Cardiorespiratory effects of rapid saline infusion in normal man

1975 ◽  
Vol 38 (5) ◽  
pp. 786-775 ◽  
Author(s):  
A. L. Muir ◽  
D. C. Flenley ◽  
B. J. Kirby ◽  
M. F. Sudlow ◽  
A. R. Guyatt ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Control Period ◽  
Lung Compliance ◽  
Saline Infusion ◽  
Tidal Range ◽  
Closing Volume ◽  
Rapid Infusion ◽  
Pulmonary Arterial

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.

Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs

1982 ◽  
Vol 52 (3) ◽  
pp. 705-709 ◽  
Author(s):  
B. R. Walker ◽  
N. F. Voelkel ◽  
J. T. Reeves
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Conscious Dogs ◽  
Pulmonary Pressure ◽  
Time Control ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.

Mechanism and pharmacology of endotoxin shock in sheep

1963 ◽  
Vol 18 (3) ◽  
pp. 544-552 ◽  
Author(s):  
D. F. J. Halmagyi ◽  
B. Starzecki ◽  
G. J. Horner
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Arterial Oxygen Saturation ◽  
Lung Compliance ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Arterial Oxygen ◽  
Marked Rise ◽  
Pulmonary Arterial ◽  
Pressure Fall

The cardiopulmonary consequences of coli-lipopolysaccharide and staphylococcus toxin administration were studied in sheep. Circulatory changes consisted mainly of a marked rise in pulmonary arterial and pulmonary arterial wedge pressure (with left atrial pressure unchanged), and a fall in cardiac output and in systemic arterial pressure. Fall in the latter closely followed the onset of pulmonary hypertension. The respiratory response consisted mainly of a severe fall in lung compliance produced by terminal airway closure. Continued perfusion of the nonventilated alveoli resulted in venous admixture. Premedication with antihistaminic, antiserotonin, or adrenolytic agents failed to affect the response. Norepinephrine or hypertensin administered after toxin injection had virtually no effect while isoproterenol treatment reduced pulmonary arterial pressure, increased cardiac output, arterial oxygen saturation, and, in cases of endotoxin shock, promptly raised systemic arterial pressure. Endotoxin-resistant sheep proved nonresponsive to minor pulmonary embolism and to incompatible blood transfusion. It is suggested that a common mediator agent is responsible for the similar cardiopulmonary consequences of these three diverse conditions. Submitted on November 26, 1962

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

Low exercise pulmonary resistance is not dependent on vasodilator prostaglandins

1983 ◽  
Vol 55 (2) ◽  
pp. 558-561 ◽  
Author(s):  
J. Lindenfeld ◽  
J. T. Reeves ◽  
L. D. Horwitz
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Cyclooxygenase Inhibitors ◽  
Pulmonary Resistance ◽  
Before And After ◽  
Pulmonary Arterial

In resting conscious dogs, administration of cyclooxygenase inhibitors results in modest increases in pulmonary arterial pressure and pulmonary vascular resistance, suggesting that vasodilator prostaglandins play a role in maintaining the low vascular resistance in the pulmonary bed. To assess the role of these vasodilator prostaglandins on pulmonary vascular resistance during exercise, we studied seven mongrel dogs at rest and during exercise before and after intravenous meclofenamate (5 mg/kg). Following meclofenamate, pulmonary vascular resistance rose both at rest (250 24 vs. 300 +/- 27 dyn . s . cm-5, P less than 0.01) and with exercise (190 +/- 9 vs. 210 +/- 12 dyn . s . cm-5, P less than 0.05). Systemic vascular resistance rose slightly following meclofenamate both at rest and during exercise. There were no changes in cardiac output. The effects of cyclooxygenase inhibition, although significant, were less during exercise than at rest. This suggests that the normal fall in pulmonary vascular resistance during exercise depends largely on factors other than vasodilator prostaglandins.

Atrial natriuretic peptide correlates with pulmonary arterial pressure and cardiac output

Peptides ◽  
1987 ◽  
Vol 8 (2) ◽  
pp. 285-290 ◽  
Author(s):  
K. Naruse ◽  
M. Naruse ◽  
T. Honda ◽  
K. Obana ◽  
H. Sakurai ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Atrial Natriuretic

Comparative effects of arachidonic acid, bisenoic prostaglandins, and an endoperoxide analog on the canine pulmonary vascular bed

1977 ◽  
Vol 55 (6) ◽  
pp. 1369-1377 ◽  
Author(s):  
Philip J. Kadowitz ◽  
Ernst W. Spannhake ◽  
Stan Greenberg ◽  
Larry P. Feigen ◽  
Albert L. Hyman
Keyword(s):  
Cardiac Output ◽  
Arachidonic Acid ◽  
Arterial Pressure ◽  
Superior Vena Cava ◽  
Right Atrium ◽  
Pulmonary Arterial Pressure ◽  
Superior Vena ◽  
Vena Cava ◽  
Aortic Pressure ◽  
Pulmonary Arterial

The effects of bolus injections of the postaglandin precursor, arachidonic acid, and PGD2, PGF2α, PGE2, and the PGH2 analog ((15S)-hydroxyl-9α,11α(epoxymethano)-prosta-5Z-dienoic acid) were compared on the pulmonary circulation in the intact spontaneously breathing pentobarbital-anesthetized dog. Arachidonic acid increased pulmonary arterial pressure, decreased aortic pressure, and increased cardiac output when injected into the superior vena cava or right atrium. PGE2, like arachidonic acid, increased pulmonary arterial pressure and cardiac output and decreased aortic pressure, whereas PGF2α and PGD2 increased pulmonary arterial pressure but did not affect cardiac output or aortic pressure when injected into the superior vena cava or right atrium. The PGH2 analog increased pulmonary arterial pressure and to a lesser extent, aortic pressure, without affecting cardiac output. None of these substances changed left atrial or right atrial pressure. The cardiopulmonary effects of arachidonic acid were blocked by indomethacin whereas the rise in pulmonary arterial pressure in response to the bisenoic prostaglandins and the analog were enhanced by the cyclooxygenase inhibitor. These data suggest that the increase in pulmonary vascular resistance in response to arachidonic acid may be due to conversion of the precursor into vasoactive intermediates and products such as bisenoic prostaglandins whereas the decrease in systemic vascular resistance is probably due to the formation of PGE2 and other peripheral vasodilator substances.

Ventilation-perfusion relationships with high cardiac output in lobar atelectasis

1981 ◽  
Vol 50 (2) ◽  
pp. 341-347 ◽  
Author(s):  
P. T. Schumacker ◽  
J. C. Newell ◽  
T. M. Saba ◽  
S. R. Powers
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
Shunt Fraction ◽  
Mechanically Ventilated ◽  
Arteriovenous Fistulas ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial ◽  
Mixed Venous

Pulmonary gas exchange was evaluated in 10 anesthetized mechanically ventilated dogs. Cardiac output (QT) was increased approximately 50% by opening peripheral arteriovenous fistulas. With both lungs ventilated, increasing QT increased mixed venous O2 both pressure (PO2) and pulmonary arterial pressure, but neither shunt fraction nor the distribution of ventilation-perfusion was consistently altered. During left lung atelectasis, increasing QT again increased mixed venous PO2 and pulmonary arterial pressure, but two different responses in shunt-like perfusion were measured. In four dogs, left lung atelectasis caused a shunt fraction of 46 +/- 6% that was not changed by high QT (P greater than 0.05). In six dogs, atelectasis caused a shunt fraction of 24 +/- 3% during normal QT that increased to 42 +/- 2% during high QT (P less than 0.001). Dogs whose shunt fraction during atelectasis was high and unchanged by QT had lower arterial pH (7.24 +/- 0.03) than dogs whose shunt fraction was initially lower and was increased with QT (7.36 +/- 0.02) (P less than 0.01). We conclude that increased QT can worsen shunt flow during lobar atelectasis when hypoxic vasoconstriction has been effective in limiting perfusion to the collapsed region at normal levels of QT.

Effects of arteriovenous fistula on systemic and pulmonary circulations

1964 ◽  
Vol 207 (6) ◽  
pp. 1319-1324 ◽  
Author(s):  
Jiro Nakano ◽  
Christian De Schryver
Keyword(s):  
Cardiac Output ◽  
Blood Transfusion ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Pulmonary Arterial

The effects of arteriovenous fistulas of different magnitudes on cardiovascular dynamics were studied in anesthetized dogs. It was found that A-V fistula decreases mean systemic arterial pressure, effective systemic blood flow, total and pulmonary peripheral resistances, whereas it increases heart rate, total cardiac output, stroke volume, left atrial pressure, pulmonary arterial pressure, and systemic peripheral resistance. The magnitude of the above hemodynamic changes was essentially proportional to the size of the fistula. At equivalent increments in total cardiac output produced by A-V fistula and blood transfusion, the former condition causes a greater increase in pulmonary arterial pressure than the latter, although both conditions decrease the pulmonary peripheral resistance by the same degree. It was also found that, at equivalent left atrial pressures, left ventricular stroke work with A-V fistula was greater than that with blood transfusion.

Hemodynamic effects of arginine vasopressin in rats adapted to chronic hypoxia

1989 ◽  
Vol 66 (1) ◽  
pp. 151-160 ◽  
Author(s):  
H. K. Jin ◽  
R. H. Yang ◽  
Y. F. Chen ◽  
R. M. Thornton ◽  
R. M. Jackson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Pulmonary Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Systemic Hemodynamic ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Air Control

Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.

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