TY - JOUR
T1 - Global myocardial ischemia and reperfusion impair endothelium-dependent relaxations to aggregating platelets in the canine coronary artery
T2 - A possible cause of vasospasm after cardiopulmonary bypass
AU - Pearson, P. J.
AU - Lin, P. J.
AU - Schaff, H. V.
PY - 1992
Y1 - 1992
N2 - Experiments were designed to determine whether endothelial cell injury contributes to increased coronary vascular tone after global cardiac ischemia and reperfusion. Canine hearts were exposed to global ischemia for 45 minutes and were reperfused for 60 minutes. Rings (5 to 6 mm long) of the left anterior descending coronary artery from reperfused hearts and from normal (control) hearts were suspended for isometric force measurement in organ chambers containing physiologic salt solution (37° C, and 95% oxygen and 5% carbon dioxide). After contraction with prostaglandin F(2α), reperfused coronary arteries had significant impairment of endothelium-dependent relaxations to aggregating platelets (52% ± 12% relaxation versus 102% ± 11% for control segments; p < 0.05). Reperfused arterial rings also exhibited impaired endothelium-dependent relaxations to the receptor-dependent agonist acetylcholine and the platelet-derived compounds adenosine diphosphate and serotonin. Importantly, endothelium-dependent relaxations to the non- receptor-dependent agonist A23187 were normal after ischemia and reperfusion. Quiescent (noncontracted) reperfused arterial rings lost the ability to counteract the constrictive effect of aggregating platelets on the coronary vascular smooth muscle (24% ± 7% contraction versus 5% ± 2% relaxation for control segments; p < 0.05). Endothelium-independent contractions to potassium chloride and prostaglandin F(2α) were similar in reperfused and normal arteries. Also, endothelium-independent relaxations to nitric oxide and isoproterenol were comparable in reperfused arteries and normal vessels. Thus global cardiac ischemia and reperfusion impair the normal endothelium- dependent relaxations to aggregating platelets and other receptor-dependent vasoactive drugs. This impairment of platelet-mediated coronary vasodilation may explain increased coronary vascular tone after cardiopulmonary bypass and could be an important pathophysiologic mechanism of postoperative coronary vasospasm.
AB - Experiments were designed to determine whether endothelial cell injury contributes to increased coronary vascular tone after global cardiac ischemia and reperfusion. Canine hearts were exposed to global ischemia for 45 minutes and were reperfused for 60 minutes. Rings (5 to 6 mm long) of the left anterior descending coronary artery from reperfused hearts and from normal (control) hearts were suspended for isometric force measurement in organ chambers containing physiologic salt solution (37° C, and 95% oxygen and 5% carbon dioxide). After contraction with prostaglandin F(2α), reperfused coronary arteries had significant impairment of endothelium-dependent relaxations to aggregating platelets (52% ± 12% relaxation versus 102% ± 11% for control segments; p < 0.05). Reperfused arterial rings also exhibited impaired endothelium-dependent relaxations to the receptor-dependent agonist acetylcholine and the platelet-derived compounds adenosine diphosphate and serotonin. Importantly, endothelium-dependent relaxations to the non- receptor-dependent agonist A23187 were normal after ischemia and reperfusion. Quiescent (noncontracted) reperfused arterial rings lost the ability to counteract the constrictive effect of aggregating platelets on the coronary vascular smooth muscle (24% ± 7% contraction versus 5% ± 2% relaxation for control segments; p < 0.05). Endothelium-independent contractions to potassium chloride and prostaglandin F(2α) were similar in reperfused and normal arteries. Also, endothelium-independent relaxations to nitric oxide and isoproterenol were comparable in reperfused arteries and normal vessels. Thus global cardiac ischemia and reperfusion impair the normal endothelium- dependent relaxations to aggregating platelets and other receptor-dependent vasoactive drugs. This impairment of platelet-mediated coronary vasodilation may explain increased coronary vascular tone after cardiopulmonary bypass and could be an important pathophysiologic mechanism of postoperative coronary vasospasm.
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U2 - 10.1016/s0022-5223(19)34880-9
DO - 10.1016/s0022-5223(19)34880-9
M3 - Article
C2 - 1597979
AN - SCOPUS:0026708646
SN - 0022-5223
VL - 103
SP - 1147
EP - 1154
JO - Journal of Thoracic and Cardiovascular Surgery
JF - Journal of Thoracic and Cardiovascular Surgery
IS - 6
ER -