Age-dependent changes in myocardial ultrastructure during anoxia.
We have examined left ventricular function and structure of male C57BL/6J mice at 3 and 24 months of age prior to, during and 5 min following a 3-min exposure to anoxia. During anoxia young hearts were characterized structurally by the presence of clear, abnormal non-membrane bound lipid-like vacuoles closely associated to mitochondria. Myelin figures were also present, and mitochondrial ATPase was considerably reduced. By the end of the 3-min period of anoxia hearts in young mice had irreversibly failed, and upon reoxygenation mitochondria underwent further degradation, including loss of internal structure. While continuing to function throughout anoxia, hearts of old mice had normal appearing myofibrillar, mitochondrial and sarcoplasmic structures. During reoxygenation occasional myelin figures were seen in senescent myocardium, although mitochondrial ATPase was not affected. At all times of anoxia and recovery pathological changes were more extensive in young mice than in their aged counterparts.
D000251:Adenosine Triphosphatases / Q000032:analysis; D000375:Aging; D000818:Animals; D000860:Hypoxia / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000201:enzymology; D009206:Myocardium / Q000648:ultrastructure*; D010101:Oxygen Consumption
D000251:Adenosine Triphosphatases