ABSTRACT
OBJECTIVE: To investigate the role of the opioid receptors agonist butorphanol on mice myocardial ischemia reperfusion (I/R) injury. MATERIALS AND METHODS: The left anterior descending of coronary artery was ligatured for 30 min and then reperfusion for 6 h was performed to mimic the mouse myocardial I/R injury. All mice were randomly divided into three groups: sham group, I/R group and I/R + butorphanol group. Blood samples were collected for the measurement of cardiac troponin I (CTnI) and creatine kinase MB (CK-MB) levels. The infarct size was stained by triphenyltetrazolium chloride. The mitochondria morphology was observed by electron microscopy. The expressions of cleaved caspase-9 and -3, p38, ERK and JNK were detected by Western blot. RESULTS: The myocardial infarct size, serum CK-MB and CTn I levels, expression of cleaved caspase-9 and -3, phosphorylation of p38 and JNK were all increased in the I/R group compared with the sham group (all p < 0.01). Butorphanol reduced the myocardial infarct size, serum CTn I and CK-MB levels, expression of cleaved caspase-9 and -3, and phosphorylation levels of p38 and JNK (all p < 0.01). The number of mitochondria and the individual mitochondrial cross-sectional areas were decreased in the I/R mice compared with the sham-operated mice (all p < 0.01). Butorphanol reversed these changes in mitochondrial morphology (all p < 0.01). CONCLUSIONS: Butorphanol attenuates myocardial I/R injury through reducing cardiomyocyte apoptosis by inhibiting mitochondria-mediated apoptotic pathway, and blockage of p38 and JNK phosphorylation.
Subject(s)
Apoptosis/drug effects , Butorphanol/therapeutic use , Mitochondria/drug effects , Myocardial Reperfusion Injury/drug therapy , Animals , Butorphanol/pharmacology , Caspase 9 , Creatine Kinase, MB Form/blood , Male , Mice , Mice, Inbred C57BL , Mitochondria/pathology , Myocardial Infarction/drug therapy , Phosphorylation , p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors , p38 Mitogen-Activated Protein Kinases/metabolismABSTRACT
The Ã(2)A' --> &Xtilde;(2)A" electronic band system of HO(2) has been simulated in emission using an extended version of the program RENNER (P. Jensen, M. Brumm, W. P. Kraemer, and P. R. Bunker, J. Mol. Spectrosc. 171, 31-57 (1995)). The two electronic states involved in this transition have strongly bent equilibrium geometries but they correlate together to form a (2)Pi state at linearity. As a result the energy level pattern in the states is affected by electronic angular momentum effects (i.e., the Renner effect and spin-orbit coupling). To simulate the spectrum, we have calculated ab initio the potential energy surfaces, electric dipole moment surfaces, magnetic dipole moment surfaces, spin-orbit coupling parameter, and the electronic angular momentum matrix elements. Some of the forbidden DeltaK(a) = 0 transitions occurring in the spectrum are induced by the magnetic dipole transition moment, and the others are electric dipole transitions that gain intensity because of the Renner interaction, spin-orbit coupling, or because of rotation-vibration interaction. All of these effects are allowed for in our calculation. The electric dipole transition moment is very small (0.017 D at the ground state equilibrium geometry) and because of this the magnetic dipole transitions are quite visible; the strongest magnetic dipole transitions are calculated to be about 10 times weaker than the strongest electric dipole transitions. In this way previous experimental assignments (E. H. Fink and D. A. Ramsay, J. Mol. Spectrosc. 185, 304-324 (1997)) are confirmed theoretically. Copyright 1999 Academic Press.
