Influence of bronchial arterial PO2 on pulmonary vascular resistance

1991 ◽  
Vol 70 (1) ◽  
pp. 405-415 ◽  
Author(s):  
B. E. Marshall ◽  
C. Marshall ◽  
M. Magno ◽  
P. Lilagan ◽  
G. G. Pietra
Keyword(s):  
Vascular Resistance ◽  
Bronchial Artery ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Arteries ◽  
Vasa Vasorum ◽  
Pulmonary Vasculature ◽  
Mechanically Ventilated ◽  
Bronchial Circulation ◽  
Pulmonary Vasodilation ◽  
Pulmonary Vasoconstriction

In six anesthetized and mechanically ventilated adult sheep, the bronchial artery was perfused with blood from an oxygenator-pump circuit. When the lungs were ventilated with 100% O2 and the bronchial O2 tension (PbrO2) was approximately 600 Torr, the mean of the pulmonary vascular resistances (PVR) measured at the beginning (3.32 +/- 0.29 units) and end (3.17 +/- 0.13 units) of the experiment was 3.24 +/- 0.20 units. When the PbrO2 was changed to 58 +/- 1 Torr, the PVR (2.99 +/- 0.14 units) did not change significantly. However, when the lungs were ventilated with air as PbrO2 was decreased to 91 +/- 4, 77 +/- 3, 56 +/- 2, and 42 +/- 1 Torr, the PVR increased to 3.67 +/- 0.18, 4.03 +/- 0.16, 4.79 +/- 0.19, and 4.71 +/- 0.35 units, respectively. However, when the PbrO2 was decreased further to 26 +/- 1 and 13 +/- 1 Torr, the PVR decreased to 3.77 +/- 0.28 and 3.91 +/- 0.30 units, respectively. In contrast, the bronchial vascular resistance decreased monotonically as PbrO2 decreased. The bronchial circulation supplies vasa vasorum to the walls of all but the smallest pulmonary arteries, and it is therefore suggested that the PO2 of the bronchial circulation is responsible for the bimodal response of the pulmonary vasculature, with stimulation of hypoxic pulmonary vasoconstriction at moderate hypoxemia and of hypoxic pulmonary vasodilation at profound hypoxemia. The physiological and pathophysiological significance of the influence of systemic PO2 on pulmonary vascular tone is discussed.

Development of the pulmonary vasculature in newborn lambs: structure-function relationships

1991 ◽  
Vol 70 (3) ◽  
pp. 1255-1264 ◽  
Author(s):  
R. P. Michel ◽  
J. B. Gordon ◽  
K. Chu
Keyword(s):  
Light Microscopy ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Venous Pressure ◽  
Pulmonary Arteries ◽  
Muscle Thickness ◽  
Pulmonary Vasculature ◽  
Pressure Gradients ◽  
Middle Segment ◽  
Pulmonary Vasoconstriction ◽  
Quantitative Light Microscopy

Our objectives were 1) to describe the quantitative light microscopy and ultrastructure of newborn lamb lungs and 2) to correlate hemodynamic changes during normoxia and hypoxia with the morphology. By light microscopy, we measured the percent muscle thickness (%MT) and peripheral muscularization of pulmonary arteries and veins from 25 lambs aged less than 24 h, 2-4 days, 2 wk, and 1 mo. At the same ages, lungs were isolated and perfused in situ and, after cyclooxygenase blockade with indomethacin, total, arterial (delta Pa), middle (delta Pm), and venous pressure gradients at inspired O2 fractions of 0.28 (mild hyperoxia) and 0.04 (hypoxia) were determined with inflow-outflow occlusion. During mild hyperoxia, delta Pa and delta Pm fell significantly between 2-4 days and 2 wk, whereas during hypoxia, only delta Pm fell. The %MT of all arteries (less than 50 to greater than 1,000 microns diam) decreased, and peripheral muscularization of less than 100-microns-diam arteries fell between less than 4 days and greater than 2 wk. Our data suggest that 1) the %MT of arteries determines normoxic pulmonary vascular resistance, because only arterial and middle segment resistance fell, 2) peripheral muscularization is a major determinant of hypoxic pulmonary vasoconstriction, because we observed a fall with age in peripheral muscularization of less than 100-micron-diam arteries and in delta Pm with hypoxia, and 3) the arterial limit of the middle segment defined by inflow-outflow occlusion lies in 100- to 1,000-microns-diam arteries.

scholarly journals Almitrine as a non ventilatory strategy to improve intrapulmonary shunt in COVID-19 patients

2020 ◽  
Author(s):  
MARIE REINE LOSSER ◽  
COLINE LAPOIX ◽  
BENOIT CHAMPIGNEULLE ◽  
MATTHIEU DELANNOY ◽  
JEAN FRANCOIS PAYEN ◽  
...  
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Dose Effect ◽  
Pharmacological Intervention ◽  
Severe Hypoxemia ◽  
Intrapulmonary Shunt ◽  
Ventilatory Strategy ◽  
Control Series ◽  
Mechanically Ventilated ◽  
Pulmonary Vasodilation ◽  
Pulmonary Vasoconstriction

In severe COVID-19 pulmonary failure, hypoxia is mainly related to pulmonary vasodilation with altered hypoxic pulmonary vasoconstriction (HPV). Besides prone positioning, other non-ventilatory strategies may reduce the intrapulmonary shunt. This study has investigated almitrine, a pharmacological option to improve oxygenation. Patients and Method. A case control series of 17 confirmed COVID-19 mechanically ventilated patients in prone or supine positioning was collected: 10 patients received two doses of almitrine (4 and 12 mcg/kg/min) at 30-45 min interval each, and were compared to 7 control COVID-matched patients conventionally treated. The end-point was the reduction of intra-pulmonary shunt increasing the PaO2 and ScvO2. Results Patients were male (59%) with median (25th, 75th percentiles) age of 70 (54-78) years and a BMI of 29 (23-34). At stable mechanical ventilatory settings, PaO2 (mmHg) at FiO2 1 (135 (85, 195) to 214 (121, 275); p = 0.06) tended to increase with almitrine. This difference was significant when the best PaO2 between the 2 doses was used : 215 (123,294) vs baseline (p = 0.01). A concomitant increase in ScvO2 occurred ((73 (72, 76) to 82 (80, 87); p = 0.02). Eight over 10 almitrine-treated patients increased their PaO2, with no clear dose-effect. During the same time, the controls did not change PaO2. In conclusion, in early COVID-19 with severe hypoxemia, almitrine infusion is associated with improved oxygenation in prone or supine positioning. This pharmacological intervention may offer an alternative and/or an additional effect to proning and might delay or avoid more demanding modalities such as ECMO.

Analysis of flow resistance in the pulmonary arterial circulation: Implications for hypoxic pulmonary vasoconstriction

2021 ◽  
Author(s):  
David Walter Johnson ◽  
Tuhin K. Roy ◽  
Timothy W. Secomb
Keyword(s):  
Essential Role ◽  
Scaling Laws ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Arteries ◽  
Blood Oxygenation ◽  
Pulmonary Vasculature ◽  
Arterial Circulation ◽  
Pulmonary Vasoconstriction ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial

Hypoxic pulmonary vasoconstriction (HPV) plays an essential role in distributing blood in the lung to enhance ventilation-perfusion matching and blood oxygenation. In this study, a theoretical model of the pulmonary vasculature is used to predict the effects of vasoconstriction over specified ranges of vessel diameters on pulmonary vascular resistance (PVR). The model is used to evaluate the ability of hypothesized mechanisms of HPV to account for observed levels of PVR elevation during hypoxia. The vascular structure from pulmonary arteries to capillaries is represented using scaling laws. Vessel segments are modeled as resistive elements and blood flow rates are computed from physical principles. Direct vascular responses to intravascular oxygen levels have been proposed as a mechanism of HPV. In the lung, significant changes in oxygen level occur only in vessels less than 60 μm in diameter. The model shows that observed levels of hypoxic vasoconstriction in these vessels alone cannot account for the elevation of PVR associated with HPV. However, the elevation in PVR associated with HPV can be accounted for if larger upstream vessels also constrict. These results imply that upstream signaling by conducted responses to engage constriction of arterioles plays an essential role in the elevation of PVR during HPV.

Ceramide inhibits Kv currents and contributes to TP-receptor-induced vasoconstriction in rat and human pulmonary arteries

2011 ◽  
Vol 301 (1) ◽  
pp. C186-C194 ◽  
Author(s):  
Javier Moral-Sanz ◽  
Teresa Gonzalez ◽  
Carmen Menendez ◽  
Miren David ◽  
Laura Moreno ◽  
...  
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Arteries ◽  
Inhibitory Effect ◽  
Mesenteric Arteries ◽  
Regulatory Subunit ◽  
Pulmonary Vasculature ◽  
Specific Response ◽  
Pulmonary Vasoconstriction ◽  
293 Cells ◽  
Pkc Ζ

Neutral sphingomyelinase (nSMase)-derived ceramide has been proposed as a mediator of hypoxic pulmonary vasoconstriction (HPV), a specific response of the pulmonary circulation. Voltage-gated K+ (Kv) channels are modulated by numerous vasoactive factors, including hypoxia, and their inhibition has been involved in HPV. Herein, we have analyzed the effects of ceramide on Kv currents and contractility in rat pulmonary arteries (PA) and in mesenteric arteries (MA). The ceramide analog C6-ceramide inhibited Kv currents in PA smooth muscle cells (PASMC). Similar effects were obtained after the addition of bacterial sphingomyelinase (SMase), indicating a role for endogenous ceramide in Kv channel regulation. Kv current was reduced by stromatoxin and diphenylphosphine oxide-1 (DPO-1), selective inhibitors of Kv2.1 and Kv1.5 channels, respectively. The inhibitory effect of ceramide was still present in the presence of stromatoxin or DPO-1, suggesting that this sphingolipid inhibited both components of the native Kv current. Accordingly, ceramide inhibited Kv1.5 and Kv2.1 channels expressed in Ltk− cells. Ceramide-induced effects were reduced in human embryonic kidney 293 cells expressing Kv1.5 channels but not the regulatory subunit Kvβ2.1. The nSMase inhibitor GW4869 reduced the thromboxane-endoperoxide receptor agonist U46619-induced, but not endothelin-1-induced pulmonary vasoconstriction that was partly restored after addition of exogenous ceramide. The PKC-ζ pseudosubstrate inhibitor (PKCζ-PI) inhibited the Kv inhibitory and contractile effects of ceramide. In MA ceramide had no effect on Kv currents and GW4869 did not affect U46619-induced contraction. The effects of SMase were also observed in human PA. These results suggest that ceramide represents a crucial signaling mediator in the pulmonary vasculature.

Adenosine A1-receptor mechanisms antagonize beta-adrenergic pulmonary vasodilation in hypoxia

1994 ◽  
Vol 267 (6) ◽  
pp. H2179-H2185 ◽  
Author(s):  
R. C. McIntyre ◽  
A. Banerjee ◽  
D. D. Bensard ◽  
E. C. Brew ◽  
A. R. Hahn ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Arteries ◽  
Receptor Subtype ◽  
Receptor Blockade ◽  
Beta Adrenergic ◽  
Pulmonary Vasodilation ◽  
Pulmonary Vasoconstriction ◽  
A1 Receptor ◽  
Receptor Beta

Hypoxic pulmonary vasoconstriction is refractory to beta-adrenergic receptor (beta-AR)-mediated pulmonary vasodilation. We hypothesized that hypoxic pulmonary arteries release adenosine (Ado) that antagonizes beta-AR-mediated pulmonary vasodilation. Using isolated rat pulmonary artery rings, we investigated 1) the effect of hypoxia and exogenous Ado on beta-AR-mediated pulmonary vasodilation, 2) the intracellular site of dysfunctional beta-AR-mediated pulmonary vasodilation in hypoxia, and 3) the Ado receptor subtype responsible for dysfunction of beta-AR-mediated pulmonary vasodilation. Hypoxia attenuated normal beta-AR-mediated pulmonary vasodilation to isoproterenol (97.5 +/- 0.8 vs. 71.5 +/- 2.3%, P < 0.01). In contrast, forskolin induced the same vasorelaxation in hypoxic pulmonary rings as controls (P = 0.09). Incubation of normoxic rings with Ado attenuated the vasorelaxation response induced by beta-AR stimulation (71.5 +/- 5.9%, P < 0.01), similar to the effect observed in hypoxia. Both nonspecific Ado receptor blockade (8-sulfophenyl-theophylline) and specific A1-receptor blockade (8-cyclopentyl-1,3-dimethylxanthine) restored the vasorelaxation response of hypoxic rings induced by beta-AR stimulation (93.3 +/- 2.3 and 92.2 +/- 2.8%, P < 0.01). The effects of hypoxia and Ado were reproduced by a specific A1 agonist (2-chloro-N6-cyclopentyladenosine), demonstrating impaired vasorelaxation induced by beta-AR stimulation in normoxia (70.6 +/- 4.5%, P < 0.01). From these data, we conclude that hypoxia antagonizes beta-AR-mediated pulmonary vasodilation via an Ado A1-receptor mechanism.

Increased pulmonary vascular resistance and defective pulmonary artery filling in caveolin-1−/− mice

2008 ◽  
Vol 294 (5) ◽  
pp. L865-L873 ◽  
Author(s):  
Nikolaos A. Maniatis ◽  
Vasily Shinin ◽  
Dean E. Schraufnagel ◽  
Shigenori Okada ◽  
Stephen M. Vogel ◽  
...  
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Type I Collagen ◽  
Pulmonary Arteries ◽  
Lung Parenchyma ◽  
Negative Regulator ◽  
Pulmonary Vasculature ◽  
Type I ◽  
Caveolin 1 ◽  
Pulmonary Vasodilation

Caveolin-1, the structural and signaling protein of caveolae, is an important negative regulator of endothelial nitric oxide synthase (eNOS). We observed that mice lacking caveolin-1 ( Cav1−/−) had twofold increased plasma NO levels but developed pulmonary hypertension. We measured pulmonary vascular resistance (PVR) and assessed alterations in small pulmonary arteries to determine the basis of the hypertension. PVR was 46% greater in Cav1−/− mice than wild-type (WT), and increased PVR in Cav1−/− mice was attributed to precapillary sites. Treatment with NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NOS activity raised PVR by 42% in WT but 82% in Cav1−/− mice, indicating greater NO-mediated pulmonary vasodilation in Cav1−/− mice compared with WT. Pulmonary vasculature of Cav1−/− mice was also less reactive to the vasoconstrictor thromboxane A2 mimetic (U-46619) compared with WT. We observed redistribution of type I collagen and expression of smooth muscle α-actin in lung parenchyma of Cav1−/− mice compared with WT suggestive of vascular remodeling. Fluorescent agarose casting also showed markedly decreased density of pulmonary arteries and artery filling defects in Cav1−/− mice. Scanning electron microscopy showed severely distorted and tortuous pulmonary precapillary vessels. Thus caveolin-1 null mice have elevated PVR that is attributed to remodeling of pulmonary precapillary vessels. The elevated basal plasma NO level in Cav1−/− mice compensates partly for the vascular structural abnormalities by promoting pulmonary vasodilation.

scholarly journals A STUDY OF THE RELATION OF PULMONARY AND BRONCHIAL CIRCULATION

1913 ◽  
Vol 18 (5) ◽  
pp. 500-506 ◽  
Author(s):  
Albert A. Ghoreyeb ◽  
Howard T. Karsner
Keyword(s):  
Pulmonary Artery ◽  
Lung Tissue ◽  
Bronchial Artery ◽  
Venous Blood ◽  
Pulmonary Arteries ◽  
The Other ◽  
Main Trunk ◽  
Intimate Contact ◽  
Bronchial Arteries ◽  
Bronchial Circulation

The most striking point brought out in this study is that as long as a definite pressure is maintained in either the pulmonary or bronchial circulations, the admixture of bloods is extremely limited. It is easily conceivable that more mixture occurs normally than under the conditions of the experiment, but there is no reason for considering this to be a large difference. If, however, in either system the pressure sinks to zero the possibility of supply by the other system becomes evident. It takes much longer for the mass injected through the bronchial arteries to penetrate to all parts of the lung than when the mass is injected through the pulmonary artery; but when accomplished, the injection reaches to all capillaries including those of the pleura, the only vessels remaining uninjected being the larger trunks of the pulmonary artery. On the other hand, the injection of the bronchial vessels by way of the pulmonary arteries is not complete with normal pressure, but occurs rapidly when a high pulmonary pressure is employed. It is therefore probable that either circulation can suffice for the simple nutritive demands of the lung if the other system is interfered with. It has been shown that embolism of the pulmonary artery, without other circulatory disturbance, does not lead to necrosis of the affected area of the lung, but it is probable that the preservation of circulation is not due to collateral bronchial circulation so much as to the free anastomosis and early division into capillaries of the pulmonary artery. In support of this statement is the fact that the appearance is not altered when the bronchials are ligated at their origin. The same ligation shows no subsequent interference with the nutrition of the bronchi up to a period of five weeks, demonstrating that the pulmonary circulation is sufficient to provide for the nutrition of the bronchi. If, however, as Virchow has shown, the pulmonary artery supplying an entire lobe be occluded, the bronchial circulation can and does suffice for the nutrition of the lobe. In the case of the occlusion of a branch of the pulmonary artery the pressure in the area interfered with does not sink to zero because of the collateral circulation in this area; whereas, if the main trunk is occluded no collateral supply is available, the pressure sinks to zero, and the bronchial artery becomes available as a source of blood supply. It must be remembered that the lung tissue, as a whole, has ready access to oxygen and this gas is the nutritive element acquired by the blood in the lungs. From these studies it would appear that the part of the lung tissue not in intimate contact with oxygen in the air is supplied by oxygenated blood of the bronchial arteries, and that the tissues through which the pulmonary blood circulates take up whatever organized nutriment they need from the pulmonary blood and possibly provide for their oxygen and carbon dioxide interchange (which must be very slight) either directly with the alveolar air, or by finding sufficient oxygen in the venous blood of the pulmonary artery. The studies of the injected specimens confirm Küttner's findings of a very rapid breaking up of the pulmonary artery into capillaries. In all the specimens studied it was found that although the pleural vessels can be injected by way of the bronchial arteries when there is zero pressure in the pulmonary arteries, yet when the two sets of vessels are injected simultaneously in the dog, the pleural vessels invariably derive their supply of injection mass from the pulmonary artery.

Inhibition of hypoxic pulmonary vasoconstriction by antagonists of store-operated Ca2+ and nonselective cation channels

2005 ◽  
Vol 289 (1) ◽  
pp. L5-L13 ◽  
Author(s):  
Letitia Weigand ◽  
Joshua Foxson ◽  
Jian Wang ◽  
Larissa A. Shimoda ◽  
J. T. Sylvester
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Acute Hypoxia ◽  
Pulmonary Arteries ◽  
Cation Channels ◽  
Pulmonary Vasoconstriction ◽  
Nonselective Cation Channels ◽  
Pressor Responses ◽  
Intracellular Ca ◽  
Pulmonary Arterial

Previous studies indicated that acute hypoxia increased intracellular Ca2+ concentration ([Ca2+]i), Ca2+ influx, and capacitative Ca2+ entry (CCE) through store-operated Ca2+ channels (SOCC) in smooth muscle cells from distal pulmonary arteries (PASMC), which are thought to be a major locus of hypoxic pulmonary vasoconstriction (HPV). Moreover, these effects were blocked by Ca2+-free conditions and antagonists of SOCC and nonselective cation channels (NSCC). To test the hypothesis that in vivo HPV requires CCE, we measured the effects of SOCC/NSCC antagonists (SKF-96365, NiCl2, and LaCl3) on pulmonary arterial pressor responses to 2% O2 and high-KCl concentrations in isolated rat lungs. At concentrations that blocked CCE and [Ca2+]i responses to hypoxia in PASMC, SKF-96365 and NiCl2 prevented and reversed HPV but did not alter pressor responses to KCl. At 10 μM, LaCl3 had similar effects, but higher concentrations (30 and 100 μM) caused vasoconstriction during normoxia and potentiated HPV, indicating actions other than SOCC blockade. Ca2+-free perfusate and the voltage-operated Ca2+ channel (VOCC) antagonist nifedipine were potent inhibitors of pressor responses to both hypoxia and KCl. We conclude that HPV required influx of Ca2+ through both SOCC and VOCC. This dual requirement and virtual abolition of HPV by either SOCC or VOCC antagonists suggests that neither channel provided enough Ca2+ on its own to trigger PASMC contraction and/or that during hypoxia, SOCC-dependent depolarization caused secondary activation of VOCC.

Abstract 276: Heme Oxygenase-1 Induction Modulates Hypoxic Pulmonary Vasoconstriction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Mansoor Ahmad ◽  
Nader G Abraham ◽  
Michael S Wolin
Keyword(s):  
Organ Culture ◽  
Heme Oxygenase ◽  
Cobalt Chloride ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Arteries ◽  
Heme Oxygenase 1 ◽  
Force Development ◽  
Pulmonary Vasoconstriction ◽  
Copper Chelator ◽  
Relaxing Effect

Endothelium removed Bovine pulmonary arteries (BPA) contract to hypoxia through a mechanism potentially involving lowering of superoxide-derived hydrogen peroxide and removing its basal relaxing effect. Induction of heme oxygenase-1 (HO-1) in BPA by 24 hr organ culture with 0.1mM cobalt chloride was accompanied by a decrease in 5μM lucigenin-detectable superoxide and an increase in horseradish peroxidase-luminol detectable peroxide levels. Force development to 20mM KCl in BPA was not affected by HO-1, but hypoxic pulmonary vasoconstriction (HPV) was significantly reduced. Organ culture with a HO-1 inhibitor (10μM chromium mesoporphyrin) reversed the effects of HO-1 on HPV and peroxide. Pretreatment of BPA with a copper chelator 10mM diethyldithiocarbamate (DETCA) to inactivate Cu,Zn-SOD, prevented the conversion of superoxide to peroxide, and attenuated HPV. DETCA treatment increased superoxide and decreased peroxide to similar levels in control and HO-1 induced BPA. Peroxide scavenging with 0.1mM ebselen increased force development to 20mM KCl and partially reversed the decrease in HPV seen on induction of HO-1. Thus HO-1 induction in BPA causes an increase in superoxide scavenging by Cu,Zn-SOD resulting in increased levels of peroxide, leading to an attenuation of HPV. The generation of superoxide in BPA is not affected by HO-1 induction as DETCA treated control and HO-1 BPA show similar levels of superoxide. Thus, HO-1 induction appears to attenuate HPV in BPA by increasing the conversion of superoxide to peroxide, leading to peroxide levels which may not be adequately lowered by hypoxia.

Hypoxic induction of Ca2+-dependent action potentials in small pulmonary arteries of the cat

1985 ◽  
Vol 59 (5) ◽  
pp. 1389-1393 ◽  
Author(s):  
D. R. Harder ◽  
J. A. Madden ◽  
C. Dawson
Keyword(s):  
Action Potentials ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Arteries ◽  
Input Resistance ◽  
Potential Generation ◽  
Applied Current ◽  
Pulmonary Vasoconstriction ◽  
Ionic Conductances ◽  
The Relationship ◽  
K Permeability

Small pulmonary arteries (less than 300 micron) from cats were mounted in myographs to record mechanical and electrical responses to hypoxia. When these preparations were exposed to a PO2 of 30–50 Torr after equilibration at 300 Torr they consistently developed active force, which increased or decreased in amplitude as [Ca2+] was raised or lowered, respectively, and was blocked on addition of verapamil. Intracellular electrical recording with glass microelectrodes demonstrated membrane depolarization and action potential generation when PO2 was lowered. Steady-state voltage vs. applied current curves obtained before and during hypoxia showed a significant reduction in input resistance. The relationship between membrane potential and extracellular K+ was not different during hypoxia compared with control, suggesting that there were not marked changes in K+ permeability under this condition. In the presence of verapamil to block Ca2+ inward current the hypoxia-induced action potentials were abolished concomitant with partial membrane repolarization. The results of these studies suggest that in certain isolated pulmonary arteries hypoxia induces contraction by a mechanism involving an increased Ca2+ conductance. These data suggest that the sensor involved in hypoxic pulmonary vasoconstriction may lie within the vessel wall and somehow mediates changes in smooth muscle ionic conductances.

Sign in / Sign up

Export Citation Format

Share Document