부산대학교 도서관

Acute myocardial ischemia was produced in rabbit Langendorff hearts by ligation of the left anterior descending coronary artery for 2 h. This was accompanied by a significant increase in creatine kinase-specific activity of the ischemic myocardium as compared to sham-operated nonischemic controls (p ± 0.05) and a significant decrease (p ± 0.01) in ATP levels from 2.25–0.29 mol/g wet wt. in the nonischemic area to 0.95 ± 0.21 mol/g wet wt in the ischemic area, indicating a considerable degree of tissue damage. There was a decrease in the norepinephrine ratio between infarcted and noninfarcted myocardium from 1.08 ± 0.08 in sham-operated controls to 0.66 ± 0.06 in ischemic hearts (p ± 0.01). Histochemistry revealed a nearly complete loss of fluorescence in perivascular adrenergic nerves in the ischemic area. Infusion of prostacyclin (PGI2) (1.1 nmol min), starting 10 min prior to ischemia, abolished the increase in creatine kinase activity (p ± 0.05) and the decrease in ATP levels of the ischemic myocardium (p ± 0.05). Furthermore, PGI2prevented the ischemia-induced alterations in catecholamine content and the decrease in adrenergic fiber fluorescence. PGI2did not significantly influence myocardial dynamics and oxygen consumption. To determine the effect of PGI2on nerve stimulation-induced catecholamine release, a separate group of Langendorff rabbit hearts with intact right sympathetic nerves were stimulated twice for 1 min at 0 and 13 min. PCI2at 30 nM 3μM had no significant effect on catecholamine overflow when compared to control hearts. It is concluded that PGI2exerts a stabilizing effect on cell membranes that prevents ischemia-induced destruction of adrenergic nerve endings, This cytoprotective effect is restricted to the ischemic area and does not interfere with the physiological nerve-stimulation-induced norepinephrine release.