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Effects of N-n-butyl haloperidol iodide on rat myocardial ischemia and reperfusion injury and L-type calcium current.
Acta Pharmacol Sin. 2003 Aug; 24(8):757-63.AP

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<0.01) and shifted the current-voltage of ICa upward, without affecting the voltage-depend-ent properties of ICa.

CONCLUSION

F2 played a protective role against rat heart I/R injury in a dose-dependent manner, and inhibited ICa in rat ventricular myocytes. The cardioprotective and vasodilatory mechanisms of F2 may be related to its inhibitory effect on L-type calcium channel.

Authors+Show Affiliations

Department of Pharmacology, Shantou University Medical College, Shantou 515031, China.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12904274

Citation

Huang, Zhan-Qin, et al. "Effects of N-n-butyl Haloperidol Iodide On Rat Myocardial Ischemia and Reperfusion Injury and L-type Calcium Current." Acta Pharmacologica Sinica, vol. 24, no. 8, 2003, pp. 757-63.
Huang ZQ, Shi GG, Zheng JH, et al. Effects of N-n-butyl haloperidol iodide on rat myocardial ischemia and reperfusion injury and L-type calcium current. Acta Pharmacol Sin. 2003;24(8):757-63.
Huang, Z. Q., Shi, G. G., Zheng, J. H., & Liu, B. (2003). Effects of N-n-butyl haloperidol iodide on rat myocardial ischemia and reperfusion injury and L-type calcium current. Acta Pharmacologica Sinica, 24(8), 757-63.
Huang ZQ, et al. Effects of N-n-butyl Haloperidol Iodide On Rat Myocardial Ischemia and Reperfusion Injury and L-type Calcium Current. Acta Pharmacol Sin. 2003;24(8):757-63. PubMed PMID: 12904274.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of N-n-butyl haloperidol iodide on rat myocardial ischemia and reperfusion injury and L-type calcium current. AU - Huang,Zhan-Qin, AU - Shi,Gang-Gang, AU - Zheng,Jin-Hong, AU - Liu,Bing, PY - 2003/8/9/pubmed PY - 2004/3/17/medline PY - 2003/8/9/entrez SP - 757 EP - 63 JF - Acta pharmacologica Sinica JO - Acta Pharmacol Sin VL - 24 IS - 8 N2 - 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<0.01) and shifted the current-voltage of ICa upward, without affecting the voltage-depend-ent properties of ICa. CONCLUSION: F2 played a protective role against rat heart I/R injury in a dose-dependent manner, and inhibited ICa in rat ventricular myocytes. The cardioprotective and vasodilatory mechanisms of F2 may be related to its inhibitory effect on L-type calcium channel. SN - 1671-4083 UR - https://www.unboundmedicine.com/medline/citation/12904274/Effects_of_N_n_butyl_haloperidol_iodide_on_rat_myocardial_ischemia_and_reperfusion_injury_and_L_type_calcium_current_ DB - PRIME DP - Unbound Medicine ER -