EFFECTS OF HYPOXIA, SIMULATED ISCHEMIA AND REOXYGENATION ON THE CONTRACTILE FUNCTION OF HUMAN ATRIAL TRABECULAE

Hypoxia, ischemia and reoxygenation cause contractile dysfunction whic h will be characterized by the time course of isometric contraction of human atrial trabeculae. Post-rest potentiation (PRP) and postextrast imulatory potentiation (PEP) were elicited to obtain indirect informat ion about the role of the sarcoplasmic reticulum (SR) in excitation-co ntraction coupling. As lipid peroxidation could cause SR dysfunction, thiobarbituric acid reactive substances (TBARS) were measured. After 3 0 min of hypoxia (H) or simulated ischemia (H combined with acidosis-S 1), contractile force decreased to 15% and 6%, respectively, of contro l (p less than or equal to 0.05), whereas the normalized rate of both contraction and relaxation increased. In group H, rapid reoxygenation produced a recovery of contractile force to about 60%. After post-hypo xic reoxygenation the TBARS concentration was increased. In group S1, rapid reoxygenation and a rather gradual correction of acidosis produc ed complete recovery of contractile force. PRP and PEP were maintained during H and S1. Particularly post-ischemic reoxygenation caused a ma rked depression of PRP and partly of PEP. Thus, alteration of SR Ca2handling occurs predominantly during reoxygenation rather than during H or S1, probably associated with the damaging effect of increased oxy gen radicals. The depression of potentiation occured along with delaye d relaxation, temporary increased resting force, mechanical alternans, and spontaneous activity which are further characteristics for SR dys function. Thus, for a possibly beneficial effect of low pH during S1 c ombined with its gradual correction during reoxygenation on the recove ry of contractile function, developed force should not be the only ind ex.