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Articles in PresS, published online ahead of print February 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00833.2001
Submitted on September 24, 2001
Accepted on February 5, 2002
1 Department of Physiology, Texas Tech University Health Sciences Center, Lubbock, TX, USA
* To whom correspondence should be addressed. E-mail: phyrdn{at}physiology.ttuhsc.edu.
The purpose of this study was to investigate the mechanisms responsible for ischemia-induced changes in spontaneous electrical activity. An ischemic-like Tyrode solution (pH 6.6) reversibly depolarized the maximum diastolic potential (MDP) and reduced the action potential (AP) overshoot (OS). We used SNARF-1, an indicator of intracellular pH (pHi), and perforated-patch techniques to test the hypothesis that acidosis caused these effects. Acidic but otherwise normal Tyrode (pH 6.8) produced similar effects. Basic Tyrode (pH 8.5) hyperpolarized the MDP, shortened the AP and slowed the firing rate. In the presence of "ischemic" Tyrode, hyperpolarizing current restored the MDP and OS to control values. HOE 642, an inhibitor of Na-H exchange, did not alter pHi or electrical activity, and did not prevent the effects of "ischemic" Tyrode or recovery following washout. Time-independent, net inward current, but not hyperpolarization-activated inward current, was enhanced by "ischemic" Tyrode or by 30 µM BaCl2, a selective blocker of inward rectifying K currents at this concentration. The results suggest that: 1) acidosis was responsible for the "ischemia"-induced effects, but Na-H exchange was not involved; 2) the OS was reduced because of depolarization-induced inactivation of inward currents that generate the AP upstroke; 3) reduction of an inward rectifying, outward K current contributed to the depolarization.
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