Preconditioning stimuli do not benefit the myocardium of hypoxia-tolerant rainbow trout (Oncorhynchus mykiss).
In many vertebrates, a short episode of oxygen lack protects against myocardial necrosis during a subsequent, longer period of oxygen deprivation. This protective effect, termed preconditioning, also improves the functional recovery. Improved functional recovery has been reported for hypoxia-sensitive, in situ perfused rainbow trout hearts, but appears absent in another strain of rainbow trout that has a more hypoxia-tolerant heart. The results for the hypoxia-tolerant rainbow trout heart, however, might have occurred because the preconditioning stimuli were insufficient in either intensity or type to elicit cardioprotective effects. In the present study, we attempted to induce preconditioning in in situ perfused hearts from hypoxia-tolerant rainbow trout ( Oncorhynchus mykiss), acclimated and tested at 10 degrees C, by either doubling the anoxic preconditioning stimulus (PO(2) of the perfusate <0.5 kPa) relative to earlier studies or by using short exposures to high concentrations of adrenaline. In addition, anoxic-preconditioning experiments were conducted at an acutely elevated temperature (15 degrees C) to increase myocardial sensitivity to oxygen lack. The effect of preconditioning stimuli was assessed by measuring cardiac performance before and after exposure to a 20-min anoxic challenge. In addition, myocardial condition was evaluated at the termination of the experiment by measuring myocardial concentrations of glycogen, high energy phosphates and lactate, as well as activities of pyruvate kinase and lactate dehydrogenase. Maximal cardiac performance in oxygenated control hearts was unchanged by the 2-h experimental protocol, whereas inclusion of a 20-min period of anoxia led to 25 and 35% reductions in maximal cardiac performance at 10 and 15 degrees C, respectively. Reduced contractility, however, could not be ascribed to myocardial necrosis, as the biochemical and energy state of the hearts was unaffected. Hence, anoxic exposure merely stunned the myocardium. At 10 degrees C, neither the anoxic nor adrenergic preconditioning protocols improved post-anoxic cardiac performance. Further, the preconditioning protocols did not reduce post-anoxic myocardial dysfunction at 15 degrees C, despite the increased cardiac sensitivity to anoxia at this temperature. Thus, despite using strong and different preconditioning stimuli compared with earlier studies, the cardio-protective effect of preconditioning seems to be absent in rainbow trout hearts that are inherently more hypoxia-tolerant.
Overgaard
Johannes
J
Department of Zoophysiology, Institute of Biological Sciences, University of Aarhus, Building 131, 8000 Aarhus C, Denmark. Johannes.Overgaard@biology.au.dk
Stecyk
Jonathan A W
JA
Gesser
Hans
H
Wang
Tobias
T
Gamperl
A Kurt
AK
Farrell
Anthony P
AP
D000704:Analysis of Variance; D000818:Animals; D002302:Cardiac Output; D004837:Epinephrine; D006003:Glycogen / Q000378:metabolism; D006321:Heart / Q000502:physiology*; D006339:Heart Rate; D000860:Hypoxia / Q000503:physiopathology*; D019157:Ischemic Preconditioning, Myocardial; D019344:Lactic Acid / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D017686:Oncorhynchus mykiss / Q000502:physiology*; D013053:Spectrophotometry; D013696:Temperature
D019344:Lactic Acid; D006003:Glycogen; D004837:Epinephrine