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J. Gordon Wright, MD; John C. Kerr; C. Robert Valeri, MD; Robert W Hobson, II, MD

Arch Surg. 1988;123(4):470-472.

Abstract
• The mechanisms of ischemia-reperfusion injury in skeletal muscle remain controversial. Some investigators have demonstrated that heparin can ameliorate ischemic injury to heart, brain, and renal tissue. We investigated the ability of heparin sodium to decrease ischemia-reperfusion injury in an isolated gracilis muscle model in ten anesthetized mongrel dogs. One gracilis muscle was perfused normally while the contralateral muscle was subjected to six hours of ischemia followed by one hour of reperfusion. Five dogs were given a preischemic bolus of heparin sodium (200 U/kg, intravenously followed by a continuous infusion (15 U/kg/h, intravenously), and five control dogs received no heparin. Quantitation of skeletal muscle ischemia-reperfusion injury was determined by histochemical staining with triphenyl tetrazolium-chloride and computerized planimetry of the infarct size. Results from the ischemic muscle demonstrate a significant beneficial effect of heparinization. The nonheparinized dogs had a 72%±5% infarct size, which was significantly reduced to 24%±8% in the heparinized dogs. The mechanism of this protective effect may be due to heparin's anticoagulant, antiplatelet, or anti-inflammatory action.

(Arch Surg 1988;123:470-472)

Author Affiliations
From the Departments of Surgery (Drs Wright, Valeri, and Hobson and Mr Kerr), and the Naval Blood Laboratory (Dr Valeri), Boston University School of Medicine.

Footnotes
Accepted for publication Sept 25, 1987.

Read before the Association of Veterans Administration Surgeons, Portland, Ore, May 8, 1987.

The opinions and assertions contained herein are those of the authors and are not to be construed as official or reflecting the views of the Navy Department or Naval services at large.

Reprint requests to Department of Surgery, Boston University Medical Center, 80 E Concord St, Boston, MA 02118 (Dr Wright).

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