title: Impaired endothelium-dependent coronary microvascular relaxation after cold potassium cardioplegia and reperfusion.
abstract: Myocardial dysfunction after cardiac operations might be influenced by altered myocardial perfusion in the postoperative period. To investigate possible alterations in vascular reactivity, in vitro coronary microvascular responses were examined after ischemic cardioplegia with use of a porcine model of cardiopulmonary bypass. Since myocardial perfusion is primarily regulated by arteries less than 200 microns in diameter, these vascular segments were examined. After 1 hour of ischemic arrest with cold crystalloid cardioplegia and 1 hour of reperfusion, microvessels (100 to 190 microns in diameter) were pressurized in a no-flow state, preconstricted by 30% to 60% of the baseline diameter with acetylcholine, and examined with video microscopic imaging and electronic dimension analysis. Endothelium-dependent relaxations to bradykinin (55% +/- 13% versus 99% +/- 1% = maximum relaxation of the preconstricted diameter in cardioplegia-reperfusion vessels versus control vessels, respectively; p < 0.05) and the calcium ionophore A 23187 (33% +/- 6% versus 90% +/- 4%; p < 0.05) were markedly impaired while endothelium-independent relaxation to sodium nitroprusside was similar to control value. After 1 hour of ischemic cardioplegia without reperfusion, endothelium-dependent relaxation was only slightly affected. Transmission electron microscopy showed minimal endothelial damage after ischemic cardioplegia and reperfusion. These findings have important implications regarding coronary spasm and cardiac dysfunction after cardiac operations.
authors.affiliation: Department of Surgery, Beth Israel Hospital, Boston, MA 02215.
authors.forename: F W
authors.initials: FW
authors.lastname: Sellke
authors.forename: T
authors.initials: T
authors.lastname: Shafique
authors.forename: F J
authors.initials: FJ
authors.lastname: Schoen
authors.forename: R M
authors.initials: RM
authors.lastname: Weintraub
mesh_terms: D000109:Acetylcholine; D000634:Aminoquinolines; D000818:Animals; D001920:Bradykinin; D000001:Calcimycin; D003331:Coronary Vessels / Q000503:physiopathology / Q000648:ultrastructure*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000503:physiopathology / Q000648:ultrastructure*; D005069:Evaluation Studies as Topic; D006324:Heart Arrest, Induced / Q000009:adverse effects* / Q000379:methods; D006979:Hyperthermia, Induced / Q000009:adverse effects* / Q000379:methods; D007213:Indomethacin; D008833:Microcirculation / Q000503:physiopathology / Q000648:ultrastructure; D017348:Microscopy, Electron, Scanning Transmission; D017202:Myocardial Ischemia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D009599:Nitroprusside; D011188:Potassium / Q000009:adverse effects*; D013189:SRS-A / Q000037:antagonists & inhibitors; D012503:Saponins; D013552:Swine; D014664:Vasodilation / Q000502:physiology*
chemical_list: D000634:Aminoquinolines; D013189:SRS-A; D012503:Saponins; D009599:Nitroprusside; D000001:Calcimycin; C041715:6-anilino-5,8-quinolinedione; D000109:Acetylcholine; D011188:Potassium; D001920:Bradykinin; D007213:Indomethacin