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Cardiovascular Research Laboratories, Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7
To investigate cardiac stunning, we recorded intracellular [Ca2+], contractions, and electrical activity in isolated guinea pig ventricular myocytes exposed to simulated ischemia and reperfusion. After equilibration, ischemia was simulated by exposing myocytes to hypoxia, acidosis, hyperkalemia, hypercapnia, lactate accumulation, and substrate deprivation for 30 min at 37°C. Reperfusion was simulated by exposure to Tyrode solution. Field-stimulated myocytes exhibited stunning upon reperfusion. By 10 min of reperfusion, contraction amplitude decreased to 43.0 ± 5.5% of preischemic values (n = 15, P < 0.05), although action potential configuration and sarcoplasmic reticulum Ca2+ stores, assessed with caffeine, were normal. Diastolic [Ca2+] and Ca2+ transients (fura 2) were also normal in stunned myocytes. In voltage-clamped cells, peak L-type Ca2+ current was reduced to 47.4 ± 4.5% of preischemic values at 10 min of reperfusion (n = 21, P < 0.05). Contractions elicited by Ca2+-induced Ca2+ release and the voltage-sensitive release mechanism were both depressed in reperfusion. Our observations suggest that stunning is associated with reduced L-type Ca2+ current but that alterations in Ca2+ homeostasis and release are not directly responsible for stunning.
ischemia; reperfusion; contractile function; Ca2+ transients
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