Electrophysiological response of vascularized hamster cardiac transplants to ischemia.

Abstract

To study transmembrane electrophysiological properties of blood-perfused mammalian heart cells during normal perfusion and during acute ischemia, 1- to 2-mm cubes of neonatal hamster atrial and ventricular myocardium were transplanted to the adult hamster cheek pouch and studied with microelectrodes 4--7 days later, when vascularization and spontaneous contractions occurred. Action potentials recorded from the transplants were similar to those recorded from neonatal and adult hamster myocardium studied in vitro. Interrupting blood flow to spontaneously beating transplants reduced diastolic depolarization and suppressed automaticity. After automaticity ceased, the transplants were paced with a bipolar electrode or intracellular microelectrode. Action potential amplitude, resting potential, and dV/dtmax decreased during ischemia. Action potential duration and the intracellular current threshold for excitation increased initially, subsequently decreased to values less than control, and increased again prior to the onset of inexcitability. Conduction delay and block occurred during the late stages of ischemia. Depressed action potentials recorded during ischemia were suppressed by tetrodotoxin (10(-5) M) but not by verapamil (2 x 10(-6) M). These data indicate that: (1) the electrophysiological properties of cheek pouch cardiac transplants are normal, (2) ischemia suppresses transplant automaticity, (3) cellular excitability increases during the early stages of ischemia and decreases at a time when conduction delay and block occur, and (4) action potentials generated during the later stages of ischemia appear to be depressed fast responses, rather than slow responses.