@article{APS9135,
author = {Zhan-Qin Huang and Gang-Gang Shi and Jin-Hong Zheng and Bing Liu},
title = {Effects of N-n-butyl haloperidol iodide on rat myocardial ischemia and reperfusion injury and L-type calcium current},
journal = {Acta Pharmacologica Sinica},
volume = {24},
number = {8},
year = {2016},
keywords = {},
abstract = {AIM: To study the effects of N-n-butyl haloperidol iodide (F2) on rat heart ischemia/reperfusion (I/R) injury and L-type calcium current (ICa) in rat ventricular myocytes.
METHODS: Rat heart I/R injury was induced by occluding the left anterior descending coronary artery for 30 min and restoring perfusion for 30 min. F2 (1, 2, and 4 mg/kg) were i.v. injected before ischemia. Plasma creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBDH), glutamic-oxaloacetic transaminase (GOT), malondialdehyde (MDA) concentrations, and superoxide dismutase (SOD) activity were measured. The pathologic changes of I/R myocardium were assessed by the transmission electron microscopy. Single rat ventricular myocyte was obtained by enzymatic dissociation method. The currents were recorded with the whole-cell configuration of the patch-clamp technique.
RESULTS: F2 reduced the release of CK, CK-MB, LDH, HBDH and GOT, preserved the activity of SOD, and decreased the MDA contents dose-dependently. For morphology, F2 mollified the pathologic changes of myocardium induced by I/R injury. F2 1 micromol/L decreased ICa from (1775+/-360) pA to (464+/-129) pA (n=8, P},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/9135}
}