A nonheparinized muscle model for studies of ischemia-reperfusion injury.

An understanding of the basic metabolic, functional, and histologic features of skeletal muscle injury secondary to ischemia and reperfusion has thus far been hampered by the lack of an adequate animal model. We have developed an in vivo isolated skeletal muscle preparation amenable to ischemia-reperfusion studies and the investigation of therapeutic modalities. The model is autoperfused and, most importantly, nonheparinized. The use of a nonheparinized model is essential following the work of Hardaway, recently confirmed by Fry, showing that alterations of flow in the shock state occur when heparin is used, invalidating other models as true replicas of clinical situations. The gracilis muscle in the canine hindlimb and its contralateral control are isolated on their neurovascular pedicles after detachment of fascial boundaries and meticulous ligation of all collateral vascular supply. Prolonged arterial occlusion can be accomplished by clamping proximal and distal to the point of origin of the gracilis artery from the superficial femoral artery. In a similar fashion, occlusion above and below the gracilis vein is effected intermittently to collect venous efluent during reperfusion. Preliminary studies of 100 muscle preparations subjected to 3 or 15 hr of ischemia, followed by 2 hr of reperfusion, demonstrate depression of oxygen utilization of 5% of control values during early reperfusion with improvement to 30% of control values over 2 hr. Contractility, abolished during ischemia, returns to 20% of control values after 2 hr of reperfusion.