title: [Effects of urotensin II on isolated rat hearts under normal perfusion and ischemia reperfusion].
abstract: To shed light on cardiac effects of the potent vasoconstrictive peptide urotensin II (U II), Langendorff-perfused isolated rat hearts were consecutively perfused with 0.1, 1 and 10 nmol/L U II, for 5 min at each dose, followed by 5-min washout. Moreover, isolated hearts subjected to 20-min global no-flow ischemia were reperfused with U II (1 or 10 nmol/L) for 20 min. Heart function parameters including heart rate, left ventricular pressure and dP/dt were monitored; content of protein and myoglobin, and activity of lactate dehydrogenase (LDH) in coronary effluent were determined; malondialdehyde (MDA) in myocardium and [(125)I]-U II binding sites in plasma membrane were measured after the completion of perfusion. The results showed that: (1) In normal rat hearts, the coronary flow was decreased and the heart function was suppressed by U II dose-dependently, and these changes were not abolished by washout. The leakage of cardiac protein, myoglobin and LDH increased with the increment of U II, but it diminished rapidly after washout. In contrast, MDA content in U II -treated myocardium was not statistically different from that in normal myocardium. (2) Ischemia-reperfusion caused significant decreases in coronary flow, suppression of heart function, and leakage of protein and LDH. In U II -reperfused hearts, all these disorders were significantly aggravated and myocardial MDA content significantly increased (P<0.01), to a greater extent in the presence of higher dose of U II. (3) The maximal binding capacity (B(max)) of U II receptors in plasma membrane from ischemia-reperfusion myocardium increased significantly as compared with that of normal myocardium (20.53+/-1.98 vs 14.65+/-1.78 fmol/mg pr, P<0.01), while Kd remained unchanged. These results indicate that U II caused injury to the isolated rat hearts under normal perfusion, and worsened the injury of the hearts under ischemia-reperfusion, in which U II receptors were up-regulated.
authors.affiliation: Cardiovascular Institute, First Hospital, Peking University, Beijing 100034.
authors.forename: Ping
authors.initials: P
authors.lastname: Zhou
authors.forename: Sheng-Ying
authors.initials: SY
authors.lastname: Wu
authors.forename: Cheng-Fan
authors.initials: CF
authors.lastname: Yu
authors.forename: Hua
authors.initials: H
authors.lastname: Wang
authors.forename: Chao-Shu
authors.initials: CS
authors.lastname: Tang
authors.forename: Li
authors.initials: L
authors.lastname: Lin
authors.forename: Wen-Jun
authors.initials: WJ
authors.lastname: Yuan
mesh_terms: D000818:Animals; D005260:Female; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D014579:Urotensins / Q000494:pharmacology*
chemical_list: D014579:Urotensins; C029677:urotensin II