Effects of urotensin II on isolated rat hearts under normal perfusion and ischemia reperfusion.
- Author:
Ping ZHOU
1
;
Sheng-Ying WU
;
Cheng-Fan YU
;
Hua WANG
;
Chao-Shu TANG
;
Li LIN
;
Wen-Jun YUAN
Author Information
1. Cardiovascular Institute, First Hospital, Peking University, Beijing 100034.
- Publication Type:Journal Article
- MeSH:
Animals;
Female;
Heart;
drug effects;
physiopathology;
In Vitro Techniques;
Male;
Myocardial Ischemia;
metabolism;
physiopathology;
Myocardial Reperfusion Injury;
metabolism;
physiopathology;
Myocardium;
metabolism;
pathology;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Urotensins;
pharmacology
- From:
Acta Physiologica Sinica
2003;55(4):442-448
- CountryChina
- Language:Chinese
-
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.
