wang, Tobias, and Skovgaard, Nini
- Abstract
Pythons exhibit a doubling of heart rate when metabolism increases several times during digestion. Pythons, therefore, represent a promising model organism to study autonomic cardiovascular regulation during the postprandial state, and previous studies show that the postprandial tachycardia is governed by a release of vagal tone as well as a pronounced stimulation from nonadrenergic, noncholinergic (NANC) factors. Here we show that infusion of plasma from digesting donor pythons elicit a marked tachycardia in fasting snakes, demonstrating that the NANC factor resides in the blood. Injections of the gastrin and cholecystokinin receptor antagonist proglumide had no effect on double-blocked heart rate or blood pressure. Histamine has been recognized as a NANC factor in the early postprandial period in pythons, but the mechanism of its release has not been identified. Mast cells represent the largest repository of histamine in vertebrates, and it has been speculated that mast cells release histamine during digestion. Treatment with the mast cell stabilizer cromolyn significantly reduced postprandial heart rate in pythons compared with an untreated group but did not affect double-blocked heart rate. While this study indicates that histamine induces postprandial tachycardia in pythons, its release during digestion is not stimulated by gastrin or cholecystokinin nor is its release from mast cells a stimulant of postprandial tachycardia. [ABSTRACT FROM AUTHOR]
- Published
- 2012
- Full Text
- View/download PDF
19. Histamine induces postprandial tachycardia through a direct effect on cardiac H2-receptors in pythons.
- Author
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Skovgaard, Nini, M&3x00F8;Iler, Kate, Gesser, Hans, and Wang, Tobias
- Subjects
- *
HISTAMINE , *HEART beat , *TACHYCARDIA , *INFLAMMATORY mediators , *BLOOD pressure , *ANTIHISTAMINES , *BIOCHEMISTRY - Abstract
The intrinsic heart rate of most vertebrates studied, including humans, is elevated during digestion, suggesting that a nonadrenergic-noncholinergic factor contributes to the postprandial tachycardia. The regulating factor, however, remains elusive and difficult to identify. Pythons can ingest very large meals, and digestion is associated with a marked rise in metabolism that is sustained for several days. The metabolic rise causes more than a doubling of heart rate and a fourfold rise in cardiac output. This makes the python an interesting model to investigate the postprandial tachycardia. We measured blood pressure and heart rate in fasting Python regius, and at 24 and 48 h after ingestion of a meal amounting to 25% of body wt. Digestion caused heart rate to increase from 25 to 56 mm, whereas blood pressure was unchanged. The postprandial rise in heart rate was partially due to a doubling of intrinsic heart rate. The H2-antagonist did not affect heart rate of fasting snakes but decreased heart rate by 15-20 mm at 24 h into digestion, whereas it had no effects at 48 h. Thus, the histaminergic tone on the heart rose from none to 30% at 24 h but vanished after 48 h. In anesthetized snakes, histamine caused a systemic vasodilatation and a marked increase in heart rate and cardiac output mediated through a direct effect on H2- receptors. Our study strongly indicates that histamine regulates heart rate during the initial phase of digestion in pythons. This study describes a novel regulation of the vertebrate heart. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
20. Reappraisal of H2S/sulfide concentration in vertebrate blood and its potential significance in ischemic preconditioning and vascular signaling.
- Author
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Whitfield, Nathan L., Kreimier, Edward L., Verdial, Francys C., Skovgaard, Nini, and Olson, Kenneth R.
- Subjects
HYDROGEN sulfide ,MOLECULES ,BLOOD plasma ,MYOCARDIUM ,HYPOXEMIA - Abstract
Hydrogen sulfide (H
2 S) is rapidly emerging as a biologically significant signaling molecule. Studies published before 2000 report low or undetectable H2 S (usually as total sulfide) levels in blood or plasma, whereas recent work has reported sulfide concentrations between 10 and 300 µM. suggesting it acts as a circulating signal. In the first series of experiments, we used a recently developed polarographic sensor to measure the baseline level of endogenous H2 S gas and turnover of exogenous H2 S gas in real time in blood from numerous animals, including lamprey, trout, mouse, rat, pig, and cow. We found that, contrary to recent reports, H2 S gas was essentially undetectable (<100 nM total sulfide) in all animals. Furthermore, exogenous sulfide was rapidly removed from blood, plasma, or 5% bovine serum albumin in vitro and from intact trout in vivo. To determine if blood H2 S could transiently increase, we measured oxygen-dependent H2 5 production by trout hearts in vitro and in vivo. H2 S has been shown to mediate ischemic preconditioning (IPC) in mammals. IPC is present in trout and, unlike mammals, the trout myocardium obtains its oxygen from relatively hypoxic systemic venous blood. In vitro, myocardial H2 S production was inversely related to Po2 , whereas we failed to detect H2 S in ventral aortic blood from either normoxic or hypoxic fish in vivo. These results provide an autocrine or paracrine mechanism for myocardial coupling of hypoxia to H2 S in IPC, i.e., oxygen sensing, but they fail to provide any evidence that H2 S signaling is mediated by the circulation. [ABSTRACT FROM AUTHOR]- Published
- 2008
- Full Text
- View/download PDF
21. Cardiovascular changes under normoxic and hypoxic conditions in the air-breathing teleost Synbranchus marmoratus: importance of the venous system.
- Author
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Skals, Marianne, Skovgaard, Nini, Taylor, Edwin W., Leite, Cleo A. C., Abe, Augusto S., and Wang, Tobias
- Subjects
- *
FISHES , *VENTILATION , *ADRENALINE , *ISOPROTERENOL , *ADRENERGIC receptors , *HYPOXEMIA - Abstract
Synbranchus marmoratus is a facultative air-breathing fish, which uses its buccal cavity as well as its gills for air-breathing. S. marmoratus shows a very pronounced tachycardia when it surfaces to air-breathe. An elevation of heart rate decreases cardiac filling time and therefore may cause a decline in stroke volume (Vs), but this can be compensated for by an increase in venous tone to maintain stroke volume. Thus, the study on S. marmoratus was undertaken to investigate how stroke volume and venous function are affected during air-breathing. To this end we measured cardiac output (a), heart rate (fH), central venous blood pressure (PCV), mean circulatory filling pressure (MCFP), and dorsal aortic blood pressures (PDA) in S. marmoratus. Measurements were performed in aerated water (PO2>130 mmHg), when the fish alternated between gill ventilation and prolonged periods of apnoeas, as well as during hypoxia (PO2⩽50 mmHg), when the fish changed from gill ventilation to air-breathing. Q increased significantly (luring gill ventilation compared to apnoea in aerated water through a significant increase in both fH and Vs. PCV and MCFP also increased significantly. During hypoxia, when the animals surface to ventilate air, we found a marked rise in fH, PCV, MCFP, Q and VS, whereas FDA decreased significantly. Simultaneous increases in PCV and MCFP in aerated, as well as in hypoxic water, suggests that the venous system plays an important regulatory role for cardiac filling and Vs in this species. In addition, we investigated adrenergic regulation of the venous system through bolus infusions of adrenergic agonists (adrenaline, phenylephrine and isoproterenol; 2 µg kg-1). Adrenaline and phenylephrine caused a marked rise in FCV and MCFP, whereas isoproterenol led to a marked decrease in FCV, and tended to decrease MCFP. Thus, it is evident that stimulation of both α- and β-adrenoreceptors affects venous tone in S. marmoratus. [ABSTRACT FROM AUTHOR]
- Published
- 2006
- Full Text
- View/download PDF
22. Endothelin-1 causes systemic vasodilatation in anaesthetised turtles (Trachemys scripta) through activation of ETB--receptors.
- Author
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Skovgaard, Nini, Warren, Daniel E., Jackson, Donald C., and Wang, Tobias
- Subjects
- *
TRACHEMYS scripta , *TURTLES , *BLOOD flow , *BLOOD circulation , *ENDOTHELINS - Abstract
The effects of endothelin-1 (ET-1) on systemic and pulmonary circulation were investigated in anaesthetised freshwater turtles (Trachemys scripta) instrumented with arterial catheters and blood flow probes. Bolus intra-arterial injections of ET-1 (0.4–400 pmol kg-1) caused a dose-dependent systemic vasodilatation that was associated with a decrease in systemic pressure (Psys) and a rise in systemic blood flow (Qsys), causing systemic conductance (Gsys) to increase. ET-1 had no significant effects on the pulmonary vasculature, heart rate (fH) or total stroke volume (VStot). This response differs markedly from mammals, where ET-1 causes an initial vasodilatation that is followed by a pronounced pressor response. In mammals, the initial dilatation is caused by stimulation of ETB-receptors, while the subsequent constriction is mediated by ETA-receptors. In the turtles, infusion of the ETB-receptor agonist BQ-3020 (150 pmol kg-1) elicited haemodynamic changes that were similar to those of ET-1, and the effects of ET-1 were not affected by the ETA-antagonist BQ-610 (0.15 μmol kg-1). Conversely, all effects of ET-1 were virtually abolished after specific ETB-receptor blockade with the ETB-antagonist BQ-788 (0.15 μmol kg-1). The subsequent treatment with the general ET-receptor antagonist tezosentan (15.4 μmol kg-1) did not produce effects that differed from the treatment with ETB-antagonist, and the blockade of ET-1 responses persisted. This present study indicates, therefore, that ETB-receptors are responsible for the majority of the cardiovascular responses to ET-1 in Trachemys. [ABSTRACT FROM AUTHOR]
- Published
- 2005
- Full Text
- View/download PDF
23. Venous tone and cardiac function in the South American rattlesnake Crotalus durissus: mean circulatory filling pressure during adrenergic stimulation in anaesthetised and fully recovered animals.
- Author
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Skals, Marianne, Skovgaard, Nini, Abe2, Augusto S., and Wang, Tobias
- Subjects
- *
RATTLESNAKES , *CROTALUS , *SNAKES , *SYMPATHOMIMETIC agents , *BLOOD - Abstract
The effects of adrenergic stimulation on mean circulatory filling pressure (MCFP), central venous pressure (PCV) and stroke volume (Vs), as well as the effects of altered MCFP through changes of blood volume were investigated in rattlesnakes (Crotalus durissus). MCFP is an estimate of the upstream pressure driving blood towards the heart and is determined by blood volume and the activity of the smooth muscle cells in the veins (venous tone). MCFP can be determined as the plateau in PCV during a total occlusion of blood flow from the heart. VS decreased significantly when MCFP was lowered by reducing blood volume in anaesthetised snakes, whereas increased MCFP through infusion of blood (up to 3 ml kg-1) only led to a small rise in Vs. Thus, it seems that end-diastolic volume is not affected by an elevated MCFP in rattlesnakes. To investigate adrenergic regulation on venous tone, adrenaline as well as phenylephrine and isoproterenol (α- and β-adrenergic agonists, respectively) were infused as bolus injections (2 and 10 μg kg-1). Adrenaline and phenylephrine caused large increases in MCFP and PCV, whereas isoproterenol decreased both parameters. This was also the case in fully recovered snakes. Therefore, adrenaline affects venous tone through both α- and β-adrenergic receptors, but the α-adrenergic receptor dominates at the dosages used in the present study. Injection of the nitric oxide donor SNP caused a significant decrease in PCV and MCFP. Thus, nitric oxide seems to affect venous tone. [ABSTRACT FROM AUTHOR]
- Published
- 2005
- Full Text
- View/download PDF
24. Cardiovascular actions of rattlesnake bradykinin ([Val¹,Thr6]bradykinin) in the anesthetized South American rattlesnake Crotalus durissus terrificus.
- Author
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Galli, Gina L.J., Skovgaard, Nini, Abe, Augusto S., Taylor, Edwin W., Conlon, J. Michael, and Wang, Tobias
- Subjects
- *
BRADYKININ , *CROTALUS , *CATECHOLAMINES , *NITRIC oxide , *ADRENERGIC receptors , *KININS - Abstract
Incubation of heat-denatured plasma from the rattlesnake Crotalus atrox with trypsin generated a bradykinin (BK) that contained two amino acid substitutions (Arg¹ → Val and Ser6 → Thr) compared with mammalian BK. Bolus intra-arterial injections of synthetic rattlesnake BK (0.01-10 nmol/kg) into the anesthetized rattlesnake, Crotalus durissus terrificus, produced a pronounced and concentration-dependent increase in systemic vascular conductance (Gsys). This caused a fall in systemic arterial blood pressure (Psys) and an increase in blood flow. Heart rate and stroke volume also increased. This primary response was followed by a significant rise in Psys and pronounced tachycardia (secondary response). Pretreatment with NG-nitro-L-arginine methyl ester reduced the NK-induced systemic vasodilatation, indicating that the effect is mediated through increased NO synthesis. The tachycardia associated with the late primary and secondary response to BK was abolished with propranolol and the systemic vasodilatation produced in the primary phase was also significantly attenuated by pretreatment, indicating that the responses are caused, at least in part, by release of cathecholamines and subsequent stimulation of β-adrenergic receptors. In contrast, the pulmonary circulation was relatively unresponsive to BK. [ABSTRACT FROM AUTHOR]
- Published
- 2005
- Full Text
- View/download PDF
25. Involvement of Potassium Channels and Calcium-Independent Mechanisms in Hydrogen Sulfide-Induced Relaxation of Rat Mesenteric Small Arteries.
- Author
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Hedegaard ER, Gouliaev A, Winther AK, Arcanjo DD, Aalling M, Renaltan NS, Wood ME, Whiteman M, Skovgaard N, and Simonsen U
- Subjects
- Animals, Electron Transport Complex I drug effects, Electron Transport Complex III antagonists & inhibitors, Hydrogen Sulfide metabolism, In Vitro Techniques, KCNQ Potassium Channels drug effects, Mesenteric Arteries metabolism, Muscle, Smooth, Vascular metabolism, Myosin Light Chains drug effects, Myosin Light Chains metabolism, Myosin-Light-Chain Phosphatase antagonists & inhibitors, Phosphorylation, Potassium Channel Blockers pharmacology, Protein Kinase Inhibitors pharmacology, Rats, Rats, Wistar, Vasodilation drug effects, Calcium metabolism, Hydrogen Sulfide pharmacology, Mesenteric Arteries drug effects, Muscle Relaxation drug effects, Muscle, Smooth, Vascular drug effects, Potassium Channels drug effects
- Abstract
Endogenous hydrogen sulfide (H2S) is involved in the regulation of vascular tone. We hypothesized that the lowering of calcium and opening of potassium (K) channels as well as calcium-independent mechanisms are involved in H2S-induced relaxation in rat mesenteric small arteries. Amperometric recordings revealed that free [H2S] after addition to closed tubes of sodium hydrosulfide (NaHS), Na2S, and GYY4137 [P-(4-methoxyphenyl)-P-4-morpholinyl-phosphinodithioic acid] were, respectively, 14%, 17%, and 1% of added amount. The compounds caused equipotent relaxations in isometric myographs, but based on the measured free [H2S], GYY4137 caused more relaxation in relation to released free H2S than NaHS and Na2S in rat mesenteric small arteries. Simultaneous measurements of [H2S] and tension showed that 15 µM of free H2S caused 61% relaxation in superior mesenteric arteries. Simultaneous measurements of smooth muscle calcium and tension revealed that NaHS lowered calcium and caused relaxation of NE-contracted arteries, while high extracellular potassium reduced NaHS relaxation without corresponding calcium changes. In NE-contracted arteries, NaHS (1 mM) lowered the phosphorylation of myosin light chain, while phosphorylation of myosin phosphatase target subunit 1 remained unchanged. Protein kinase A and G, inhibitors of guanylate cyclase, failed to reduce NaHS relaxation, whereas blockers of voltage-gated KV7 channels inhibited NaHS relaxation, and blockers of mitochondrial complex I and III abolished NaHS relaxation. Our findings suggest that low micromolar concentrations of free H2S open K channels followed by lowering of smooth muscle calcium, and by another mechanism involving mitochondrial complex I and III leads to uncoupling of force, and hence vasodilation., (Copyright © 2015 by The American Society for Pharmacology and Experimental Therapeutics.)
- Published
- 2016
- Full Text
- View/download PDF
26. Protection against high intravascular pressure in giraffe legs.
- Author
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Petersen KK, Hørlyck A, Ostergaard KH, Andresen J, Broegger T, Skovgaard N, Telinius N, Laher I, Bertelsen MF, Grøndahl C, Smerup M, Secher NH, Brøndum E, Hasenkam JM, Wang T, Baandrup U, and Aalkjaer C
- Subjects
- Adaptation, Physiological, Animals, Brachial Artery diagnostic imaging, Brachial Artery pathology, Capillary Permeability, Edema physiopathology, Hydrostatic Pressure, Male, Tibial Arteries diagnostic imaging, Tibial Arteries pathology, Time Factors, Ultrasonography, Vascular Resistance, Vasoconstriction, Arterial Pressure, Brachial Artery physiopathology, Capillaries physiopathology, Edema prevention & control, Lower Extremity blood supply, Ruminants, Tibial Arteries physiopathology
- Abstract
The high blood pressure in giraffe leg arteries renders giraffes vulnerable to edema. We investigated in 11 giraffes whether large and small arteries in the legs and the tight fascia protect leg capillaries. Ultrasound imaging of foreleg arteries in anesthetized giraffes and ex vivo examination revealed abrupt thickening of the arterial wall and a reduction of its internal diameter just below the elbow. At and distal to this narrowing, the artery constricted spontaneously and in response to norepinephrine and intravascular pressure recordings revealed a dynamic, viscous pressure drop along the artery. Histology of the isolated median artery confirmed dense sympathetic innervation at the narrowing. Structure and contractility of small arteries from muscular beds in the leg and neck were compared. The arteries from the legs demonstrated an increased media thickness-to-lumen diameter ratio, increased media volume, and increased numbers of smooth muscle cells per segment length and furthermore, they contracted more strongly than arteries from the neck (500 ± 49 vs. 318 ± 43 mmHg; n = 6 legs and neck, respectively). Finally, the transient increase in interstitial fluid pressure following injection of saline was 5.5 ± 1.7 times larger (n = 8) in the leg than in the neck. We conclude that 1) tissue compliance in the legs is low; 2) large arteries of the legs function as resistance arteries; and 3) structural adaptation of small muscle arteries allows them to develop an extraordinary tension. All three findings can contribute to protection of the capillaries in giraffe legs from a high arterial pressure.
- Published
- 2013
- Full Text
- View/download PDF
27. Hydrogen sulfide mediates hypoxic vasoconstriction through a production of mitochondrial ROS in trout gills.
- Author
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Skovgaard N and Olson KR
- Subjects
- Animals, Antioxidants pharmacology, Ditiocarb pharmacology, Dose-Response Relationship, Drug, Female, Glutathione pharmacology, Hydrogen Peroxide metabolism, Hydrogen Sulfide pharmacology, Male, Models, Animal, Pulmonary Gas Exchange, Superoxide Dismutase antagonists & inhibitors, Vasoconstriction drug effects, Gills metabolism, Hydrogen Sulfide metabolism, Hypoxia physiopathology, Mitochondria metabolism, Reactive Oxygen Species metabolism, Trout physiology, Vasoconstriction physiology
- Abstract
Hypoxic pulmonary vasoconstriction (HPV) is an adaptive response that diverts pulmonary blood flow from poorly ventilated and hypoxic areas of the lung to more well-ventilated parts. This response is important for the local matching of blood perfusion to ventilation and improves pulmonary gas exchange efficiency. HPV is an ancient and highly conserved response, expressed in the respiratory organs of all vertebrates, including lungs of mammals, birds, and reptiles; amphibian skin; and fish gills. The mechanism underlying HPV and how cells sense low Po(2) remains elusive. In perfused trout gills (Oncorhynchus mykiss), acute hypoxia, as well as H(2)S, caused an initial and transient constriction of the vasculature. Inhibition of the enzymes cystathionine-β-synthase and cystathionine-γ-lyase, which blocks H(2)S production, abolished the hypoxic response. Individually blocking the four complexes in the electron transport chain abolished both the hypoxic and the H(2)S-mediated constriction. Glutathione, an antioxidant and scavenger of superoxide, attenuated the vasoconstriction in response to hypoxia and H(2)S. Furthermore, diethyldithiocarbamate, an inhibitor of superoxide dismutase, attenuated the hypoxic and H(2)S constriction. This strongly suggests that H(2)S mediates the hypoxic vasoconstriction in trout gills. H(2)S may stimulate the mitochondrial production of superoxide, which is then converted to hydrogen peroxide (H(2)O(2)). Thus, H(2)O(2) may act as the "downstream" signaling molecule in hypoxic vasoconstriction.
- Published
- 2012
- Full Text
- View/download PDF
28. Vasoactivity of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta).
- Author
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Stecyk JA, Skovgaard N, Nilsson GE, and Wang T
- Subjects
- Alkynes pharmacology, Anesthesia, Animals, Blood Pressure drug effects, Blood Pressure physiology, Body Temperature physiology, Female, Glycine analogs & derivatives, Glycine pharmacology, Hydrogen Sulfide blood, Hydroxylamine pharmacology, Male, Mesenteric Arteries drug effects, Mesenteric Arteries physiology, Oxygen pharmacology, Pulmonary Artery drug effects, Pulmonary Artery physiology, Stroke Volume drug effects, Stroke Volume physiology, Vasoconstriction drug effects, Vasoconstriction physiology, Hydrogen Sulfide pharmacology, Hypoxia physiopathology, Turtles physiology, Vascular Resistance drug effects, Vascular Resistance physiology
- Abstract
Systemic vascular resistance (R(sys)) of freshwater turtles increases substantially during anoxia, but the underlying mechanisms are not fully understood. We investigated whether hydrogen sulfide (H(2)S), an endogenously produced metabolite believed to be an O(2) sensor/transducer of vasomotor tone, contributes to the increased R(sys) of anoxic red-eared slider turtles (Trachemys scripta). Vascular infusion of the H(2)S donor NaHS in anesthetized turtles at 21 degrees C and fully recovered normoxic turtles at 5 degrees C and 21 degrees C revealed H(2)S to be a potent vasoconstrictor of the systemic circulation. Likewise, wire myography of isolated turtle mesenteric and pulmonary arteries demonstrated H(2)S to mediate an anoxia-induced constriction. Intriguingly, however, NaHS did not exert vasoconstrictory effects during anoxia (6 h at 21 degrees C; 14 days at 5 degrees C) when plasma H(2)S concentration, estimated from the colorimetric measurement of plasma acid-labile sulfide concentration, likely increased by approximately 3- and 4-fold during anoxia at 21 degrees C, and 5 degrees C, respectively. Yet, blockade of endogenous H(2)S production by DL-propargylglycine or hydroxylamine (0.44 mmol/kg) partially reversed the decreased systemic conductance (G(sys)) exhibited by 5 degrees C anoxic turtles. These findings suggest that the signal transduction pathway of H(2)S-mediated vasoactivity is either maximally activated in the systemic circulation of anoxic turtles and/or that it is oxygen dependent.
- Published
- 2010
- Full Text
- View/download PDF
29. Histamine induces postprandial tachycardia through a direct effect on cardiac H2-receptors in pythons.
- Author
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Skovgaard N, Møller K, Gesser H, and Wang T
- Subjects
- Anesthesia, Animals, Blood Pressure drug effects, Female, Histamine blood, Histamine Agonists pharmacology, Histamine H1 Antagonists pharmacology, Histamine H2 Antagonists pharmacology, Male, Receptors, Histamine H1 drug effects, Regional Blood Flow drug effects, Sinoatrial Node drug effects, Tachycardia physiopathology, Boidae physiology, Histamine pharmacology, Postprandial Period drug effects, Postprandial Period physiology, Receptors, Histamine H2 drug effects, Tachycardia chemically induced
- Abstract
The intrinsic heart rate of most vertebrates studied, including humans, is elevated during digestion, suggesting that a nonadrenergic-noncholinergic factor contributes to the postprandial tachycardia. The regulating factor, however, remains elusive and difficult to identify. Pythons can ingest very large meals, and digestion is associated with a marked rise in metabolism that is sustained for several days. The metabolic rise causes more than a doubling of heart rate and a fourfold rise in cardiac output. This makes the python an interesting model to investigate the postprandial tachycardia. We measured blood pressure and heart rate in fasting Python regius, and at 24 and 48 h after ingestion of a meal amounting to 25% of body wt. Digestion caused heart rate to increase from 25 to 56 min, whereas blood pressure was unchanged. The postprandial rise in heart rate was partially due to a doubling of intrinsic heart rate. The H(2)-antagonist did not affect heart rate of fasting snakes but decreased heart rate by 15-20 min at 24 h into digestion, whereas it had no effects at 48 h. Thus, the histaminergic tone on the heart rose from none to 30% at 24 h but vanished after 48 h. In anesthetized snakes, histamine caused a systemic vasodilatation and a marked increase in heart rate and cardiac output mediated through a direct effect on H(2)- receptors. Our study strongly indicates that histamine regulates heart rate during the initial phase of digestion in pythons. This study describes a novel regulation of the vertebrate heart.
- Published
- 2009
- Full Text
- View/download PDF
30. Hydrogen sulfide as an oxygen sensor in trout gill chemoreceptors.
- Author
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Olson KR, Healy MJ, Qin Z, Skovgaard N, Vulesevic B, Duff DW, Whitfield NL, Yang G, Wang R, and Perry SF
- Subjects
- Animals, Cells, Cultured, Chemoreceptor Cells drug effects, Chemoreceptor Cells physiopathology, Cystathionine beta-Synthase antagonists & inhibitors, Cystathionine beta-Synthase metabolism, Cystathionine gamma-Lyase antagonists & inhibitors, Cystathionine gamma-Lyase metabolism, Disease Models, Animal, Dose-Response Relationship, Drug, Enzyme Inhibitors pharmacology, Female, Gills drug effects, Gills enzymology, Gills physiopathology, Heart Rate, Hydrogen Sulfide administration & dosage, Hydrogen Sulfide blood, Hypoxia genetics, Hypoxia physiopathology, Injections, Ion-Selective Electrodes, Male, Membrane Potentials, Mitochondria metabolism, Neuroepithelial Cells metabolism, Oncorhynchus mykiss, Polarography, RNA, Messenger metabolism, Receptors, Cell Surface, Reflex, Respiratory Mechanics, Zebrafish, Chemoreceptor Cells metabolism, Gills metabolism, Hydrogen Sulfide metabolism, Hypoxia metabolism, Oxygen metabolism, Signal Transduction drug effects
- Abstract
O2 chemoreceptors elicit cardiorespiratory reflexes in all vertebrates, but consensus on O2-sensing signal transduction mechanism(s) is lacking. We recently proposed that hydrogen sulfide (H2S) metabolism is involved in O2 sensing in vascular smooth muscle. Here, we examined the possibility that H2S is an O2 sensor in trout chemoreceptors where the first pair of gills is a primary site of aquatic O2 sensing and the homolog of the mammalian carotid body. Intrabuccal injection of H2S in unanesthetized trout produced a dose-dependent bradycardia and increased ventilatory frequency and amplitude similar to the hypoxic response. Removal of the first, but not second, pair of gills significantly inhibited H2S-mediated bradycardia, consistent with the loss of aquatic chemoreceptors. mRNA for H2S-synthesizing enzymes, cystathionine beta-synthase and cystathionine gamma-lyase, was present in branchial tissue. Homogenized gills produced H2S enzymatically, and H2S production was inhibited by O2, whereas mitochondrial H2S consumption was O2 dependent. Ambient hypoxia did not affect plasma H2S in unanesthetized trout, but produced a PO2-dependent increase in a sulfide moiety suggestive of increased H2S production. In isolated zebrafish neuroepithelial cells, the putative chemoreceptive cells of fish, both hypoxia and H2S, produced a similar approximately 10-mV depolarization. These studies are consistent with H2S involvement in O2 sensing/signal transduction pathway(s) in chemoreceptive cells, as previously demonstrated in vascular smooth muscle. This novel mechanism, whereby H2S concentration ([H2S]) is governed by the balance between constitutive production and oxidation, tightly couples tissue [H2S] to PO2 and may provide an exquisitely sensitive, yet simple, O2 sensor in a variety of tissues.
- Published
- 2008
- Full Text
- View/download PDF
31. Reappraisal of H2S/sulfide concentration in vertebrate blood and its potential significance in ischemic preconditioning and vascular signaling.
- Author
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Whitfield NL, Kreimier EL, Verdial FC, Skovgaard N, and Olson KR
- Subjects
- Animals, Biomarkers blood, Cattle, Oncorhynchus mykiss, Petromyzon, Polarography, Rats, Rats, Inbred Strains, Sus scrofa, Hydrogen Sulfide blood, Ischemic Preconditioning, Myocardial, Signal Transduction physiology
- Abstract
Hydrogen sulfide (H(2)S) is rapidly emerging as a biologically significant signaling molecule. Studies published before 2000 report low or undetectable H(2)S (usually as total sulfide) levels in blood or plasma, whereas recent work has reported sulfide concentrations between 10 and 300 microM, suggesting it acts as a circulating signal. In the first series of experiments, we used a recently developed polarographic sensor to measure the baseline level of endogenous H(2)S gas and turnover of exogenous H(2)S gas in real time in blood from numerous animals, including lamprey, trout, mouse, rat, pig, and cow. We found that, contrary to recent reports, H(2)S gas was essentially undetectable (<100 nM total sulfide) in all animals. Furthermore, exogenous sulfide was rapidly removed from blood, plasma, or 5% bovine serum albumin in vitro and from intact trout in vivo. To determine if blood H(2)S could transiently increase, we measured oxygen-dependent H(2)S production by trout hearts in vitro and in vivo. H(2)S has been shown to mediate ischemic preconditioning (IPC) in mammals. IPC is present in trout and, unlike mammals, the trout myocardium obtains its oxygen from relatively hypoxic systemic venous blood. In vitro, myocardial H(2)S production was inversely related to Po(2), whereas we failed to detect H(2)S in ventral aortic blood from either normoxic or hypoxic fish in vivo. These results provide an autocrine or paracrine mechanism for myocardial coupling of hypoxia to H(2)S in IPC, i.e., oxygen sensing, but they fail to provide any evidence that H(2)S signaling is mediated by the circulation.
- Published
- 2008
- Full Text
- View/download PDF
32. Evidence that neurotensin mediates postprandial intestinal hyperemia in the python, Python regius.
- Author
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Skovgaard N, Conlon JM, and Wang T
- Subjects
- Anesthesia, Animals, Biological Evolution, Cardiovascular Physiological Phenomena drug effects, Intestines drug effects, Neurotensin pharmacology, Postprandial Period drug effects, Pulmonary Circulation drug effects, Pulmonary Circulation physiology, Splanchnic Circulation drug effects, Stroke Volume drug effects, Stroke Volume physiology, Vasodilation drug effects, Hyperemia physiopathology, Intestines blood supply, Intestines physiology, Neurotensin physiology, Postprandial Period physiology, Snakes physiology
- Abstract
Digestion of large meals in pythons produces substantial increases in heart rate and cardiac output, as well as a dilation of the mesenteric vascular bed leading to intestinal hyperemia, but the mediators of these effects are unknown. Bolus intra-arterial injections of python neurotensin ([His(3), Val(4), Ala(7)]NT) (1 - 1,000 pmol/kg) into the anesthetized ball python Python regius (n = 7) produced a dose-dependent vasodilation that was associated with a decrease in systemic pressure (P(sys)) and increase in systemic blood flow (Q(sys)). There was no effect on pulmonary pressure and conductance. A significant (P < 0.05) increase in heart rate (f(H)) and total cardiac output (Q(tot)) was seen only at high doses (>30 pmol/kg). The systemic vasodilation and increase in Q(tot) persisted after beta-adrenergic blockade with propranolol, but the rise in f(H) was abolished. Also, the systemic vasodilation persisted after histamine H(2)-receptor blockade. In unanesthetized pythons (n = 4), bolus injection of python NT in a dose as low as 1 pmol/kg produced a significant increase in blood flow to the mesenteric artery (177% +/- 54%; mean +/- SE) and mesenteric conductance (219% +/- 74%) without any increase in Q(sys), systemic conductance, P(sys), and f(H). The data provide evidence that NT is an important hormonal mediator of postprandial intestinal hyperemia in the python, but its involvement in mediating the cardiac responses to digestion may be relatively minor.
- Published
- 2007
- Full Text
- View/download PDF
33. Hypoxic pulmonary vasoconstriction in reptiles: a comparative study of four species with different lung structures and pulmonary blood pressures.
- Author
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Skovgaard N, Abe AS, Andrade DV, and Wang T
- Subjects
- Alligators and Crocodiles, Animals, Blood Pressure, Crotalus, Hemodynamics physiology, Lizards, Species Specificity, Hypoxia physiopathology, Lung blood supply, Lung physiopathology, Pulmonary Circulation, Vasoconstriction
- Abstract
Low O2 levels in the lungs of birds and mammals cause constriction of the pulmonary vasculature that elevates resistance to pulmonary blood flow and increases pulmonary blood pressure. This hypoxic pulmonary vasoconstriction (HPV) diverts pulmonary blood flow from poorly ventilated and hypoxic areas of the lung to more well-ventilated parts and is considered important for the local matching of ventilation to blood perfusion. In the present study, the effects of acute hypoxia on pulmonary and systemic blood flows and pressures were measured in four species of anesthetized reptiles with diverse lung structures and heart morphologies: varanid lizards (Varanus exanthematicus), caimans (Caiman latirostris), rattlesnakes (Crotalus durissus), and tegu lizards (Tupinambis merianae). As previously shown in turtles, hypoxia causes a reversible constriction of the pulmonary vasculature in varanids and caimans, decreasing pulmonary vascular conductance by 37 and 31%, respectively. These three species possess complex multicameral lungs, and it is likely that HPV would aid to secure ventilation-perfusion homogeneity. There was no HPV in rattlesnakes, which have structurally simple lungs where local ventilation-perfusion inhomogeneities are less likely to occur. However, tegu lizards, which also have simple unicameral lungs, did exhibit HPV, decreasing pulmonary vascular conductance by 32%, albeit at a lower threshold than varanids and caimans (6.2 kPa oxygen in inspired air vs. 8.2 and 13.9 kPa, respectively). Although these observations suggest that HPV is more pronounced in species with complex lungs and functionally divided hearts, it is also clear that other components are involved.
- Published
- 2005
- Full Text
- View/download PDF
34. Endothelin-1 causes systemic vasodilatation in anaesthetised turtles (Trachemys scripta) through activation of ETB-receptors.
- Author
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Skovgaard N, Warren DE, Jackson DC, and Wang T
- Subjects
- Analysis of Variance, Animals, Blood Pressure, Dose-Response Relationship, Drug, Endothelin Receptor Antagonists, Endothelins pharmacology, Oligopeptides pharmacology, Peptide Fragments pharmacology, Piperidines pharmacology, Pyridines pharmacology, Stroke Volume, Tetrazoles pharmacology, Blood Circulation drug effects, Endothelin-1 pharmacology, Receptors, Endothelin metabolism, Turtles metabolism, Vasodilation drug effects
- Abstract
The effects of endothelin-1 (ET-1) on systemic and pulmonary circulation were investigated in anaesthetised freshwater turtles (Trachemys scripta) instrumented with arterial catheters and blood flow probes. Bolus intra-arterial injections of ET-1 (0.4-400 pmol kg(-1)) caused a dose-dependent systemic vasodilatation that was associated with a decrease in systemic pressure (P(sys)) and a rise in systemic blood flow (Q(sys)), causing systemic conductance (G(sys)) to increase. ET-1 had no significant effects on the pulmonary vasculature, heart rate (fh) or total stroke volume (Vs(tot)). This response differs markedly from mammals, where ET-1 causes an initial vasodilatation that is followed by a pronounced pressor response. In mammals, the initial dilatation is caused by stimulation of ET(B)-receptors, while the subsequent constriction is mediated by ET(A)-receptors. In the turtles, infusion of the ET(B)-receptor agonist BQ-3020 (150 pmol kg(-1)) elicited haemodynamic changes that were similar to those of ET-1, and the effects of ET-1 were not affected by the ET(A)-antagonist BQ-610 (0.15 micromol kg(-1)). Conversely, all effects of ET-1 were virtually abolished after specific ET(B)-receptor blockade with the ET(B)-antagonist BQ-788 (0.15 micromol kg(-1)). The subsequent treatment with the general ET-receptor antagonist tezosentan (15.4 micromol kg(-1)) did not produce effects that differed from the treatment with ET(B)-antagonist, and the blockade of ET-1 responses persisted. This present study indicates, therefore, that ET(B)-receptors are responsible for the majority of the cardiovascular responses to ET-1 in Trachemys.
- Published
- 2005
- Full Text
- View/download PDF
35. Cardiovascular actions of rattlesnake bradykinin ([Val1,Thr6]bradykinin) in the anesthetized South American rattlesnake Crotalus durissus terrificus.
- Author
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Galli GL, Skovgaard N, Abe AS, Taylor EW, Conlon JM, and Wang T
- Subjects
- Amino Acid Sequence, Anesthesia, General veterinary, Animals, Bradykinin chemistry, Bradykinin isolation & purification, Bradykinin pharmacology, Injections, Intra-Arterial veterinary, Time Factors, Bradykinin analogs & derivatives, Crotalus physiology, Hemodynamics drug effects
- Abstract
Incubation of heat-denatured plasma from the rattlesnake Crotalus atrox with trypsin generated a bradykinin (BK) that contained two amino acid substitutions (Arg1 --> Val and Ser6 --> Thr) compared with mammalian BK. Bolus intra-arterial injections of synthetic rattlesnake BK (0.01-10 nmol/kg) into the anesthetized rattlesnake, Crotalus durissus terrificus, produced a pronounced and concentration-dependent increase in systemic vascular conductance (Gsys). This caused a fall in systemic arterial blood pressure (Psys) and an increase in blood flow. Heart rate and stroke volume also increased. This primary response was followed by a significant rise in Psys and pronounced tachycardia (secondary response). Pretreatment with N(G)-nitro-L-arginine methyl ester reduced the NK-induced systemic vasodilatation, indicating that the effect is mediated through increased NO synthesis. The tachycardia associated with the late primary and secondary response to BK was abolished with propranolol and the systemic vasodilatation produced in the primary phase was also significantly attenuated by pretreatment, indicating that the responses are caused, at least in part, by release of cathecholamines and subsequent stimulation of beta-adrenergic receptors. In contrast, the pulmonary circulation was relatively unresponsive to BK.
- Published
- 2005
- Full Text
- View/download PDF
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