We studied the effect of 1.0 μM ryanodine and 0.1 μM BAY K 8644 (putative modulators of intracellular calcium) on the changes in action potential characteristics, cellular coupling, and longitudinal conduction induced by simulated ischemia (9.0 mM K, 6.5 pH, 0 glucose, 20 mmHg PO2) in superfused guinea pig papillary muscles. Simulated ischemia (SI) depolarized the resting membrane by 5 mV and caused a 28% decrease in action potential upstroke (V(max)), a 65% decrease in action potential duration at 90% (APD90), a 40% increase in internal longitudinal resistance (r(i)), and a 17% decrease in conduction velocity as compared with the 9-K Tyrode control solution. These changes were reversible and reproducible. The decrease in V(max) induced by SI was greater than that associated with a K+-induced change in resting membrane potential (RMP). Ryanodine lessened the SI-induced APD90 shortening by 26%, the decrease in V(max) by 42%, the increase in r(i) by 33%, and the decrease in conduction velocity by 21%. BAY K 8644 did not alter SI-induced APD90 shortening but augmented the decrease in V(max) by 23%, the increase in r(i) by 67%, and the decrease in conduction velocity by 59%. Neither ryanodine nor BAY K 8644 altered the SI-induced changes in RMP. Our results suggest that changes in intracellular calcium during SI not only influence cellular coupling but also contribute to the apparent non-RMP-dependent component of the change in V(max) and to the change in APD90 induced by SI.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||6 30-6|
|Publication status||Published - 1991|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)