Electrophysiological responses of hypertrophied rat myocardium to combined hypoxia, hyperkalemia, and acidosis.

We studied whether electrophysiological response to ischemia could be different in hypertrophied left ventricle of spontaneously hypertensive rats (SHRs) and in normal left ventricle of normotensive Wistar-Kyoto (WKY) rats. For that purpose, we used a two-compartment tissue bath in which one-half of a left ventricular strip was exposed to normal conditions and the other part to ischemic conditions (low pH, hypoxia, and hyperkalemia). Electrical activity was recorded using standard microelectrodes in normal and hypertrophied preparations. Under basal conditions, the action potential duration (APD) and effective refractory period (ERP) were longer in SHRs than in WKY rats (118 +/- 9 ms vs 81 +/- 3 ms, p less than 0.05 and 90 +/- 9 ms vs. 74 +/- 4 ms, p less than 0.05, respectively). During ischemia, the APD and ERP changed in opposite ways in both groups and we observed the development of postrepolarization refractoriness that was greater in hypertrophied than in normal hearts. Maximum upstroke velocity (Vmax) values were 229 +/- 12 and 227 +/- 10 V/s in the SHR and the WKY preparations, respectively. Three minutes after the induction of ischemia, Vmax values decreased to 46 +/- 7 V/s in SHRs and to 106 +/- 12 V/s in WKY rats. A significant increase in subendocardial collagen density was measured in SHR left ventricle compared to WKY rats (4.39 +/- 0.34% vs. 1.66 +/- 0.15%, p less than 0.05), which might partly explain the impaired conduction observed in hypertrophied preparations during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)