scholarly journals INTERRELATIONSHIPS AMONG PULMONARY “CAPILLARY” PRESSURE, BLOOD FLOW AND VALVE SIZE IN MITRAL STENOSIS. THE LIMITED REGULATORY EFFECTS OF THE PULMONARY VASCULAR RESISTANCE 1

1952 ◽  
Vol 31 (12) ◽  
pp. 1082-1088 ◽  
Author(s):  
Jorge Araujo ◽  
Daniel S. Lukas
Keyword(s):  
Blood Flow ◽  
Capillary Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Mitral Stenosis ◽  
Pulmonary Capillary ◽  
Valve Size ◽  
Pulmonary Capillary Pressure ◽  
Regulatory Effects

Pulmonary capillary pressure in intact dog lungs

1978 ◽  
Vol 235 (5) ◽  
pp. H569-H573
Author(s):  
J. C. Gabel ◽  
R. E. Drake
Keyword(s):  
Capillary Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pressure Range ◽  
Gravimetric Method ◽  
Average Value ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure

We used a gravimetric method to determine the ratio (gamma) of pulmonary venous to total pulmonary vascular resistance in intact dog lungs. From this ratio, pulmonary capillary pressure (Pc) can be calculated. The average value of gamma was 0.50 +/- 0.06 (mean +/- SD) in 10 dogs. We found no correlation between gamma and PO2, PCO2, pH, or hematocrit in the narrow ranges of these experiments. Over the capillary pressure range of 22.4--35.2 mmHg we found no correlation between gamma and Pc. The value of gamma found in this study is not significantly different from the value found in isolated perfused lungs.

Phasic capillary pressure determined by arterial occlusion in intact dog lung lobes

1989 ◽  
Vol 67 (6) ◽  
pp. 2205-2211 ◽  
Author(s):  
Y. Yamada ◽  
M. Suzukawa ◽  
M. Chinzei ◽  
T. Chinzei ◽  
N. Kawahara ◽  
...  
Keyword(s):  
Capillary Pressure ◽  
Vascular Resistance ◽  
Control Period ◽  
Arterial Occlusion ◽  
Lung Lobe ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure ◽  
Lower Lung ◽  
Pulmonary Arterial ◽  
Electrocardiogram Ecg

In six open-chest dogs, electrocardiogram- (ECG) controlled pulmonary arterial occlusion was performed during the control period and during the infusions of serotonin and histamine. A temporal series of instantaneous pulmonary capillary pressure and the longitudinal distributions of vascular resistance and compliance were evaluated in the intact left lower lung lobe. In the control period, we found a significant phasic variation of pulmonary capillary pressure (Pc) with the cardiac cycle. The ratio of arterial to venous resistances (Ra/Rv) was 6:4, and the ratio of arterial to capillary compliances (Ca/Cc) was 1:11. During the infusions of serotonin and histamine, Pc showed similar phasic variations, despite significant hemodynamic changes induced by these agents. Serotonin predominantly increased Ra, whereas histamine predominantly increased Rv. The ratio of Rv to the total resistance decreased significantly from 0.42 to 0.32 during the infusion of serotonin and increased significantly to 0.62 during the infusion of histamine. The data suggest that phasic Pc determined by ECG-controlled arterial occlusion reflects the pulsatility in the pulmonary microvascular bed under control conditions and after alterations of the pulmonary vascular resistance by serotonin and histamine.

PAF increases capillary pressure but not vascular permeability in isolated blood-perfused canine lungs

1993 ◽  
Vol 264 (5) ◽  
pp. H1454-H1459 ◽  
Author(s):  
T. Shibamoto ◽  
Y. Yamaguchi ◽  
T. Hayashi ◽  
Y. Saeki ◽  
M. Kawamoto ◽  
...  
Keyword(s):  
Capillary Pressure ◽  
Vascular Permeability ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Autologous Blood ◽  
Platelet Activating Factor ◽  
Fold Increase ◽  
Lung Weight ◽  
Pulmonary Capillary ◽  
Dose Dependent Increase

We determined the effects of platelet-activating factor (PAF) on pulmonary vascular resistance, lung weight, and microvascular permeability in isolated canine lungs perfused at constant pressure with autologous blood. PAF caused a dose-dependent increase in total pulmonary vascular resistance (Rt) and pulmonary capillary pressure assessed as double-occlusion pressure. PAF (33 micrograms; n = 7) caused a 10-fold increase in Rt and a decrease in precapillary-to-postcapillary vascular resistance ratio from 0.97 +/- 0.10 to 0.38 +/- 0.03, suggesting predominant pulmonary venoconstriction. Shortly after PAF, lung weight decreased transiently and then increased, reaching a plateau above baseline (112.5 +/- 1.6%) at 30 min. In lungs perfused in the antidromic direction from the pulmonary vein to the artery (n = 5), PAF (33 micrograms) produced marked precapillary vasoconstriction, consistent with pulmonary venoconstriction, and a remarkable and sustained decrease in lung weight below baseline by 30 min. Vascular permeability, measured 30 min after PAF using the capillary filtration coefficient and isogravimetric capillary pressure, did not change significantly from baseline. Thus we conclude that PAF produces lung weight gain by means of an increase in capillary pressure predominantly due to pulmonary venoconstriction without significant changes in vascular permeability in isolated blood-perfused canine lungs.

Factors regulating pulmonary “capillary” pressure in mitral stenosis. IV

1951 ◽  
Vol 41 (6) ◽  
pp. 834-854 ◽  
Author(s):  
R. Gorlin ◽  
B.M. Lewis ◽  
F.W. Haynes ◽  
R.J. Spiegl ◽  
L. Dexter
Keyword(s):  
Capillary Pressure ◽  
Mitral Stenosis ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure

Effects of inhaled NO and inhibition of endogenous NO synthesis in oxidant-induced acute lung injury

1994 ◽  
Vol 76 (3) ◽  
pp. 1324-1329 ◽  
Author(s):  
B. P. Kavanagh ◽  
A. Mouchawar ◽  
J. Goldsmith ◽  
R. G. Pearl
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Capillary Permeability ◽  
Lung Weight ◽  
Pulmonary Capillary ◽  
Injury Model ◽  
Pulmonary Capillary Pressure ◽  
Inhaled No

Inhaled nitric oxide (NO) decreases pulmonary arterial pressure (Ppa) and improves oxygenation in the adult respiratory distress syndrome. Endogenous NO can modulate the development of acute tissue injury. We investigated the effects of inhaled NO and of inhibition of endogenous NO synthase in oxidant-induced acute lung injury in the isolated buffer-perfused rabbit lung. A rapid (45 min) and a more gradual (3 h) model of oxidant-induced acute lung injury were developed using the production of superoxide free radicals from the reaction of purine with low and high doses of xanthine oxidase, respectively. The effects of rapid injury included increases in Ppa, precapillary pulmonary vascular resistance, capillary filtration coefficient (Kfc), and lung weight. In the gradual-injury model, only lung weight and Kfc increased. Pretreatment with inhaled NO (90–120 ppm) prevented the rise in Ppa and precapillary pulmonary vascular resistance in the rapid-injury model and prevented elevation of Kfc in the gradual-injury model. Pretreatment with an inhibitor of endogenous NO synthase (NG-nitro-L-arginine methyl ester) resulted in increased pulmonary capillary pressure and postcapillary pulmonary vascular resistance in the rapid-injury model and increased peak Ppa, pulmonary capillary pressure, and pulmonary vascular resistance in the gradual-injury model. These data suggest that in oxidant-induced acute lung injury 1) inhaled NO may attenuate increases in capillary permeability and 2) endogenous NO may function as a modulator of pulmonary vascular tone without affecting capillary permeability.

Correlation of Data Obtained by Radiocardiography and Right-Heart Catheterization in Cardiac Patients

1968 ◽  
Vol 07 (02) ◽  
pp. 125-129
Author(s):  
J. Měštan ◽  
V. Aschenbrenner ◽  
A. Michaljanič
Keyword(s):  
Capillary Pressure ◽  
Transit Time ◽  
Right Heart Catheterization ◽  
Heart Catheterization ◽  
Right Heart ◽  
Pulmonary Capillary ◽  
Filling Time ◽  
Pulmonary Capillary Pressure ◽  
The Mean ◽  
Pulmonary Transit Time

SummaryIn patients with acquired and congenital valvular heart disease correlations of the parameters of the radiocardiographic curve (filling time of the right heart, minimal pulmonary transit time, peak-to-peak pulmonary transit time, and the so-called filling time of the left heart) with the mean pulmonary artery pressure and the mean pulmonary “capillary” pressure were studied. Further, a regression equation was determined by means of which the mean pulmonary “capillary” pressure can be predicted.

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