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At least 1,135 records · Page 63Linked to original sources
PubMed1986

Effect of chronic vanadate administration on pulmonary circulation in the rat.

The effect of prolonged dietary vanadate administration on pulmonary hemodynamics was investigated. Rats treated with vanadate for 2 months developed pulmonary hypertension, as indicated by significantly (p less than 0.001) higher mean and systolic right ventricular pressure. Cardiac output was not affected by vanadate administration, while the calculated pulmonary vascular resistance was found to be significantly (p less than 0.05) higher in rats treated with vanadium. Right ventricular hypertrophy was also noted in vanadium-treated animals. Vanadium treatment did not significantly affect systemic circulation. The results indicate that vanadium administration induces pulmonary hypertension.

Animals↗
PubMed1998

Time domain method to identify simultaneously parameters of the windkessel model applied to the pulmonary circulation.

Lumped models are frequently used to provide a satisfactory description of the hemodynamic properties of the pulmonary vasculature. The purpose of this study is to describe a method to identify simultaneously the parameters values of windkessel models components. The following equation was used to obtain R1 (characteristic resistance), R2 (peripheral resistance), C (total compliance) and L (inertance): [formula: see text] where ki are the following functions of L, R1, R2 and C: [formula: see text] To assess the accuracy of the method, estimates of R1, R2, and C were compared to characteristic impedance Rc, vascular resistance PVR and pulmonary arterial compliance Cd respectively computed from referenced methods. Comparison between R1 and Rc, PVR and R1 + R2, C and Cd were obtained in 5 anaesthetised pigs during basal conditions and after endotoxin-shock. The results indicate that in both conditions, comparisons evidenced highly significant correlations between values computed by the different approaches (p < 0.0001). Although our method yielded to consistently lower values than values provided by referenced methods, the results were concordant with respect to the expected response of pulmonary vasculature to endotoxin insult. We conclude that our method of identification is suitable for the assessment of lumped parameters windkessel model estimates. The main interest is that actual resistance and compliance values can be obtained easily and simultaneously by a global method approach.

Animals↗
PubMed1984

Regional pulmonary blood volume in patients with abnormal blood pressure or flow in the pulmonary circulation.

We studied the effects of a chronic increase in flow and of chronic hypertension on regional pulmonary blood volume and extravascular lung density (lung tissue and interstitial water per unit thoracic volume) in one group of patients with intracardiac, left-to-right shunt and in another group with Eisenmenger's syndrome or primary pulmonary hypertension. We used positron computerized tomography to measure regional lung density (transmission scans) and blood volume (labelling with 11CO). The distribution of pulmonary blood volume was more uniform in patients with a chronic increase in pulmonary blood flow than in normal subjects. There were also indications of an absolute increase in intrapulmonary blood volume. In patients with chronic pulmonary arterial hypertension, the regional distribution of blood volume was abnormally uniform, but there were no indications of substantial abnormalities in overall intrapulmonary blood volume.

Adolescent↗
PubMed1993

Endothelial control of the pulmonary circulation in normal and chronically hypoxic rats.

1. The effect of blockade of nitric oxide synthesis in pulmonary endothelium by two L-arginine analogues was tested in isolated blood-perfused lungs of normal rats and rats exposed chronically to 10% O2. 2. In both groups of rats the analogues (N-monomethyl-L-arginine (L-NMMA) and N-nitro-L-arginine methyl ester (L-NAME)) enhanced hypoxic vasoconstriction. In normal rats, with rare exceptions, these analogues had little or no effect on pulmonary artery pressure (Ppa) at constant blood flow during normoxia. However, chronically hypoxic rats have pulmonary hypertension and in these rats the analogues always raised Ppa; the rise in Ppa after L-NMMA but not L-NAME could be partially reversed by L-arginine. L-NAME was more potent than L-NMMA. 3. To see whether the difference between rat groups was due to the high Ppa in chronically hypoxic rats, in control rats we raised Ppa passively by lung inflation to values higher than found in chronically hypoxic rats. L-NAME did not alter the effects of lung inflation on Ppa. 4. Ppa was also raised passively by plotting pressure-flow lines up to high flow rates; the lines were changed minimally by both analogues in control rats but in chronically hypoxic rats the lines were raised to higher pressures and steepened substantially. 5. In control rats, during vasoconstriction caused by hypoxia, endothelin 1 and almitrine, L-NAME caused further rises in pressure. We conclude that a stimulus for nitric oxide release in control rats is the narrowing of vessels caused by vasoconstriction rather than passive increases in intravascular pressure. 6. In chronically hypoxic rats arterioles are narrowed by growth of new muscle and there is some muscle tone even in normoxia. Thus narrowing of the vascular lumen is the stimulus common to both groups of rats which leads to nitric oxide synthesis and attenuation of Ppa by a negative feedback process. Narrowing is associated with a large increase in shear stress due to two factors; the pressure drop along a vessel segment is increased and the surface area of the lining of the affected segment is decreased. 7. Atrial natriuretic peptide caused dose-dependent pulmonary vasodilation in both rat groups but had a greater effect in chronically hypoxic rats. The action persisted and was enhanced after blockade of NO synthesis.

Almitrine↗
PubMed1996

Effects of zaprinast and dissolved nitric oxide on the pulmonary circulation of fetal sheep.

This study was designed to determine indirectly if the changes in ovine fetal pulmonary vascular tone caused by i.v. injections of nitric oxide-containing solutions are mediated by cGMP. We first characterized the dose-response relationship of bolus intrapulmonary injections of zaprinast (a cGMP-selective phosphodiesterase inhibitor) and nitric oxide solutions. Injections of nitric oxide solutions as well as zaprinast solutions resulted in dose-dependent decreases in pulmonary arterial pressure that were greater than reductions in systemic arterial pressure. We also evaluated the effects of simultaneous infusions of zaprinast and U46619 (a thromboxane mimetic) on the response to bolus injections of 1.0 micrograms of acetylcholine, 100 ng of endothelin-1, and 10.0 microL of ethanol saturated with nitric oxide. Zaprinast was infused at a rate of 1.5 mg/min, and the concentration of U46619 was titrated to raise mean left pulmonary arterial pressure (LPAP) to the steady state level that was present before infusing zaprinast. All bolus injections reduced left pulmonary arterial pressure more than they reduced mean systemic arterial pressure. However, neither the response magnitudes nor the response durations were affected by simultaneous infusions of zaprinast and U46619. We therefore suggest that modulation of fetal pulmonary vascular tone by endogenously produced nitric oxide may involve mechanisms other than raising smooth muscle cytoplasmic cGMP concentrations.

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