Hypoxic pulmonary vasoconstriction in reptiles: a comparative study of four species with different lung structures and pulmonary blood pressures

2005 ◽  
Vol 289 (5) ◽  
pp. R1280-R1288 ◽  
Author(s):  
Nini Skovgaard ◽  
Augusto S. Abe ◽  
Denis V. Andrade ◽  
Tobias Wang
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Blood Perfusion ◽  
Pulmonary Vasculature ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Pulmonary Vasoconstriction ◽  
Local Ventilation

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.

Hypoxia elicits an increase in pulmonary vasculature resistance in anaesthetised turtles (Trachemys scripta)

1998 ◽  
Vol 201 (24) ◽  
pp. 3367-3375 ◽  
Author(s):  
D. Crossley ◽  
J. Altimiras ◽  
T. Wang
Keyword(s):  
Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Trachemys Scripta ◽  
Pulmonary Vasculature ◽  
Low Oxygen ◽  
Systemic Blood Flow ◽  
Oxygen Levels ◽  
Blood Flows ◽  
Pulmonary Vasoconstriction ◽  
Cervical Vagotomy

In mammals and birds, low oxygen levels in the lungs cause a constriction of the pulmonary vasculature. This response is locally mediated and is considered to be important for local matching of perfusion and ventilation. It is not known whether reptiles respond in a similar fashion. The present study describes the effects of altering lung oxygen levels (at a constant FCO2 of 0.03) on systemic and pulmonary blood flows and pressures in anaesthetised (Nembumal, 50 mg kg-1) and artificially ventilated turtles Trachemys scripta. During severe hypoxia (1.5-3 kPa PO2), pulmonary blood flow decreased in all animals; systemic blood flow increased, resulting in an increased net right-to-left shunt blood flow. The redistribution of blood flows was associated with reciprocal changes in the vascular resistances within the pulmonary and the systemic circulations(Rpul and Rsys, respectively). At 1.5 kPa O2, Rpul increased from 0.09 0.01 to 0.15 0.03 kPa ml-1 min kg during normoxia (means 1 s.e.m., N=5). Concurrently, Rsys tended to decrease from a normoxic value of 0.12 0.01 to 0.09 0.02 kPa ml-1 min kg (P=0.08). The effects of hypoxia on the haemodynamic variables persisted following atropinisation (1 mg kg-1) and cervical vagotomy, suggesting that the increased Rpul during hypoxia is locally mediated. This study therefore demonstrates that turtles exhibit hypoxic pulmonary vasoconstriction, although the threshold is low compared with that of mammals.

Predicting The Influence Of Hypoxic Pulmonary Vasoconstriction On The Distribution Of Pulmonary Blood Flow

2011 ◽  
Author(s):  
Kelly S. Burrowes ◽  
Annalisa J. Swan ◽  
Alys R. Clark ◽  
Quentin P.P. Croft ◽  
Keith L. Dorrington ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasoconstriction

Leukotriene inhibitors do not block hypoxic pulmonary vasoconstriction in dogs

1987 ◽  
Vol 62 (5) ◽  
pp. 1808-1813 ◽  
Author(s):  
D. P. Schuster ◽  
D. R. Dennis
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Lower Lobe ◽  
Left Lower Lobe ◽  
The Other ◽  
Pulmonary Vasoconstriction ◽  
Other Hand ◽  
Alveolar Hypoxia

We studied whether intravenously administered inhibitors of leukotriene synthesis (diethylcarbamazine, DEC) or end-organ effect (FPL-55712) would change the distribution of regional pulmonary blood flow (rPBF) caused by left lower lobe (LLL) alveolar hypoxia in dogs. Both drugs failed to alter rPBF. In addition, the pressor response to whole-lung hypoxia was not blocked by an FPL-55712 infusion. On the other hand, nitroprusside, as a nonspecific vasodilator also administered intravenously, was able to partially reverse the effects of LLL hypoxia on rPBF. Thus our data do not support a role for leukotriene mediation of hypoxic pulmonary vasoconstriction in dogs.

Chemoreflex blunting of hypoxic pulmonary vasoconstriction is vagally mediated

1989 ◽  
Vol 66 (2) ◽  
pp. 782-791 ◽  
Author(s):  
L. B. Wilson ◽  
M. G. Levitzky
Keyword(s):  
Blood Flow ◽  
Nervous System ◽  
Pulmonary Blood Flow ◽  
Parasympathetic Nervous System ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Left Lung ◽  
Pulmonary Vasoconstriction ◽  
Anesthetized Dogs ◽  
Bilateral Vagotomy ◽  
Carotid Body Chemoreceptors

We investigated the role of the autonomic nervous system in the arterial chemoreceptor attenuation of hypoxic pulmonary vasoconstriction (HPV) using anesthetized dogs. Total pulmonary blood flow (Qt) and left pulmonary blood flow (Ql) were determined using electromagnetic flow probes. Carotid body chemoreceptors were perfused using blood pumped from an extracorporeal circuit containing an oxygenator. Four groups were used: 1) prevagotomy (control), 2) bilateral vagotomy, 3) post-atropine, and 4) post-propranolol. Left lung hypoxia decreased Ql/Qt from 42.9 +/- 2.9 to 28.1 +/- 3.0%, from 41.1 +/- 5.3 to 26.7 +/- 4.2%, from 38.6 +/- 1.3 to 22.2 +/- 2.4%, and from 48.2 +/- 4.2 to 28.5 +/- 3.7% in the four groups, respectively. Chemoreceptor stimulation during unilateral hypoxia increased Ql/Qt from 28.1 +/- 3.0 to 39.1 +/- 4.9% and from 28.5 +/- 3.7 to 40.6 +/- 3.7% in the control and propranolol groups. However, chemoreceptor stimulation had no effect on Ql/Qt during left lung hypoxia after vagotomy or atropine, as Ql/Qt went from 26.7 +/- 4.2 to 29.3 +/- 5.2% and from 22.2 +/- 2.4 to 24.1 +/- 1.5% in groups 2 and 3, respectively. Because chemoreceptor stimulation did not affect HPV in groups 2 and 3, we conclude that the chemoreceptor attenuation of HPV is mediated by the parasympathetic nervous system.

Hydrogen sulfide mediates hypoxic vasoconstriction through a production of mitochondrial ROS in trout gills

2012 ◽  
Vol 303 (5) ◽  
pp. R487-R494 ◽  
Author(s):  
Nini Skovgaard ◽  
Kenneth R. Olson
Keyword(s):  
Adaptive Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Blood Perfusion ◽  
Amphibian Skin ◽  
Downstream Signaling ◽  
Pulmonary Vasoconstriction ◽  
Mitochondrial Ros ◽  
Transport Chain ◽  
Hypoxic Vasoconstriction

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 Po2 remains elusive. In perfused trout gills ( Oncorhynchus mykiss), acute hypoxia, as well as H2S, caused an initial and transient constriction of the vasculature. Inhibition of the enzymes cystathionine-β-synthase and cystathionine-γ-lyase, which blocks H2S production, abolished the hypoxic response. Individually blocking the four complexes in the electron transport chain abolished both the hypoxic and the H2S-mediated constriction. Glutathione, an antioxidant and scavenger of superoxide, attenuated the vasoconstriction in response to hypoxia and H2S. Furthermore, diethyldithiocarbamate, an inhibitor of superoxide dismutase, attenuated the hypoxic and H2S constriction. This strongly suggests that H2S mediates the hypoxic vasoconstriction in trout gills. H2S may stimulate the mitochondrial production of superoxide, which is then converted to hydrogen peroxide (H2O2). Thus, H2O2 may act as the “downstream” signaling molecule in hypoxic vasoconstriction.

Changes in Regional Pulmonary Blood Flow during Lobar Bronchial Occlusion in Man

1994 ◽  
Vol 86 (5) ◽  
pp. 639-644 ◽  
Author(s):  
N. W. Morrell ◽  
K. S. Nijran ◽  
T. Biggs ◽  
W. A. Seed
Keyword(s):  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Time Course ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Normal Subjects ◽  
Fibreoptic Bronchoscopy ◽  
Pulmonary Vasoconstriction ◽  
Partial Pressures ◽  
Entire Lung ◽  
Alveolar Hypoventilation

1. Acute hypoxic pulmonary vasoconstriction is important in the restoration of ventilation—perfusion balance in the presence of regional alveolar hypoventilation. However, the magnitude and time course of this response in man has not been adequately characterized in regions smaller than an entire lung. We have studied the effectiveness of hypoxic vasoconstriction in diverting blood from hypoxic lobes in normal supine subjects, and have documented the redistribution of pulmonary blood flow under these conditions. 2. Lobar hypoxia was induced for 80–300 s by placing occluding balloon-tipped catheters in lobar bronchi during fibreoptic bronchoscopy in 10 normal subjects. Respiratory gas partial pressures within occluded lobes were measured with a mass spectrometer. The percentage reduction in blood flow to the hypoxic lobes was assessed after injection of 99mTc-labelled albumin by γ-scintigraphy, and compared with a control scan performed 1 week later. A computer program was used to analyse changes in regional pulmonary perfusion. 3. During lobar bronchial occlusion respiratory gas partial pressures rapidly approached reported values for mixed venous partial pressures. After a mean time of occlusion of 3.5 min lobar blood flow was reduced by 47 ± 5%. During occlusions pulmonary blood flow was not evenly redistributed, but was preferentially redistributed to more cranial lung regions. 4. We conclude that acute hypoxic pulmonary vasoconstriction in occluded lobes is more effective at rapidly diverting pulmonary blood flow away from hypoxic lung regions than has previously been reported in man during unilateral hypoxia of an entire lung. Non-uniform redistribution of pulmonary blood flow in the supine subject is likely to be due to compression of the lung bases by the diaphragm in the supine position.

Hypoxic pulmonary vasoconstriction: role of ion channels

2005 ◽  
Vol 98 (1) ◽  
pp. 415-420 ◽  
Author(s):  
Joseph R. H. Mauban ◽  
Carmelle V. Remillard ◽  
Jason X.-J. Yuan
Keyword(s):  
Ion Channels ◽  
Structural Changes ◽  
Chronic Hypoxia ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Vasculature ◽  
Cellular Mechanisms ◽  
Pulmonary Vasoconstriction ◽  
Intracellular Ca ◽  
Medial Hypertrophy

Acute hypoxia induces pulmonary vasoconstriction and chronic hypoxia causes structural changes of the pulmonary vasculature including arterial medial hypertrophy. Electro- and pharmacomechanical mechanisms are involved in regulating pulmonary vasomotor tone, whereas intracellular Ca2+ serves as an important signal in regulating contraction and proliferation of pulmonary artery smooth muscle cells. Herein, we provide a basic overview of the cellular mechanisms involved in the development of hypoxic pulmonary vasoconstriction. Our discussion focuses on the roles of ion channels permeable to K+ and Ca2+, membrane potential, and cytoplasmic Ca2+ in the development of acute hypoxic pulmonary vasoconstriction and chronic hypoxia-mediated pulmonary vascular remodeling.

Nonsustained pulmonary vasoconstriction during acute hypoxia in anesthetized dogs

1975 ◽  
Vol 228 (3) ◽  
pp. 756-761 ◽  
Author(s):  
A Tucker ◽  
JT Reeves
Keyword(s):  
Pulmonary Blood Flow ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Chemical Mediator ◽  
Pulmonary Vasoconstriction ◽  
Initial Rise ◽  
Pulmonary Vasodilator ◽  
Anesthetized Dogs ◽  
Muscle Contractile ◽  
Sustained Increase

The objectives of this study were to describe in greater detail the initial rise and spontaneous decline in acute hypoxic pulmonary vasoconstriction and to investigate a number of mechanisms that could have caused this secondary vasodilation. With the onset of isocapnic hypoxia (Pao2 of 28, 44, or 56 mmHg), pulmonary vascular resistances increased to maximum values at 3 min and then spontaneously declined toward control values. Pulmonary perfusion pressures rose to maxima at approximately 4 min and then also declined. During severe hypoxic exposures (Pao2 of 30-37 mmHg) this secondary vasodilation was found not to be due to beta-adrenergic-induced vasodilation, withdrawal of alpha-adrenergic-induced vasoconstriction, vasodilation caused by a sustained increase in pulmonary blood flow, fatigue of the vascular smooth muscle contractile mechanism, or release of vasodilatory prostaglandins. It is suggested that the decline in hypoxic pulmonary vasoconstriction may be due to an exhaustion of a chemical mediator, release of a pulmonary vasodilator agent, or myogenic stress relaxation.

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