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PubMed1985

Influence of carbon dioxide tension in the cephalic circulation on hind-limb vascular resistance in anaesthetized dogs.

In dogs anaesthetized with chloralose, the effects were determined of changes in cephalic blood PCO2 on vascular resistance and on the reflex vascular responses to stimulation of baroreceptors and chemoreceptors. Both vagus nerves were cut above the nodose ganglia, both carotid sinus regions were perfused with blood at controlled pressures and the cephalic circulation was perfused with blood, equilibrated with various levels of CO2, through the brachiocephalic and left subclavian arteries. Increases in cephalic blood PCO2 between 4 and 6 kPa resulted in increases in arterial perfusion pressure in a vascularly isolated hind limb. These responses were inhibited at high carotid sinus pressures and the responses to changes in carotid pressure were enhanced at high levels of cephalic PCO2. The reflex increase in vascular resistance resulting from stimulation of carotid chemoreceptors, however, was unaffected by the level of cephalic blood CO2. These results indicate that the carbon dioxide tension in the cephalic circulation is of importance in the control of vascular resistance in the hind limb.

Animals↗

PubMedDate not supplied

Relationship of cardiac allograft size and pulmonary vascular resistance to long-term cardiopulmonary function.

The purpose of this study was to evaluate the long-term cardiopulmonary function of heart transplant patients who received disproportionately sized allografts for varying levels of pulmonary vascular resistance. Resting hemodynamics and oxygen uptake during exercise were recorded at 1 year after transplantation in 52 patients. No differences in resting heart rate, cardiac output, stroke volume, peak oxygen uptake during exercise, and exercise duration were found in recipients of undersized hearts (donor:recipient weight ratio [D:R] < 0.75), sized-matched hearts (D:R = 0.75 to 1.25), and oversized (D:R > 1.25) hearts. In a further analysis according to preoperative pulmonary vascular resistance, resting cardiac output (5.8 +/- 1.3 L/min) was normal, and peak exercise oxygen uptake (22.7 +/- 8.0 ml/kg/min) was mildly decreased in recipients of size-matched allografts with a pulmonary vascular resistance of less than 3 Wood units (size-matched hearts, with mild or no pulmonary vascular resistance). Of patients with moderate pulmonary hypertension (pulmonary vascular resistance > or = 3 Wood units), resting cardiac output was normal (5.1 +/- 0.6 L/min) in recipients of oversized hearts and was reduced (4.7 +/- 1.0 L/min) in recipients of sized-matched hearts (p < 0.05 versus recipients of size-matched hearts with pulmonary vascular resistance less than 3 Wood units).(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗

PubMed2001

Uric acid in cachectic and noncachectic patients with chronic heart failure: relationship to leg vascular resistance.

BACKGROUND: Chronic heart failure (CHF) is a hyperuricemic state, and capillary endothelium is the predominant site of xanthine oxidase in the vasculature. Upregulated xanthine oxidase activity (through production of toxic free radicals) may contribute to impaired regulation of vascular tone in CHF. We aimed to study the relationship between serum uric acid levels and leg vascular resistance in patients with CHF with and without cachexia and in healthy control subjects. METHODS: In 23 cachectic and 44 noncachectic patients with CHF (age, 62 +/- 1 years, mean +/- SEM) and 10 healthy control subjects (age, 68 +/- 1 years), we assessed leg resting and postischemic peak vascular resistance (calculated from mean blood pressure and leg blood flow by venous occlusion plethysmography). RESULTS: Cachectic patients, compared with noncachectic patients and control subjects, had the highest uric acid levels (612 +/- 36 vs 459 +/- 18 and 346 +/- 21 micromol/L, respectively, both P <.0001) and the lowest peak leg blood flow and vascular reactivity (reduction of leg vascular resistance from resting to postischemic conditions: 83% vs 88% and 90%, both P <.005). In all patients, postischemic vascular resistance correlated significantly and independently of age with uric acid (r = 0.61), creatinine (r = 0.47, both P <.0001), peak VO2 (r = 0.34), and New York Heart Association class (r = 0.33, both P <.01). This correlation was not present in healthy control subjects (r = -0.04, P =.9). In multivariate and stepwise regression analyses, serum uric acid emerged as the strongest predictor of peak leg vascular resistance (standardized coefficient = 0.61, P <.0001) independent of age, peak VO2, creatinine, New York Heart Association class, and diuretic dose. CONCLUSIONS: Hyperuricemia and postischemic leg vascular resistance are highest in cachectic patients with CHF, and both are directly related independent of diuretic dose and kidney function. The xanthine oxidase metabolic pathway may contribute to impaired vasodilator capacity in CHF.

Adult↗

PubMed1997

Cerebral and umbilical vascular resistance response to vibroacoustic stimulation in growth-restricted fetuses.

OBJECTIVE: To test the hypothesis that after vibroacoustic stimulation the ratio between cerebral vascular and umbilical vascular resistance in the growth-restricted fetus is different from that in the normal fetus. METHODS: The pulsatility index (PI) of the middle cerebral artery and that of the umbilical artery (UA) were measured by pulsed Doppler velocimetry in 30 normal and 14 growth-restricted fetuses before and after vibroacoustic stimulation. The ratios of cerebral PI to UA PI and the changes in PI after vibroacoustic stimulation were calculated. Comparisons were made using the Wilcoxon rank-sum test or signed-rank test. The statistical power of the study was 80%. RESULTS: Mean (+/- standard deviation) cerebral PI values before vibroacoustic stimulation (1.50 +/- 0.29) in normals and 1.29 +/- 0.26 in the fetal growth restriction [FGR] group) and UA PI values (1.00 +/- 0.18 in normals and 1.15 +/- 0.24 in the FGR group) were significantly different between groups (P < .04) and significantly decreased after vibroacoustic stimulation (P < .05). Although the cerebral to UA PI ratios (1.50 +/- 0.38 in normals and 1.13 +/- 0.33 in the FGR group) were significantly different between groups (P < .008), the values remained the same after vibroacoustic stimulation (P = .39 and .80, respectively). In all fetuses the fetal heart rate accelerated after vibroacoustic stimulation. CONCLUSION: Cerebral vascular resistance was lower and umbilical vascular resistance higher in the growth-restricted fetuses than in normals. The vascular resistance response after vibroacoustic stimulation in the growth-restricted fetus was not significantly different from the response of the normal fetus, suggesting preservation of regulation of resistance.

Acoustic Stimulation↗

PubMed1976

The effect of temporary clamping of the renal vessels on the vascular resistance in rabbit kidneys.

In studies of 45 rabbits, either the renal artery (35 animals), or the renal artery and vein (10 animals) were clamped in situ. The effect of the clamping--of the warm ischemia--on the vascular resistance of the kidney after reestablishment of the circulation was examined in perfusion studies made after removal of the kidneys from groups of 5 animals between 1 and 5 days after revascularization. Resistance patterns were measured during hypothermic perfusion. The results confirm earlier findings that vascular resistance increases in proportion to the duration of warm ischemia up to 60 min, but not thereafter. The renal vascular resistance falls over the days following revascularization, more slowly after longer periods of ischemia. Thus after 60 min of warm ischemia the vascular resistance became normal within 24 hours, but after 180 min of warm ischemia, the normal resistance range was not reached until 96 hours after reestablishment of the circulation. When both the renal artery and the renal vein were clamped, the pattern was the same but much less emphatic. The vascular resistance never attained such high values as seen after clamping of the renal artery alone, and became normal after 24 hours of revascularization, even when the period of warm ischemia was as long as 180 min.

Animals↗

PubMed2001

Differential roles of the sodium-calcium exchanger in renin secretion and renal vascular resistance.

The intracellular free calcium concentration ([Ca2+]i) is a central regulator of renin secretion and the contractility of vascular smooth muscle cells. As [Ca2+]i results from calcium influx and calcium extrusion, we were interested in the role of the Na+/Ca2+-exchanger as an important calcium-extrusion pathway in the regulation of renin secretion. Therefore, we investigated the effects of inhibiting the Na+/Ca2+-exchanger, either by reducing the extracellular sodium concentration ([Na+]e) or using pharmacological tools, on renin secretion and vascular resistance in the isolated perfused rat kidney model. Stepwise reductions of [Na+]e led to progressive (up to sevenfold) increases in renal vascular resistance ([Na+]e 7 mM) whilst renin secretion rates were not altered significantly. Similarly, pharmacological blockade of the Na+/Ca2+-exchanger by benzamil (100 microM) or KB-R7943 (30 microM) resulted in significant vasoconstrictions without altering basal renin secretion rates. Also renin secretion that was pre-stimulated by isoproterenol (10 nM), blockade of macula densa salt transport by bumetanide (100 microM) or lowering the perfusion pressure to 40 mmHg was not attenuated by Na+/Ca2+-exchanger inhibition, although the vascular resistance increased significantly. In contrast, angiotensin II (100 pM) reduced pre-stimulated renin secretion values by 50%. The subsequent lowering of the [Na+]e however did not augment the inhibition of renin secretion, although the renal vascular resistance increased markedly. We conclude that the Na+/Ca2+-exchanger has no functional role in the regulation of [Ca2+]i in juxtaglomerular cells controlling renin secretion, whereas it markedly affects the preglomerular vascular smooth muscle cells of the renal vasculature.

Adrenergic beta-Agonists↗

PubMed1987

Fetal blood flow velocity waveforms in relation to changing peripheral vascular resistance.

In an acute experiment in Texel ewes, Doppler flow velocity waveforms from the fetal descending aorta were related to peripheral vascular resistance as calculated from perfusion pressure divided by electromagnetically measured volume flow in the descending aorta. Vascular resistance was increased by stepwise embolization of the peripheral circulation via repeated bolus administration of Sephadex G-25 microspheres. A rise in peripheral vascular resistance was associated with a reduction in peak and end-diastolic flow velocity and an increase in Pulsatility Index. Clinically, if similar changes are observed in growth retarded fetuses, the findings are usually interpreted to represent 'uteroplacental insufficiency'. Present data provide direct evidence that raised peripheral vascular resistance does indeed produce such waveform changes.

Animals↗

PubMed2003

The influence of measured versus assumed uptake of oxygen in assessing pulmonary vascular resistance in patients with a bidirectional Glenn anastomosis.

AIMS: To determine the accuracy of data relating to pulmonary vascular resistance data in patients with a bidirectional Glenn anastomosis as calculated using predicted versus measured uptake of oxygen. METHODS: We studied retrospectively the data from 33 patients with a bidirectional Glenn anastomosis who underwent cardiac catheterisation prior to surgery to complete the Fontan circulation. Their weight ranged from 5.4 to 51.7 kg, and they were aged up to 12 years. Uptake of oxygen was measured using the Deltatrac II metabolic monitor. From the calculated indexed pulmonary vascular resistance, cases were stratified according to the risk of failure of the subsequent Fontan circulation. The six patients with a resistance of greater than 4 Um2 were deemed at high risk, the six with a resistance from 3 to 4 Um2 at moderate risk, and the 21 patients with a resistance less than 3 Um2 at low risk. Uptake of oxygen was also estimated from the predictive formulas of Lindahl, Lundell et al. and LaFarge and Miettinen. The indexed resistance was similarly calculated using these formulas and a comparable stratification of risk made from this data. RESULTS: The predicted values for uptake of oxygen were consistently higher than those measured, leading to an underestimation of indexed resistance, with mean difference between -0.62 and -1.57 Um2. This difference resulted in misclassification of between five and nine of the 12 patients considered at moderate or high risk as being at low-risk. No other haemodynamic data could reliably separate the subjects deemed at low-risk from those considered to be at high-risk. A transpulmonary gradient of greater than 7 mm of mercury was found to be 100 percent specific for elevated indexed resistance, but only 60 percent sensitive. CONCLUSIONS: In patients with bidirectional Glenn anastomoses, all formulas based on predictive uptake of oxygen lead to underestimation of the true indexed pulmonary vascular resistance, to an extent that could significantly influence clinical decision-making. The transpulmonary gradient is not a reliable surrogate for indexed pulmonary vascular resistance.

Blood Pressure↗

PubMed1986

Contribution of endogenous vasoactive compounds to renal vascular resistance in neonatal chronic partial ureteral obstruction.

To evaluate the relative contribution of endogenous vasoactive compounds to maintenance of increased renal vascular resistance in neonatal obstructive nephropathy, cardiac output and renal blood flow were measured using radioactive microspheres in 25 +/- 3 day-old guinea pigs subjected to unilateral partial ureteral constriction within the first two days of life. Mass and renal blood flow of the obstructed kidney were significantly lower than those of the contralateral kidney. Following a control period, thromboxane synthesis was blocked by infusion of OKY-046, after which prostaglandin synthesis was inhibited by indomethacin. In a separate group of animals, angiotensin converting enzyme inhibitor, MK-422, was infused before or after administration of OKY-046. While neither OKY-046 nor indomethacin had a consistent effect on vascular resistance, infusion of MK-422 resulted in selective reduction of renal vascular resistance of the obstructed kidney compared to resistance in the intact kidney and other vascular beds. Removal of the contralateral kidney at the time of ureteral constriction in an additional group of animals resulted in hypertrophy and vasodilation of the obstructed kidney which was not altered by thromboxane or cyclooxygenase inhibition. We conclude that in the neonatal kidney subjected to ipsilateral chronic partial ureteral obstruction, vasoconstriction is mediated at least in part by angiotensin II, but not by thromboxane. Furthermore, vasodilation of the obstructed kidney resulting from contralateral nephrectomy is not dependent on prostaglandin synthesis. Renal vascular resistance of the kidney with prolonged partial ureteral constriction in early development thus appears to be inversely related to renal growth and is not significantly mediated by endogenous prostanoids.

Angiotensin II↗

PubMed1981

[Mechanism of the increase in peripheral vascular resistance in hypertension].

To elucidate the mechanisms determining peripheral vascular resistance in arterial hypertension the circulation in the leg was studied by venous occlusion plethysmography in 41 hypertensive patients and 11 normotensive controls. It was found that vascular resistance in the leg both at rest and during maximal vasodilatation were within the normal limits in labile and mild hypertension, but it was significantly raised in established, malignant and refractory hypertension. The increased Rmin strongly suggests structurally narrowed lumina, but not enhanced vasoconstriction of the neurohumoral origin. Moreover, vascular smooth muscle activity at rest was not increased in absolute values in hypertensive patients though it may be considered as inappropriately "high" in relation to the altered vascular design. It was concluded, that at least in the vascular bed of the leg a rise in peripheral resistance is caused by structural changes of the resistance vessels along with unchanged contractile activity of the vascular smooth muscles.

Adult↗

PubMed1996

The effect of a nitric oxide donor and an inhibitor of nitric oxide synthase on blood flow and vascular resistance in feline submandibular, parotid and pancreatic glands.

The aim was to examine whether (1) blood flow and vascular resistance are altered in response to exogenous nitric oxide and (2) whether endogenous synthesis of nitric oxide participates in the haemodynamic regulation of the submandibular, parotid and pancreatic glands. Experiments were performed on anaesthetized, artificially ventilated cats. Mean arterial blood pressure, heart rate, blood gases, cardiac output and tissue blood flow were determined before and 15 min after intravenous administration of either the nitric oxide donor SIN-1 (3-morpholinosydnonimine, 1 mg/kg, n = 10) or the competitive nitric oxide synthase inhibitor NOLA (NG-nitro-L-arginine, 30 mg/kg, n = 9) blood flow was measured by a radioactive-labelled microsphere method. In the SIN-1 group, in spite of a serious decrease in mean arterial blood pressure (p < 0.001), the blood flow in the glands remained unchanged. The vascular resistance decreased after SIN-1 in the submandibular and pancreatic glands (p < 0.001 and p < 0.05, respectively), and was slightly reduced in the parotid. The NOLA increased mean arterial blood pressure (p < 0.01) and reduced the blood flow in the submandibular and pancreatic glands (p < 0.01 and p < 0.001, respectively), but the decrease in the parotid was not significant. Vascular resistance increased after NOLA in all three glands (p < 0.05, p < 0.001 and p < 0.05). These findings suggest that basal nitric oxide production in these exocrine glands is sufficient to modulate vascular resistance. Moreover, the release of endogenous NO from the nerves and/or endothelium is probably involved in the regulation of vascular tone. The nitric oxide-dependent component of blood-flow regulation, however, seems to be less pronounced in the parotid gland.

Animals↗

PubMed1976

Comparison of alpha-MSH and several vasoactive substances on vascular resistance in the feline mesenteric vascular bed.

The effects of alpha-MSH and several other vasoactive substances on the mesenteric vascular bed were studied in the anesthetized cat under conditions of controlled blood flow. Intra-arterial injections of alpha-MSH in doses of 10, 30, and 100 mug resulted in significant dose-related decreases in mesenteric arterial perfusion pressure but little or no effect on systemic arterial pressure. The vasodilator response to alpha-MSH was breif in duration and resistance to flow was decreased 10, 18, and 26 percent at 10, 30, and 100 mug. These significant changes after alpha-MSH were of a much smaller magnitude than were observed after prostaglandins E1 and E2, isoproterenol, bradykinin or glyceryl trinitrate and differed completely from the increased resistance after angiotensin II and norepinephrine.

Angiotensin II↗

PubMed1979

Contribution of prostaglandins to the regulation of pulmonary vascular resistance in adult cats and dogs.

In order to determine the role of prostaglandins in the regulation of pulmonary vascular resistance, we investigated effects of prostaglandin cyclo-oxygenase inhibition by indomethacin (2 mg/kg), meclofenamate (2 mg/kg), and aspirin (40 mg/kg) upon canine and feline pulmonary vasoconstriction caused by two stimuli: acute hypoxia (6% O2) and exogenous PGF2 alpha. Measurements were made utilizing an open chest, pump-perfused, in situ lung preparation. Cat pulmonary vasculatures were more responsive to hypoxia and PGF2 alpha than were dog's. In dogs, indomethacin, meclofenamate, and aspirin all increased pulmonary vascular resistance and augmented pulmonary vasoconstrictor responses to hypoxia and PGF2 alpha. Neither indomethacin, meclofenamate, nor aspirin affected baseline pulmonary vascular resistance of cats. Aspirin and indomethacin augmented pulmonary vasoconstriction in the cat. Meclofenamate was without effect. Further, although aspirin and indomethacin strongly inhibited pulmonary vascular pressor responses to exogenous arachidonic acid, meclofenamate decreased pulmonary responses to arachidonic acid very little. All three inhibitors nearly abolished systemic responses to arachidonic acid in the cat. Exogenous PGI2 infusion decreased pulmonary vascular resistance in the cat. Prostaglandin cyclo-oxygenase activity produces a vasodilator influence, probably PGI2, in the canine pulmonary vasculature that may be significant in protecting the animal from pulmonary hypertension and its consequences. The role of the prostaglandin system in the feline pulmonary vasculature appears to be qualitatively similar, but quantitatively less, than in the dog.

Animals↗

PubMed1986

Augmented cardiopulmonary baroreflex control of forearm vascular resistance in young athletes.

The aim of this study was to examine the effect of exercise training on reflex control of vascular resistance in human males. Forearm vascular responses to lower body negative pressure (LBNP) at -10 and -40 mm Hg were compared between highly trained young athletes (21.5 +/- 0.5 years old, n = 14) and age-matched nonathletes (20.7 +/- 0.5 years old, n = 16). Resting heart rate was lower in athletes than in nonathletes. Resting blood pressure, central venous pressure, forearm blood flow, and forearm vascular resistance were not different between the two groups. The magnitude of reflex forearm vasoconstriction in response to LBNP at -10 mm Hg, which decreased central venous pressure but did not alter blood pressure or heart rate, was greater in athletes than in nonathletes. The slope of the regression line relating changes in central venous pressure and forearm vascular resistance was steeper in athletes than in nonathletes. Vasoconstrictive responses to intraarterially administered norepinephrine and angiotensin II did not differ between athletes and nonathletes. These results suggest that the tonic inhibitory influence of the cardiopulmonary receptors is augmented in athletes. This augmentation may contribute to some of cardiovascular and endocrine adaptations that occur with exercise training.

Adult↗

PubMed1985

Digitalis-induced augmentation of cardiopulmonary baroreflex control of forearm vascular resistance.

We sought to determine whether digitalis augments cardiopulmonary baroreflex control of forearm vascular resistance in normal young men. Cardiopulmonary baroreceptor input was reduced with lower body negative pressure (LBNP) at 10 and 20 mm Hg, which decreased central venous pressure but did not alter blood pressure or heart rate. Decreases in forearm blood flow and increases in forearm vascular resistance with LBNP were greater after administration of lanatoside C (Cedilanid) than before, and the slope of the regression line relating changes in central venous pressure and those in forearm vascular resistance was steeper after lanatoside C. Vasoconstrictor responses to the cold pressor test did not differ before and after lanatoside C, which suggested that augmented responses to LBNP after the drug were not caused by a generalized change in reflex control. These results suggest that lanatoside C augments the tonic inhibitory influence of cardiopulmonary baroreceptors in normal men.

Adult↗

PubMed1995

Inhaled nitric oxide does not alter the longitudinal distribution of pulmonary vascular resistance.

Because the effects of inhaled nitric oxide (NO) may be localized to its site of delivery, we studied the effects of inhaled NO on the longitudinal distribution of pulmonary vascular resistance during pulmonary hypertension in perfused rabbit lungs. Before NO administration, pulmonary hypertension was produced by infusion of the thromboxane A2 mimetic U-46619 in all lungs. Pulmonary vascular resistance was divided into arterial, microvascular, and venous components by arterial and venous occlusion techniques. In the buffer-perfused lung, all doses of inhaled NO (5, 20, and 80 ppm) produced small decreases (approximately 3 mmHg) in pulmonary arterial pressure (Ppa), with equivalent proportional reductions in all segmental vascular resistances. Similar results were obtained after an extended inhaled NO dose range of 20, 80, and 240 ppm. In the buffer-perfused lung, inhibition of endogenous NO synthesis with NG-nitro-L-arginine methyl ester (L-NAME) potentiated the effects of U-46619. Subsequent inhaled NO administration produced larger decreases (approximately 7 mmHg) in Ppa with equivalent proportional reductions in all segmental vascular resistances. In the blood-perfused lung, L-NAME did not alter baseline pulmonary pressures. Administration of inhaled NO during U-46619-induced pulmonary hypertension produced dose-related decreases in Ppa. The highest dose (80 ppm) of inhaled NO decreased Ppa by 3.5 mmHg, with equivalent proportional reductions in all segmental vascular resistances.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2000

Effect of magnolol on coronary vascular resistance in rabbits: measurement with pulsed Doppler velocimetry.

BACKGROUND AND PURPOSE: Magnolol is an active component purified from Magnolia officinalis that has been reported to protect the myocardium against infarction and reperfusion injury. The purpose of this study was to investigate the effect of magnolol on the coronary circulation and to determine whether a change in coronary vascular resistance could be the mechanism underlying its myocardial protective effect. METHODS: Male New Zealand white rabbits were anesthetized. A 3-mm suction-type pulsed Doppler velocimetry probe was applied to the proximal part of the left anterior descending coronary artery after median sternotomy. The 39 rabbits received intravenous injection of either vehicle (n = 5), magnolol (10(-6) g/kg, n = 6; 10(-5) g/kg, n = 5; 10(-4) g/kg, n = 5), or nitroglycerin (10(-5) g/kg, n = 6; 10(-4) g/kg, n = 6; 10(-3) g/kg, n = 6). The effects of magnolol and nitroglycerin on coronary vascular resistance were compared. RESULTS: Magnolol did not change blood pressure or coronary blood flow velocity. However, at a dose of 10(-4) g/kg, it decreased coronary vascular resistance significantly more than vehicle (88 +/- 1% vs 95 +/- 1% of baseline coronary vascular resistance, p < 0.001). Nitroglycerin increased coronary blood flow velocity and decreased coronary vascular resistance in a dose-dependent manner (p < 0.01). CONCLUSIONS: Magnolol reduced coronary vascular resistance in anesthetized, open-chest rabbits only at a high concentration. Its effect was modest compared with that of nitroglycerin. Since magnolol protects the myocardium at relatively low doses, coronary vasodilatation is unlikely to be the underlying mechanism responsible for its myocardial protective effects.

Animals↗

PubMed1992

Effects of prostaglandin E1 and hydralazine on the longitudinal distribution of pulmonary vascular resistance during vasoconstrictor pulmonary hypertension in sheep.

Pulmonary capillary pressure (Ppc) is dependent upon left atrial pressure, pulmonary venous resistance, and cardiac output. The effects of pulmonary vasodilators on Ppc will therefore depend upon any alterations in the longitudinal distribution of pulmonary vascular resistance (precapillary [arterial] and postcapillary [venous] components). We therefore studied the effects of two pulmonary vasodilators (prostaglandin E1 and hydralazine) on Ppc and the longitudinal distribution of pulmonary vascular resistance. Pulmonary hypertension was produced in sheep by the continuous administration of the thromboxane A2-mimetic U46619. Ppc was measured by analysis of pulmonary artery occlusion pressure decay curves. U46619 increased Ppc by 9 mmHg and increased both the arterial and venous components of pulmonary vascular resistance. Subsequent administration of prostaglandin E1 decreased Ppc by 5 mmHg and decreased both the arterial and venous components of pulmonary vascular resistance (by 50 and 69% respectively). Hydralazine produced smaller decreases in the arterial and venous components of pulmonary vascular resistance (by 35 and 49% respectively) and did not significantly reduce Ppc. We conclude that prostaglandin E1 but not hydralazine is effective in decreasing Ppc in this experimental model of pulmonary hypertension.

Alprostadil↗