Recovery of trout myocardial function following anoxia: preconditioning ina non-mammalian model

Studies with mammals and birds clearly demonstrate that brief preexposure t o oxygen deprivation can protect the myocardium from damage normally associ ated with a subsequent prolonged hypoxic/ischemic episode. However, is not known whether this potent mechanism of myocardial protection, termed precon ditioning, exists in other vertebrates including fishes. In this study, we used an in situ trout (Oncorhynchus mykiss) working heart preparation at 10 degreesC to examine whether prior exposure to 5 min of anoxia (PO2 less th an or equal to 5 mmHg) could reduce or eliminate the myocardial dysfunction that normally follows 15 min of anoxic exposure. Hearts were exposed eithe r to a control treatment (oxygenated perfusion) or to one of three anoxic t reatments: 1) anoxia with low P-out [15 min of anoxia at an output pressure (P-out) of 10 cmH(2)O]; 2) anoxia with high P-out [10 min of anoxia at a P -out of 10 cmH(2)O, followed by 5 min of anoxia at P-out = 50 cmH(2)O]; and 3) preconditioning [5 min of anoxia at P-out = 10 cmH(2)O, followed after 20 min of oxygenated perfusion by the protocol described for the anoxia wit h high P-out group]. Changes in maximum cardiac function, measured before a nd after anoxic exposure, were used to assess myocardial damage. Maximum ca rdiac performance of the control group was unaffected by the experimental p rotocol, whereas 15 min of anoxia at low P-out decreased maximum stroke vol ume (V-s (max)) by 15% and maximum cardiac output ((Q)over dot(max)) by 23% . When the anoxic workload was increased by raising P-out to 50 cmH(2)O, th ese parameters were decreased further (by 23 and 38%, respectively). Precon ditioning with anoxia completely prevented the reductions in V-s (max) and (Q) over dot(max) that were observed in the anoxia with high Pout group and any anoxia-related increases in the input pressure (P-in) required to main tain resting (Q) over dot (16 ml.min(-1).kg(-1)). Myocardial levels of glyc ogen and lactate were not affected by any of the experimental treatments; h owever, lactate efflux was sevenfold higher in the preconditioned hearts. T hese data strongly suggest that 1) a preconditioning-like mechanism exists in the rainbow trout heart, 2) increased anaerobic glycolysis, fueled by ex ogenous glucose, was associated with anoxic preconditioning, and 3) precond itioning represents a fundamental mechanism of cardioprotection that appear ed early in the evolution of vertebrates.