Heart biochemical responses in miniature swine subjected to +Gz acceleration.
Myocardial biochemical systems which are sensitive to hypoxic and ischemic insult were studied to determine the possible etiology of ventricular endocardial hemorrhage in miniature swine following +GZ stress. Unanesthetized animals were subjected to a single, 120-s +9 GZ acceleration. Approximately 1-2 h following +GZ exposure, the animals were anesthetized and the hearts removed for analyses. Acceleration exposure resulted in the loss of acid phosphatase enzyme activity from the membrane-bound lysosomal fraction with concomitant increased activity in the soluble fraction. This suggests that lysosomal membrane integrity had been disrupted. Mitochondrial preparations from +GZ-stressed hearts exhibited marked increases in active respiratory rate and rate of calcium transport while oxidative phosphorylation efficiency was unchanged. The results clearly indicate that +GZ acceleration is capable of altering myocardial biochemical systems. However, the results tend to suggest that these alterations in cellular processes may be mediated by influences other than hypoxia or ischemia.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002474:Cell-Free System; D005260:Female; D005969:Glutamate Dehydrogenase / Q000378:metabolism; D006112:Gravitation; D008247:Lysosomes / Q000201:enzymology; D008297:Male; D008931:Mitochondria, Muscle / Q000201:enzymology / Q000378:metabolism; D009206:Myocardium / Q000201:enzymology* / Q000648:ultrastructure; D010085:Oxidative Phosphorylation; D013312:Stress, Physiological / Q000201:enzymology*; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013552:Swine
D013385:Succinate Dehydrogenase; D005969:Glutamate Dehydrogenase; D000135:Acid Phosphatase; D002118:Calcium