TY - JOUR
T1 - Selective endothelial dysfunction in conscious dogs after cardiopulmonary bypass
AU - Zanaboni, Paul
AU - Murray, Paul A.
AU - Simon, Brett A.
AU - Zehr, Kenton
AU - Fleischer, Kirk
AU - Tseng, Elaine
AU - Nyhan, Daniel P.
PY - 1997/6
Y1 - 1997/6
N2 - 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 CPR. 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 μg · 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.
AB - 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 CPR. 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 μg · 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.
KW - Chronic instrumentation
KW - Endothelium- independent vasodilation
KW - Endothelium-dependent vasodilation
KW - Pressure-flow plots
KW - Pulmonary circulation
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U2 - 10.1152/jappl.1997.82.6.1776
DO - 10.1152/jappl.1997.82.6.1776
M3 - Article
C2 - 9173941
AN - SCOPUS:0031009416
SN - 8750-7587
VL - 82
SP - 1776
EP - 1784
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 6
ER -