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Results for “VASCULAR RESISTANCE”

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PubMed2000

Noninvasive, continuous evaluation of peripheral vascular resistance in humans.

We sought a noninvasive alternative method of monitoring peripheral vascular resistance continuously in humans, based on the analysis of arterial pressure waveforms. Radial arterial pressure waveforms were recorded noninvasively with a tonometer and analysed using a neural network method. To test the accuracy of this method, the peripheral vascular resistance was also determined by an invasive thermodilution method using a Swan-Ganz catheter in 20 subjects. To test the method in a clinical application, peripheral vascular resistance was determined by the noninvasive method before and after administration of nifedipine in 6 patients with essential hypertension. Neural network analysis of waveforms reliably yielded values between 0.00 and 1.00. Peripheral vascular resistance determined by neural network analysis and according to the invasive method showed a significant (p< 0.005) positive linear correlation. The peripheral vascular resistance measured by neural network analysis showed a significant (p< 0.05) decrease 30 min after administration of nifedipine, paralleling a decrease in blood pressure. Neural network analysis of tonometric radial artery waveforms provides an accurate, noninvasive, and continuous index of peripheral vascular resistance in human subjects. This simple method should permit more extensive homodynamic studies and larger epidemiological surveys in contrast to those undertaken using invasive techniques.

Blood Pressure↗

PubMed2000

Inhaled nitric oxide reduces pulmonary vascular resistance more than prostaglandin E(1) during heart transplantation.

UNLABELLED: Heart transplantation in patients with increased pulmonary vascular resistance is often associated with postbypass right heart failure. We therefore compared the abilities of prostaglandin E(1) (PGE(1)) and inhaled nitric oxide to reduce pulmonary vascular resistance during heart transplantation. Patients undergoing orthotopic heart transplantation for congestive heart failure were randomly assigned to either a PGE(1) infusion at a rate of 8 ng. kg. (-1)min(-1) starting 10 min before weaning from cardiopulmonary bypass (CPB) (n = 34) or inhalation of 4 ppm nitric oxide starting just before weaning from CPB (n = 34). Both treatments were increased stepwise, if necessary, and were stopped 6 h postoperatively. Hemodynamic values were recorded after the induction of anesthesia, 10 and 30 min after weaning from CPB, and 1 h and 6 h postoperatively. Immediately after weaning from CPB, pulmonary vascular resistance was nearly halved in the nitric oxide group but reduced by only 10% in the PGE(1) group. Pulmonary artery pressure was decreased approximately 30% during nitric oxide inhalation, but only approximately 16% during the PGE(1) infusion. Six hours after surgery, pulmonary vascular resistance and pulmonary artery pressure were similar in the two groups. The ratio between pulmonary vascular resistance and systemic vascular resistance was significantly less in the nitric oxide patients at all postbypass times. In contrast, the pulmonary-to-systemic vascular resistance ratio increased approximately 30% in the patients given PGE(1). Cardiac output, heart rate, mean arterial pressure, right atrial pressure, and pulmonary wedge pressure did not differ between the groups. Weaning from CPB was successful in all patients assigned to nitric oxide inhalation; in contrast, weaning failed in six patients assigned to PGE(1) (P = 0.03). IMPLICATIONS: Nitric oxide inhalation selectively reduces pulmonary vascular resistance and pulmonary artery pressure immediately after heart transplantation which facilitates weaning from cardiopulmonary bypass.

Administration, Inhalation↗

PubMed1989

[New selection criterion for Fontan procedure: pulmonary artery clamping test and pulmonary vascular resistance in increased pulmonary blood flow].

A new selection criterion for Fontan procedure, pulmonary artery clamping test (PACT) was developed and employed in 13 candidates for Fontan procedure. PACT was aimed to evaluate the response of pulmonary vascular bed to increased pulmonary blood flow and calculate the pulmonary vascular resistance in the increased pulmonary blood flow as a selection criterion for Fontan procedure, preoperatively. After a median sternotomy incision, an electromagnetic flow meter was employed for measuring the pulmonary blood flow (Qp) on the pulmonary trunk. By clamping the left pulmonary artery and the right pulmonary artery, right pulmonary vascular resistance and the left pulmonary resistance in the pulmonary blood flow of Qp were calculated respectively. By means of electrical analogue, right and left lungs were simulated as resistors in parallel. And the equivalent pulmonary vascular resistance Rpc was calculated as the predicted pulmonary vascular resistance in the increased pulmonary blood flow of two times Qp. Fontan procedure was performed in 9 cases with a Rpc of less than 3 unit.m2 with a successful result and no death. Postoperative cardiac index ranged from 2.6 to 3.7 L/min.m2 with a mean of 2.8 L/min.m2. Postoperative pulmonary vascular resistance ranged from 1.6 to 3.2 unit.m2. Postoperative cardiac index was correlated with postoperative pulmonary vascular resistance. And postoperative pulmonary vascular resistance was well correlated with equivalent pulmonary vascular resistance but was not correlated with preoperative pulmonary vascular resistance measured by Fick's method at the preoperative catheterization. In Fontan procedure, the pulmonary blood flow frequently increases to a certain degree postoperatively. And pulmonary vascular resistance is not a static resistance, but a dynamic resistance. Hence, in discussing a pulmonary vascular resistance as a selection criterion for Fontan procedure, the pulmonary blood flow in which the pulmonary vascular resistance stand should be taken into account. Equivalent pulmonary vascular resistance Qpc is a theoretical selection criterion for Fontan procedure and well reflects the postoperative pulmonary vascular resistance. Fontan procedure can be successfully performed with a Rpc of less than 3 unit.m2.

Adolescent↗

PubMed1975

The effects of prostaglandin E on fetal pulmonary vascular resistance (38588).

The effects of PGE on pulmonary vascular resistance were investigated in fetal goats using an isolated perfusion technique on otherwise intact unventilated lobes. PGE decreased perfusion pressure in the left pulmonary artery under conditions of monary vascular resistance by vasodilatation of tonically contracted vascular smooth muscle. In our preparation, intrapulmonary PGE infusion did not alter femoral arterial pressure which suggests that PGE is inactivated in the fetal lung. Implications for PGE in the newborn with respiratory distress and increased pulmonary vascular resistance are discussed.

Animals↗

PubMed1991

Calcitonin gene-related peptide (CGRP) and leg vascular resistance during head-up tilt induced hypovolaemic shock in man.

Calcitonin gene-related peptide is a potent vasodilator and its distribution in perivascular nerves suggests a role in the regulation of vascular tone. We evaluated leg vascular resistance together with total peripheral resistance and the arterial plasma concentrations of calcitonin gene-related peptide and catecholamines during 50 degrees head-up tilt induced hypotension in 7 males. During tilt mean arterial pressure, heart rate, total peripheral resistance, leg vascular resistance and plasma noradrenaline increased, while cardiac output and leg blood flow decreased. After 45 +/- 9 min (mean +/- SE) presyncopal symptoms appeared together with decreases in mean arterial pressure (81 +/- 6 to 56 +/- 9 mmHg), heart rate (97 +/- 6 to 73 +/- 8 beats min-1), leg vascular resistance (158 +/- 9 to 109 +/- 8 mmHg min l-1) and total peripheral resistance (17 +/- 3 to 10 +/- 2 mmHg min l-1) (P less than 0.01). Plasma calcitonin gene-related peptide increased from 32 +/- 3 to 35 +/- 3 pmol l-1 (P less than 0.01) and adrenaline from 1.1 +/- 0.2 to 1.7 +/- 0.3 nmol l-1 (P less than 0.01), while noradrenaline did not change. The results indicate that presyncopal symptoms induced by head-up tilt are associated with regional as well as total decreases in vascular resistance accompanied by moderate increases in arterial plasma concentrations of calcitonin gene-related peptide and adrenaline.

Adult↗

PubMed1981

Increased pulmonary vascular resistance during liquid ventilation.

The effect of liquid ventilation on pulmonary vascular resistance was studied in an isolated cat lung preparation in situ. Lungs were perfused with whole blood from a donor cat at a constant flow of 100 ml . min-1 kg-1. Pulmonary arterial venous pressures were measured, and pulmonary vascular resistance calculated during gas ventilation (control) and ventilation with fluorocarbon, FC-80. During control ventilation at a mean tidal volume (VT) of 28 +/- 1 (SEM) ml and lung volume of 108 +/- 8 (SEM) ml, pulmonary vascular resistance was 0.07 +/- 0.01 (SEM) PRU. During liquid ventilation at similar lung volumes, pulmonary vascular resistance increased by 62% to 0.12 +/- 0.03 (SEM) PRU (P less than 0.05). At greater liquid lung volumes reflecting optimum CO2 elimination, pulmonary vascular resistance increased by 115% over control values to 0.15 +/- 0.01 (SEM) PRU (P less than 0.005). These data demonstrate significant alterations in pulmonary circulation during liquid ventilation, and suggest that further studies should be completed before hyperbaric applications in human can be considered.

Animals↗

PubMed1992

Platelet activating factor-induced changes in gastric motility and vascular resistance.

Our study evaluated the hypothesis that gastric contractions may contribute to ischemia by increasing vascular resistance. Using an ex vivo segment of the dog's stomach as the experimental model, contractions were induced with platelet activating factor (PAF) and bethanechol, a cholinergic vasodilator. Spontaneous contractions produced slight increases in luminal pressure and corresponding increases in vascular resistance. PAF caused statistically significant, dose-dependent increases in the force of gastric contractions that were highly correlated with phasic changes in vascular resistance. To ensure that the relationship between contractions and vascular resistance was independent of vascular tone, we next examined responses to bethanechol. Bethanechol stimulated contractions that also transiently increased both luminal pressure and vascular resistance. Our results demonstrate that gastric contractions markedly increase vascular resistance and support the hypothesis that hypercontractility may contribute to the development of mucosal ischemia during ulceration.

Animals↗

PubMed1976

Vascular resistance in hypothermically perfused kidneys damaged by warm ischemia.

Vascular resistance was determined during hypothermic perfusion of rabbit kidneys after various periods of warm ischemia. Ischemia was induced by clamping of the renal artery, or of the renal artery and vein, in situ. Studies were made after periods of clamping ranging from 0 to 180 min. The perfusing fluid was 5% Dextran of low molecular weight in balanced saline solution (Tis-U-Sol), with addition of 5 mg % Papaverin. When the renal artery was clamped for more than 15 min, vascular resistance increased. Maximal resistance was reached after 60 min of clamping, and was 3 times as high as that value in the control group of kidneys which were not clamped. The vascular resistance attained after 60 min of clamping did not further increase when clamping was maintained for 180 min. When both the renal artery and the renal vein were clamped vascular resistance first increased after 30 min. Maximal resistance was reached after 60 min of clamping, but was only 1/2 of that level seen when the renal artery alone was clamped.

Animals↗

PubMed1984

Altered control of hindlimb vascular resistance by vagal afferents in spontaneously hypertensive rats. Difference in the early and late stage of hypertension.

The aim of this study was to examine whether control of vascular resistance by vagal afferents is altered in the early as well as late stage of hypertension. We examined the effects of vagotomy on hindlimb vascular resistance as well as on arterial baroreflex control of hindlimb vascular resistance in spontaneously hypertensive rats and Wistar-Kyoto rats, 12 and 35 weeks old. Vagotomy in rats with the intact arterial baroreceptors increased hindlimb vascular resistance in all four groups. Hindlimb vascular responses to graded sympathetic nerve stimulation were closely linear up to 6 Hz in all groups, and the slope of the response was approximately 1.4 times steeper in spontaneously hypertensive than in Wistar-Kyoto rats, in both the young and old groups. The increase in hindlimb vascular resistance after vagotomy normalized by the slope of the response to sympathetic nerve stimulation was greater in young spontaneously hypertensive rats than in young Wistar-Kyoto rats, but was less in old spontaneously hypertensive rats than in old Wistar-Kyoto rats. Vagotomy increased the gain of arterial baroreflex control of hindlimb vascular resistance in young spontaneously hypertensive rats, and in two groups of Wistar-Kyoto rats, but not in old spontaneously hypertensive rats. The percent increase in the gain of arterial baroreflex control of hindlimb vascular resistance after vagotomy tended to be greater in young spontaneously hypertensive than in young Wistar-Kyoto rats, but was less in old spontaneously hypertensive than in old Wistar-Kyoto rats. Central venous pressure and left ventricular end-diastolic pressure were higher in spontaneously hypertensive than in Wistar-Kyoto rats in both young and old groups. Left atrial distensibility assessed by obtaining the atrial pressure-volume relationship was comparable between young spontaneously hypertensive and young Wistar-Kyoto rats, but was less in old spontaneously hypertensive than in old Wistar-Kyoto rats. These results indicate that vagal afferents exert tonic inhibition on control of hindlimb vascular resistance in spontaneously hypertensive as well as in Wistar-Kyoto rats, and that tonic inhibitory influence of vagal afferents on control of hindlimb vascular resistance is altered in spontaneously hypertensive rats, augmented in young, but attenuated in old, spontaneously hypertensive rats, compared with that in age-matched Wistar-Kyoto rats. It is considered that altered control of vascular resistance by vagal afferents in spontaneously hypertensive rats may result from changes in vagal afferent activity.

Animals↗

PubMed1995

[Directional velocity of the arterial flow, systemic vascular resistance and urinary excretion of sodium in cirrhotic patients].

OBJECTIVES: We have studied the vascular resistance at the posterior tibial artery utilizing the Doppler reverse/forward flow ratio, and its relationship to systemic vascular resistance and renal function in 32 nonazotemic cirrhotic patients. METHODS: Patients were divided into three groups. Group A comprised 10 patients without ascites or oedema; group B comprised 9 patients with ascites and a relatively high sodium excretion (40 +/- 34 mmol/day); and group C comprised 13 patients with ascites and very low sodium excretion (4.9 +/- 2 mmol/day). RESULTS: No significant differences were found in urine flow, creatinine or creatinine clearance between the three groups. Renin and aldosterone levels were found increased in group C. Systemic vascular resistance differed significantly in the three groups, being lower in group C. Significant higher values in the Doppler reverse/forward ratio were observed in patients with markedly increased sodium retention and less systemic vascular resistance (group C). The Doppler reverse/forward ratio showed significant correlations with systemic vascular resistance (r = 0.65; n = 32; p < 0.001), urinary sodium excretion (r = 0.53; n = 32; p < 0.01), renin (r = 0.474; n = 32; p < 0.01) and aldosterone levels (r = 0.589; n = 32; p < 0.001). CONCLUSIONS: These preliminary results suggest in patients with hepatic cirrhosis vascular resistance, assessed non-invasively, at the posterior tibial artery, increases with the severity of sodium retention and the impairment in systemic hemodynamics. Thus, this measurement may be useful for the evaluation and follow-up of patients with cirrhosis of the liver.

Adult↗

PubMed1987

Elevated pulmonary vascular resistance and cardiac transplantation.

Severe elevation of pulmonary vascular resistance has been considered a contraindication to cardiac transplantation. Most centers exclude patients with pulmonary vascular resistance greater than 6 Wood units. Wood units, however, do not correct for variations in body size and therefore may not be the best measure for use in comparison of patients. We performed a retrospective analysis of 82 cardiac transplant recipients and compared preoperative pulmonary vascular resistance (PVR) calculated in two ways to the incidence of right ventricular failure and death. Our data show that the PVR index unit (PVRI) identifies those patients that are at risk for right heart failure better than the Wood unit, which does not correct for body size. Four patients died of right heart failure with resistance less than 6 Wood units, but had PVRI greater than 6 units. High resistance is not an absolute contraindication to cardiac transplantation; 28 of 33 patients operated on with a PVRI greater than 6 survived. The degree of elevation of PVR did not correlate with survival. Ten of 12 patients with a PVRI greater than 9 survived. Testing with nitroprusside at cardiac catheterization was helpful in determining reversibility of pulmonary vascular obstruction. No patients with a PVRI less than 6 developed right heart failure.

Adolescent↗

PubMed1990

Controlled initial hyperkalemic reperfusion after cardiac transplantation: coronary vascular resistance and blood flow.

The coronary vascular response to controlled initial hyperkalemic reperfusion after global ischemia during cardiac transplantation was studied in 11 patients. The mean global ischemic time was 206 minutes (range, 143 to 245 minutes). All donor hearts received initial hyperkalemic crystalloid cardioplegia and subsequent oxygenated crystalloid cardioplegia during implantation. Coronary blood flow was highest during the first one to two minutes of controlled reperfusion but remained normal throughout the first ten minutes of reperfusion. Coronary vascular resistance was less than normal throughout the first ten minutes of controlled reperfusion, but there was a gradual increase throughout this period. Systemic vascular resistance remained within normal limits. The time to effective contraction was highly variable, but a greater potassium load during initial reperfusion was generally associated with a longer time to effective contraction.

Aorta↗

PubMed1975

The echocardiographic assessment of pulmonary artery pressure and pulmonary vascular resistance.

Serial assessment of the status of the pulmonary vascular bed requires bed requires cardiac catheterization. We have demonstrated the right ventricular systolic time intervals (RVSTI) may be measured from the pulmonary valve echo. The right ventricular ejection time (RVET) and right pre-ejection period (RPEP) were measured in 45 normal patients. The RVET and RPEP decreased with increasing heart rate but increased with age. The RPEP/RVET, however, was uninfluenced by either age or heart rate. The RPEP/RVET was, therefore, determined from the pulmonary valve echo in 64 patients with congenital heart disease who underwent cardiac catheterization. Increased pulmonary artery diastolic pressure (PADP), pulmonary vascular resistance (PADP), pulmonary vascular resistance (PVR) and mean pulmonary artery pressure (MPAP) resulted inan increased RPEP/RVET. The use of the RPEP/RVET permitted the serial echographic evaluation of the pulmonary vascular bed in selected patients; marked elevation of the ratio indicated the presence of pulmonary hypertension.

Adolescent↗

PubMedDate not supplied

Localization of increased hepatic vascular resistance in liver cirrhosis.

To determine the localization of increased vascular resistance in cirrhotic liver, blood pressures were measured by a direct cannulation method at several key points in the hepatic vascular pathway in normal and cirrhotic rats. Cirrhosis was produced by feeding a choline-deficient diet. Blood pressures in normal rats were 110 mm H2O in the portal vein, 68 mm H2O in the terminal portal venule, 28 mm H2O in the terminal hepatic venule and 20 mm H2O in the inferior vena cava. In cirrhotic rats, blood pressures in the portal vein and the terminal portal venule were 173 and 100 mm H2O, respectively, while those in the terminal hepatic venule and the inferior vena cava were elevated only slightly above normal. These hemodynamic data suggest that an increase in vascular resistance in cirrhotic liver is present in the intrahepatic portal vein and sinusoids, but not in intrahepatic hepatic vein. In cirrhotic liver, stenosis and distortion were found in peripheral branches of the portal vein, and sinusoidal stenoses and a decrease in sinusoidal space were recognized. Accordingly, it is suggested that the increase in vascular resistance in the intrahepatic portal vein and sinusoids correlate with these structural changes. Although severe stenoses and distortion were found in hepatic vein branches, it was thought that they do not contribute to portal hypertension because of lack of increase in vascular resistance in the intrahepatic hepatic vein.

Animals↗

PubMed1988

Correlations of lung morphology, pulmonary vascular resistance, and outcome in children with congenital heart disease.

Pulmonary vascular resistance was measured in air, oxygen, and after administration of vasodilators in 14 children with pulmonary hypertension and congenital heart disease. Lung morphology was examined by light microscopy and assessed quantitatively. In this selected group of patients (a) medial muscle thickness of greater than 20% in the intra-acinar arteries and Heath-Edwards changes of I or II were significantly associated with perioperative death from pulmonary complications after cardiac surgery; (b) children with lower percentage medial muscle thickness had a higher baseline resistance (r = -0.84) associated with Heath-Edwards grade III or higher changes (most of these patients were not offered corrective surgery); (c) when the lowest pulmonary vascular resistance was less than 3 units, Heath-Edwards grading was I or II (n = 4). When the pulmonary vascular resistance was greater than 6 units, however, there was no direct correlation with Heath-Edwards grading (n = 9). Four patients with a resistance of greater than 6 units had only grade I or II changes. Three had a medial muscle thickness above 20%, and were among those who died at or soon after operation. It is concluded that (a) patients with a lowest pulmonary vascular resistance of greater than 6 units have a bad prognosis whatever their lung morphology; and (b) some patients with Heath-Edwards grade I or II will have a high resistance (this group has a high medial muscle mass and a poor prognosis and would not be detected by Heath-Edwards grading alone).

Adult↗

PubMed1996

Computer simulation of human blood flow and vascular resistance.

Organ blood flows and associated vascular resistances have been investigated through the use of a Microsoft Windows-compatible computer program which employs Monte Carlo simulations based on the system's principal components. This approach replicates the system's behavior by maintaining proper correlations between all variables in the system as well as allowing for modulation of the system by its inherent uncertainties. By applying various external constraints, such as a specific age, weight, height and/or blood pressure, the simulations allow for insights to be obtained about the behavior of individual patients. In particular, patient specific organ blood flows and associated vascular resistances can be determined as a function of a patient's age, weight, height and blood pressure.

Adult↗

PubMed1979

Carotid and cardiopulmonary baroreceptor control of splanchnic and forearm vascular resistance during venous pooling in man.

1. This study evaluated the contribution of carotid and cardiopulmonary baroreceptors to reflex splanchnic and forearm vascular adjustments during venous pooling in man. We compared (a) responses to lower body suction which produces venous pooling with (b) responses to lower body suction plus simultaneous application of neck suction. The rationale was that simultaneous application of neck suction, which stretches carotid baroreceptors, would minimize the contribution of carotid baroreceptors to circulatory adjustments produced by lower body suction.2. Lower body suction at 40 mmHg decreased central venous pressure and arterial pulse pressure and increased forearm vascular resistance (plethysmography), splanchnic vascular resistance (indocyanine green dye clearance), and heart rate. Simultaneous application of neck suction prevented the tachycardia and most of the splanchnic vasoconstriction during lower body suction, but did not significantly attenuate the forearm vasoconstriction.3. The major findings in this study are first, that the splanchnic vasoconstrictor response during venous pooling is mediated primarily through carotid baroreceptors, and secondly, that carotid and cardiopulmonary baroreceptors produce strikingly contrasting and non-uniform regional vascular responses during venous pooling. Cardiopulmonary baroreceptors exert the predominant influence on forearm vascular resistance, but appear to have only a minor influence on splanchnic vascular resistance. Carotid baroreceptors produce most of the splanchnic vasoconstriction during venous pooling. but have a minor role in the forearm vasoconstriction.

Abdomen↗

PubMed1996

Endothelium-derived nitric oxide regulates systemic and pulmonary vascular resistance during acute hypoxia in humans.

OBJECTIVES: This investigation sought to determine whether endothelium-derived nitric oxide contributes to hypoxia-induced systemic vasodilation and pulmonary vasoconstriction in humans. BACKGROUND: Endothelium-derived nitric oxide contributes to basal systemic and pulmonary vascular resistance. During hypoxia, systemic vasodilation and pulmonary vasoconstriction occur. There are some data indicating that endothelium-derived nitric oxide mediates changes in vascular resistance during hypoxia, but much of it is contradictory, and none has been derived from normal humans. METHODS: The hemodynamic effects of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase inhibitor, were studied in healthy volunteers under normoxic and hypoxic conditions. A Swan-Ganz catheter and radial artery cannula were inserted to measure right atrial, pulmonary artery, pulmonary capillary wedge and systemic blood pressures. Cardiac output was measured by thermodilution. Systemic vascular resistance and pulmonary vascular resistance were calculated. The pharmacokinetics of L-NMMA (300 mg intravenously) was studied during normoxia in six subjects. Hypoxia was induced in eight subjects who inspired a mixture of nitrogen and oxygen through a gas blender adjusted to reduce the partial pressure of oxygen from (mean +/- SE) 98 +/- 4 to 48 +/- 1 mm Hg. RESULTS: During normoxia, L-NMMA increased systemic vascular resistance from 1,108 +/- 74 to 1,705 +/- 87 dynes-s-cm-5 and increased pulmonary vascular resistance from 60 +/- 5 to 115 +/- 9 dynes-s-cm-5 (p < or = 0.01 for each). Peak effects occurred within 10 min of L-NMMA administration. Acute hypoxia alone decreased systemic vascular resistance from 1,209 +/- 78 to 992 +/- 58 dynes-s-cm-5 (p < or = 0.05) and increased pulmonary vascular resistance from 92 +/- 11 to 136 +/- 4 dynes-s-cm-5 (p < or = 0.01). While hypoxic conditions were maintained, infusion of L-NMMA increased systemic vascular resistance (to 1,496 +/- 97 dynes-s-cm-5, p < or = 0.01) and increased pulmonary vascular resistance further (to 217 +/- 25 dynes-s-cm-5, p < or = 0.01). CONCLUSIONS: Endothelium-derived nitric oxide contributes to systemic vasodilation and serves as a counterregulatory mechanism to attenuate pulmonary vasoconstriction during acute hypoxia in healthy human subjects.

Acute Disease↗