The Effects of Verapamil, Quiescence, and Cardioplegia on Calcium Exchange and Mechanical Function in Ischemic Rabbit Myocardium

• Published in: Circulation research 1982-03, Vol.50 (3), p.360-368
• Main Authors: Bourdillon, Patrick D, Poole-Wilson, Philip A
• Format: Article
• Language: English
• Subjects: Action Potentials - drug effects; Animals; Blood Flow Velocity; Calcium - metabolism; Coronary Disease - metabolism; Coronary Disease - physiopathology; Electric Stimulation; Extracellular Space - physiopathology; Heart Arrest, Induced; In Vitro Techniques; Rabbits; Verapamil - pharmacology
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.50.3.360

The effects of verapamil (1 mg/liter, 2 × 10 mol/liter), quiescence, and cardioplegia (K 16 mmol/liter, Mg 16 mmol/liter) on calcium exchange and mechanical function during ischemia and reperfusion have been investigated in the rabbit interventricular septum at 32°C. Calcium influx and efflux were recorded continuously with Ca and Ca. After 60 minutes of total ischemia and reperfusion for 30 minutes, there was a net calcium gain of 4.9 mmol/kg dry tissue. Verapamil given before total ischemia reduced net calcium gain to 1.5 mmol/kg dry tissue (n = 5, P < 0.03). When given only on reperfusion after total ischemia, or 10 minutes before reperfusion during low flow ischemia, verapamil did not affect calcium exchange. Cardioplegia begun 10 minutes before total ischemia reduced net calcium gain to 1.0 ± 0.26 mmol/kg dry tissue (n = 6, F < 0.001). Cardioplegia during the first 10 minutes of reperfusion, or lack of electrical stimulation during reperfusion, did not reduce calcium gain. Net calcium gain correlated with the maximum rise in resting tension and with the recovery of developed tension. In control experiments, neither verapamil nor cardioplegia altered influx or efflux of slowly exchanging calcium. The cardioprotective effects of cardioplegia and the calcium channel blocker verapamil appear to be due to a reduction of myocardial work rather than to any specific direct action on calcium fluxes across the myocardial cell membrane.