scholarly journals The Influence of the Pulmonary Arterial Pressure on the Pulmonary Capillary Venous Pressure in Man

1953 ◽  
Vol 1 (4) ◽  
pp. 340-344 ◽  
Author(s):  
LARS WERKÖ ◽  
E. VARNAUSKAS ◽  
H. ELIASCH ◽  
B. THOMASSON
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial

Effect of hypoxia on pulmonary artery pressure of dogs

1964 ◽  
Vol 207 (6) ◽  
pp. 1314-1318 ◽  
Author(s):  
Benson R. Wilcox ◽  
W. Gerald Austen ◽  
Harvey W. Bender
Keyword(s):  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Artery Pressure ◽  
Pulmonary Vasoconstriction ◽  
Systemic Hypoxia ◽  
Pump Output ◽  
Pulmonary Arterial

The mechanism by which the pulmonary artery pressure rises in response to hypoxia has never been clearly demonstrated. This problem was reinvestigated in experiments utilizing separate pulmonary and systemic perfusion systems. These vascular beds were perfused in such a fashion that a change in pulmonary artery pressure could only result from changes in vasomotor tone. Alveolar-pulmonary vein hypoxia was usually associated with a slight fall in pulmonary artery pressure. Systemic hypoxia resulted in elevation of pulmonary arterial pressure in 10 of the 12 animals tested with a constant-flow and constant-pulmonary venous pressure. In addition, all animals with systemic desaturation showed an increased venous return. When the "cardiac output" (pump output) was increased to match this return, the elevation in pulmonary artery pressure increased. It was concluded that the pulmonary arterial pressure elevation seen with hypoxia is the result of active pulmonary vasoconstriction coupled with an increased pulmonary blood flow.

scholarly journals Comparative Study of Capillary Filtration Coefficient (Kfc) Determination by a Manual and Automatic Perfusion System. Step by Step Technique Review

2019 ◽  
pp. 901-908
Author(s):  
C.C. Bravo-Reyna ◽  
G. Torres-Villalobos ◽  
N. Aguilar-Blas ◽  
J. Frías-Guillén ◽  
J.R. Guerra-Mora
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Ischemia Reperfusion ◽  
Venous Pressure ◽  
Filtration Coefficient ◽  
Perfusion System ◽  
Gold Standard Method ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient ◽  
Pulmonary Arterial

The purpose of calculating the capillary filtration coefficient is to experimentally evaluate edema formation in models of pulmonary ischemia-reperfusion injury. For many years, the obtaining of this coefficient implies a series of manual maneuvers during ex-vivo reperfusion of pulmonary arterial pressure, venous pressure and weight, as well as the calculation of the Kfc formula. Through automation, the calculation of capillary filtration coefficient could be easier and more efficient. To describe an automatic method designed in our laboratory to calculating the capillary filtration coefficient and compare with traditional determination of capillary filtration coefficient as gold standard method. An automatic three valve perfusion system was constructed, commanded by a mastery module connected to a graphical user interface. To test its accuracy, cardiopulmonary blocks of Wistar rats were harvested and distributed in manual (n=8) and automated (n=8) capillary filtration coefficient determination groups. Physiological parameters as pulmonary arterial pressure, pulmonary venous pressure, weight and capillary filtration coefficient were obtained. Results: Capillary filtration coefficient, pulmonary arterial pressure, venous arterial pressure shown no statistical significance difference between the groups. The automated perfusion system for obtaining Kfc was standardized and validated, giving reliable results without biases and making the process more efficient in terms of time and personal staff.

Bradykinin actively modulates pulmonary vascular pressure-cardiac index relationships

1987 ◽  
Vol 63 (1) ◽  
pp. 145-151 ◽  
Author(s):  
D. P. Nyhan ◽  
P. W. Clougherty ◽  
H. M. Goll ◽  
P. A. Murray
Keyword(s):  
Cardiac Index ◽  
Arterial Pressure ◽  
Pulmonary Capillary Wedge Pressure ◽  
Pulmonary Arterial Pressure ◽  
Vena Cava ◽  
Conscious Dogs ◽  
Beta Adrenergic ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Wedge Pressure

Our objectives were to investigate the pulmonary vascular effects of exogenously administered bradykinin at normal and reduced levels of cardiac index in intact conscious dogs and to assess the extent to which the pulmonary vascular response to bradykinin is the result of either cyclooxygenase pathway activation or reflex activation of sympathetic beta-adrenergic and -cholinergic receptors. Multipoint pulmonary vascular pressure-cardiac index (P/Q) plots were constructed during normoxia in conscious dogs by step-wise constriction of the thoracic inferior vena cava to reduce Q. In intact dogs, bradykinin (2 micrograms X kg-1 X min-1 iv) caused systemic vasodilation, i.e., systemic arterial pressure was slightly decreased (P less than 0.05), Q was markedly increased (P less than 0.01), and mixed venous PO2 and oxygen saturation (SO2) were increased (P less than 0.01). Bradykinin decreased (P less than 0.01) the pulmonary vascular pressure gradient (pulmonary arterial pressure-pulmonary capillary wedge pressure) over the entire range of Q studied (140–60 ml X min-1 X kg-1) in intact dogs. During cyclooxygenase pathway inhibition with indomethacin, bradykinin again decreased (P less than 0.05) pulmonary arterial pressure-pulmonary capillary wedge pressure at every level of Q, although the magnitude of the vasodilator response was diminished at lower levels of Q (60 ml X min-1 X kg-1). Following combined administration of sympathetic beta-adrenergic and -cholinergic receptor antagonists, bradykinin still decreased (P less than 0.01) pulmonary arterial pressure-pulmonary capillary wedge pressure over the range of Q from 160 to 60 ml X min-1 X kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

A New Look at Pulmonary Edema

Physiology ◽  
1986 ◽  
Vol 1 (5) ◽  
pp. 150-153 ◽  
Author(s):  
GA Laine ◽  
SJ Allen ◽  
JP Williams ◽  
J Katz ◽  
JC Gabel ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Critically Ill Patients ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Colloid Osmotic Pressure ◽  
Fluid Accumulation ◽  
Fatal Complication ◽  
Therapeutic Measures ◽  
Pulmonary Arterial

Fluid accumulation within the lungs is a potentially fatal complication in critically ill patients. Sepsis and increased microvascular permeability are often implicated as the cause. This article shows that edema can be prevented by lowering systemic venous pressure (to permit pulmonary lymph to drain), by lowering pulmonary arterial pressure, and by maintaining plasma colloid osmotic pressure. It points out the importance of understanding the basic physiology behind pulmonary edema and therapeutic measures.

Lowered pulmonary arterial pressure prevents edema after endotoxin in sheep

1987 ◽  
Vol 63 (3) ◽  
pp. 1008-1011 ◽  
Author(s):  
S. J. Allen ◽  
R. E. Drake ◽  
J. Katz ◽  
J. C. Gabel ◽  
G. A. Laine
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Pressure ◽  
Dry Weight ◽  
Base Line ◽  
Capillary Membrane ◽  
Significant Difference ◽  
Pulmonary Arterial ◽  
The Difference

Escherichia coli endotoxin causes increased capillary membrane permeability and increased pulmonary arterial pressure (PAP) in sheep. If the pulmonary hypertension extends to the level of the microvasculature, then the increased microvascular pressure may contribute to the pulmonary edema caused by endotoxin. We tested the hypothesis that reducing the pulmonary hypertension would reduce the amount of edema caused by endotoxin. Twelve sheep were chronically instrumented with catheters to measure PAP, left atrial pressure, and central venous pressure. The sheep were divided into two groups. One group (E) of six sheep received an intravenous infusion of 4 micrograms/kg of E. coli endotoxin. The second group (E + SNP) received the same dose of endotoxin as well as a continuous infusion of sodium nitroprusside (SNP) to reduce PAP. Three hours after the endotoxin infusions, the sheep were terminated and the extravascular fluid-to-blood-free dry weight ratios of the lungs were determined (EVF). The base-line PAP was 17.5 +/- 2.7 mmHg. A two-way analysis of variance demonstrated a significant difference (P less than 0.01) in PAP between the E and E + SNP groups. Although PAP in each group varied as a function of time, the difference between the two groups did not. The mean PAP for the E + SNP group (20.9 +/- 1.5 mmHg) was lower than the E group PAP of 27.3 +/- 2.1 mmHg after the endotoxin spike. Furthermore, the E + SNP group EVF (3.9 +/- 0.2) was significantly less than the EVF of the E group (4.7 +/- 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Heparin reversal by protamine in humans--complement, prostaglandins, blood cells, and hemodynamics

1991 ◽  
Vol 71 (4) ◽  
pp. 1415-1421 ◽  
Author(s):  
J. Hobbhahn ◽  
P. F. Conzen ◽  
H. Habazettl ◽  
R. Gutmann ◽  
W. Kellermann ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Animal Experiments ◽  
Transpulmonary Pressure ◽  
Hemodynamic Instability ◽  
Compensatory Mechanisms ◽  
Prostaglandin F2 Alpha ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Positive Correlations

Fourteen noncardiac surgical patients received heparin (10,000 IU), which was neutralized by 100 mg protamine injected within 2 min during steady-state anesthesia. After protamine application, plasma complement C3a, thromboxane B2 (TxB2), prostaglandin F2 alpha (PGF2 alpha) and KH2PGF2 alpha increased significantly, whereas prostacyclin (6-keto-PGF2 alpha) levels did not change. This mediator response was associated with transient leukopenia and thrombocytopenia. Arterial pressure, pulmonary arterial pressure, and transpulmonary pressure gradient increased significantly. Heart rate, cardiac output, pulmonary capillary wedge pressure, and arterial PO2 remained constant. Positive correlations of plasma C3a were observed with pulmonary leukosequestration and plasma TxB2. Inverse correlations of C3a were noted with the counts of leukocytes and of platelets. A positive correlation was found between TxB2 and pulmonary arterial pressure. Our results indicate that marked activation of the complement system and the cyclooxygenase pathway is common after heparin reversal by protamine in anesthetized patients. This is in contrast to previous human studies performed after cardiopulmonary bypass but agrees well with results obtained in animal experiments. The mediator response in our patients, however, was not accompanied by hemodynamic instability, suggesting appropriate compensatory mechanisms.

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