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Articles in PresS, published online ahead of print April 25, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00020.2002
Submitted on January 14, 2002
Accepted on April 19, 2002
1 Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada
* To whom correspondence should be addressed. E-mail: gregory.ferrier{at}dal.ca.
To investigate cardiac stunning, we recorded intracellular [Ca2+], contractions, and electrical activity in isolated guinea pig ventricular myocytes exposed to simulated ischemia and reperfusion. Following 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's solution. Field stimulated myocytes exhibited stunning upon reperfusion. By 10 min of reperfusion contraction amplitude decreased to 43.0 ± 5.5% of pre-ischemic values (n=15, P<0.05), although action potential configuration and SR Ca2+ stores, assessed with caffeine, were normal. Diastolic [Ca2+] and Ca2+ transients (fura-2) also were normal in stunned myocytes. In voltage-clamped cells, peak L-type Ca2+ current was reduced to 47.4 ± 4.5% of pre-ischemic values at 10 min 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.
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