Contractures and increase in internal longitudianl resistance of cow ventricular muscle induced by hypoxia.

Abstract

This study was performed to determine whether hypoxia in glucose-free solutions can increase the electrical resistance of intercellular junctions in ventricular muscle. Internal longitudinal resistance (Ri), mechanical tension, and transmembrane action potentials were measured simultaneously in cow ventricular trabeculae. The mean control value of Ri was 265 +/- 38 omegacm (mean +/- SE) at 34 degrees C. After 1 hour of hypoxia in glucose-free Tyrode's solution, it had increased by 300 +/- 41% (n = 11, P less than 0.001). The rise in Ri was closely related to the increase in resting tension (contracture). These effects were more pronounced during a second exposure to hypoxia and were potentiated by application of epinephrine, by increasing extracellular calcium concentration, and by increasing frequency of stimulation. Addition of glucose (50 mM) provided some protection against hypoxia. It is inferred that the increase in Ri is entirely due to the increase in the resistance of intercellular junctions (electrical uncoupling). Intracellular calcium may be responsible for both the contracture and the uncoupling.

Protection of rat atrial myocardium against electrical, mechanical and structural aspects of injury caused by exposure in vitro to conditions of simulated ischaemia

“…Exposure of atria to SI at a calcium concentration of 0.5 mm caused less contracture, and less shortening of refractory periods and slowing of CV than at 2 mm CaCl2. This confirms previous findings in ventricular muscle (Hearse et al, 1977;Wojtczak, 1979;Cavero et al, 1983;Koomen et al, 1983;Fitzpatrick & Karmazyn, 1984;Anno et al, 1986;Karmazyn, 1986), although contrary findings have also been published (Nayler & Williams, 1978;Lewis et al, 1979). Why mitochondria were not protected structurally against SI at 0.5 mm calcium in the present experiments is unknown, but has been reported previously for ventricular muscle in vivo (Jennings et al, 1985a;Pilati & Paradise, 1984).…”

“…It was of interest to discover whether sulphinpyrazone also protects the myocardium against the structural and mechanical changes produced by SI and whether other non-steroidal anti-inflammatory agents share these properties. In view of the association between calcium overload and myocardial injury (Hearse et al, 1977; Wojtczak, 1979;Koomen et al, 1983;Cavero et al, 1983;Fitzpatrick & Karmazyn, 1984;Karmazyn, 1986), the association between calcium ions and SI was also investigated.…”

pH-dependent modulation of voltage gating in connexin45 homotypic and connexin45/connexin43 heterotypic gap junctions

“…Studies of normal/ischemia border regions in isolated preparations of the heart showed that preservation of ischemic cells by neighboring cells exposed to normal perfusion is greater in the longitudinal than in transverse direction of the fibers, consistent with ∼7-to 10-fold stronger cell-cell coupling in the longitudinal direction (45). However, under severe ischemic conditions GJ communication is blocked (46), and this blockage may limit both the spread of damage and the cell-rescuing/ preservation effect of GJs. Thus, during mild ischemia GJs remain open to preserve ischemia-affected cells, but when ischemia worsens, GJs shut down, a response that may isolate damaged areas and improve organ survival.…”

Effect of tissue anisotropy on extracellular potential fields in canine myocardium in situ.

“…The extracellular voltage at local depolarization in small strips of muscle in vitro has been used to determine intracellular and extracellular resistivity of cardiac muscle (Weidmann, 1970;Clerc, 1976;Weingart, 1977;Wojtczak, 1979;Hermsmeyer, 1980). In the present study we did not determine wavefront voltage by simply measuring the voltage change during local depolarization.…”