Pulmonary Vasoregulation by Cyclooxygenase Metabolites and Angiotensin II after Hypoperfusion in Conscious, Pentobarbitalanesthetized, and Halothane-anesthetized Dogs

Fehr, D. M.; Nyhan, Daniel; Chen, Bessie B.; Murray, Paul A.

doi:10.1097/00000542-199108000-00014

Cited by 10 publications

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“…Our experimental approach has several unique features that allow our results to be attributed specifically to the effects of CPB. First, general anesthetics are recognized as modulators of vasoregulation, including pulmonary vasoregulation (5,12,22,23,25). The use of conscious animals avoids this potential confounding influence.…”

Section: Discussionmentioning

confidence: 99%

“…The LP-Q relationship was measured to determine the pulmonary vascular responses to endothelium-dependent and -independent vasodilators before and again 3-4 days after closed-chest CPB. This approach avoids the known effects of general anesthesia on neurohumoral (5,12,23,25) and local (12,19,22) mechanisms of pulmonary vasoregulation. Furthermore, measurement of continuous LP-Q plots avoids the inherent limitations of single-point calculations of pulmonary vascular resistance.…”

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confidence: 99%

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Selective endothelial dysfunction in conscious dogs after cardiopulmonary bypass

Zanaboni

Murray

Simon

et al. 1997

Journal of Applied Physiology

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It has previously been demonstrated that cardiopulmonary bypass (CPB) causes prolonged pulmonary vascular hyperreactivity (D.P. Nyhan, J.M. Redmond, A.M. Gillinov, K. Nishiwaki, and P.A. Murray. J. Appl. Physiol. 77: 1584-1590, 1994). This study investigated the effects of CPB on endothelium-dependent (acetylcholine and bradykinin) and endothelium-independent (sodium nitroprusside) pulmonary vasodilation in conscious dogs. Continuous left pulmonary vascular pressure-flow (LP-Q) plots were generated in conscious dogs before CPB and again in the same animals 3-4 days post-CPB. The dose of U-46619 used to acutely preconstrict the pulmonary circulation to similar levels pre- and post-CPB was decreased (0.13 +/- 0.01 vs. 0.10 +/- 0.01 mg.kg-1.min-1, P < 0.01) after CPB. Acetylcholine, bradykinin, and sodium nitroprusside all caused dose-dependent pulmonary vasodilation pre-CPB. The pulmonary vasodilator response to acetylcholine was completely abolished post-CPB. For example, at left pulmonary blood flow of 80 ml.kg-1.min-1 acetylcholine (10 micrograms.kg-1.min-1) resulted in 72 +/- 15% reversal (P < 0.01) of U-46619 preconstriction pre-CPB but caused no change post-CPB. However, the responses to bradykinin and sodium nitroprusside were unchanged post-CPB. The impaired pulmonary vasodilator response to acetylcholine, but not to bradykinin, suggests a selective endothelial defect post-CPB. The normal response to sodium nitroprusside indicates that cGMP-mediated vasodilation is unchanged post-CPB.

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