Literature DB >> 9534854

Differential roles of myocardial Ca2+ channels and Na+/Ca2+ exchange in myocardial reperfusion injury in open chest dogs: relative roles during ischemia and reperfusion.

S C Smart1, K B Sagar, D C Warltier.   

Abstract

OBJECTIVE: Compare the roles of Ca2+ channels and Na+/Ca2+ exchange in reperfusion injury (reperfusion ventricular fibrillation and myocardial stunning).
METHODS: Open chest dogs undergoing 15 minutes of left anterior descending coronary artery occlusion and 3 hours of reperfusion were randomized to controls or intracoronary infusions of the respective antagonists, nifedipine (50 micrograms/min) or amiloride (5 mg/min), according to five protocols: (A) 40 minutes before occlusion to 30 minutes after reperfusion; (B) 2 minutes before to 5 minutes after reperfusion; (C) 10 minutes before to 10 minutes after reperfusion (two step infusion for nifedipine only 5 micrograms/min during occlusion and 50 micrograms/min after reperfusion); and (D) 0 to 30 minutes after reperfusion. The role of Ca2+ channels was further investigated by infusing the agonist, Bay K 8644 (50 micrograms/min), alone or simultaneously with any protocol B, C, or D infusions altering both reperfusion ventricular fibrillation and myocardial stunning.
RESULTS: Effects of the agents on injury did not result from hemodynamic effects or alterations in blood flow. Amiloride had no effect on ventricular fibrillation. Only protocol A infusion of amiloride prevented myocardial stunning. In contrast, protocol A and B infusions of nifedipine prevented both myocardial stunning (p = ns vs. baseline, p < 0.01 vs. control) and ventricular fibrillation (0%, p < 0.01). Protocol C prevented reperfusion ventricular fibrillation, but not stunning (p = ns vs. control). Protocol D did not alter injury. Bay K 8644 co-treatment reversed the effects of Protocol B infusion of nifedipine. Ventricular fibrillation was common and postischemic function worst in dogs treated with Bay K 8644 alone (protocol B).
CONCLUSION: Myocardial Ca2+ channels contribute to both reperfusion ventricular fibrillation and stunning, whereas Na+/Ca2+ exchange contributes only to stunning. Inhibitors of myocardial Ca2+ channels are protective when infused in high doses just before reperfusion, whereas the efficacy of Na+/Ca2+ exchange inhibitors is dependent on pretreatment.

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Year:  1997        PMID: 9534854     DOI: 10.1016/s0008-6363(97)00187-9

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  3 in total

1.  Protection of the ischemic myocardium during the reperfusion: between hope and reality.

Authors:  Jean Chrisostome Bopassa
Journal:  Am J Cardiovasc Dis       Date:  2012-07-25

2.  Ventricular arrhythmias and mortality associated with isoflurane and sevoflurane in a porcine model of myocardial infarction.

Authors:  Marta Regueiro-Purriños; Felipe Fernández-Vázquez; Armando Perez de Prado; Jose R Altónaga; Carlos Cuellas-Ramón; Jose M Ajenjo-Silverio; Asuncion Orden; Jose M Gonzalo-Orden
Journal:  J Am Assoc Lab Anim Sci       Date:  2011-01       Impact factor: 1.232

3.  Inhibitory effects of AMP 579, a novel cardioprotective adenosine A1/A2A receptor agonist, on native IKr and cloned HERG current.

Authors:  Noriko Saegusa; Toshiaki Sato; Takehiko Ogura; Issei Komuro; Haruaki Nakaya
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2004-11-19       Impact factor: 3.000

  3 in total

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