Myocardial enzyme loss: factors leading to reduction or exacerbation of release.
In studies with the isolated, perfused, K+ arrested rat heart the release of four myocardial enzymes was studied during 7 hr of anoxia. The effect of several potential protective agents upon enzyme release was measured. Anoxic perfusion with exogenous supplies of glucose afforded considerable protection; the duration of anoxia that could be tolerated without significant release was greatly extended and the extent of overall release was greatly reduced. Limited oxygen availability also afforded considerable protection and the effect was additive with glucose. It is proposed that maximum protection is achieved with procedures aimed at maximizing cellular levels of ATP during hypoxia. The use of "membrane stabilizers," e.g., methyl prednisolone may also have some protective effects. It is proposed that the onset of myocardial enzyme release is associated with the transition from reversible to irreversible cellular damage. Significant metabolic protection can be achieved during the phase of reversible damage. In contrast, after the onset of irreversible damage, little can be done to halt or reduce enzyme loss. Under certain circumstances, e.g., reoxygenation after an extended period of anoxia, attempted protection may lead to exacerbation of damage.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000263:Adenylate Kinase / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D003402:Creatine Kinase / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006884:Hydroxybutyrate Dehydrogenase / Q000378:metabolism; D000860:Hypoxia / Q000201:enzymology*; D008297:Male; D009206:Myocardium / Q000201:enzymology*; D010477:Perfusion; D051381:Rats
D000255:Adenosine Triphosphate; D006884:Hydroxybutyrate Dehydrogenase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase; D000263:Adenylate Kinase; D005947:Glucose