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Hepatic Microsomal Adenosine Triphosphatase and Mitochondrial FunctionResponse to Cold and Warm Ischemia
Michael C. Townsend, MD;
Michael D. Yokum;
Donald E. Fry, MD
Arch Surg. 1987;122(7):813-816.
Abstract
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• We investigated the response of mitochondrial function and microsomal adenosine triphosphatase (ATPase) activity in rat liver tissue subjected to in vitro ischemia at either 0°C to 4°C or 37°C for 30 to 60 minutes. Mitochondrial coupling, expressed as respiratory control index, was preserved at up to 60 minutes' cold ischemia. However, respiratory control index was decreased significantly from control by 30 minutes of warm ischemia. Both microsomal magnesium-activated ATPase and sodium-potassium ATPase activity were significantly increased by 60 minutes of warm ischemia yet were unaltered by 60 minutes of ischemia at 0°C to 4°C. Warm ischemia produces deleterious effects on energy-generating (mitochondria) and energy-utilizing (ATPase) activity. Hypothermia provides a significant prolongation of cellular viability in ischemic tissue in terms of bioenergetic status. In addition to organ procurement and transplantation, hypothermic cytoprotection may prove valuable in areas such as shock, ischemia, and other clinical conditions of compromised visceral perfusion.
(Arch Surg 1987;122:813-816)
Author Affiliations
From the Department of Surgery 112W, Veterans Administration Medical Center, and the Department of Surgery, Case Western Reserve University, Cleveland. Dr Townsend is a Dudley P. Allen research fellow, Department of Surgery, Case Western Reserve University.
Footnotes
Accepted for publication April 29, 1986.
Read before the Ninth Annual Surgical Symposium of the Association of VA Surgeons, Tampa, Fla, May 10, 1985.
Reprint requests to Department of Surgery, VA Medical Center, 10701 East Blvd, Cleveland, OH 44106 (Dr Fry).
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