Correlation between antioxidant changes during hypoxia and recovery on reoxygenation.
Changes in myocardial antioxidants due to different durations of hypoxia at normal or lower temperatures were correlated with the recovery of structure and function on reoxygenation. Hearts perfused with substrate-free hypoxic buffer at 37 degrees C for 5 or 10 min and at 22 degrees C for 10 min showed a significant depression in the contractile function and rise in resting tension. Reoxygenation of these hearts at 37 degrees C for 20 min resulted in a recovery of these functions. On reoxygenation, hearts made hypoxic for 10 min at 37 degrees C showed poor recovery of the contractile function, increase in malondialdehyde content and a dramatic increase in the creatine phosphokinase activity in the coronary effluent. Addition of catalase to the perfusion medium markedly improved function recovery of these hearts. Hypoxia at 37 degrees C for 5 min or at 22 degrees C for 10 min with or without reoxygenation had no effect on superoxide dismutase (SOD) or glutathione peroxidase (GSHPx) activities. These antioxidants were depressed in hearts made hypoxic for 10 min at 37 degrees C with no further change on reoxygenation. Neither SOD nor GSHPx was detected in the coronary effluent during hypoxia or reoxygenation. Hypoxia at 37 or 22 degrees C for 10 min caused significant ultrastructural changes, and on reoxygenation 37 degrees C hypoxic hearts showed exacerbation, whereas the 22 degrees C hypoxic hearts showed recovery. These data support the hypothesis that reduced antioxidant reserve during hypoxia may contribute to the oxidative injury on reoxygenation, suggesting that maintenance of endogenous antioxidant levels during hypoxia may be important for recovery.
Dhaliwal
H
H
Cardiovascular Sciences Division, St. Boniface General Hospital Research Center, Winnipeg, Manitoba, Canada.
Kirshenbaum
L A
LA
Randhawa
A K
AK
Singal
P K
PK
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000494:pharmacology; D003402:Creatine Kinase / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008854:Microscopy, Electron; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000473:pathology / Q000648:ultrastructure*; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000494:pharmacology; D013696:Temperature
D000975:Antioxidants; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D003402:Creatine Kinase