[Muscle metabolic state in tourniquet syndrome in the rat after administration of the proteinase inhibitor aprotinin (author's transl)]. / Muskelstoffwechselstatus beim Tourniquet-Syndrom der Ratte nach Anwendung des Proteinaseninhibitors Aprotinin.

The metabolic status of rat skeletal muscle was examined after 5 h of unilateral ischemia of one hind leg and following 5 h of recirculation. There was no recovery, neither with nor without aprotinin (Trasylol) in different doses (35 000 and 125 000 KIE/kg b.w.). After 3 h of ischemia and 3 h of recirculation a significant recovery of the metabolic status occurred in animals without and with 35 000 KIE aprotinin/kg b.w. After injection of 125 000 KIE aprotinin the restoration of the metabolic status was significantly retarded. The metabolic situation of the contralateral, non-ischemic legs revealed--in comparison to normal levels--a significant deterioration in the latter group.

Effect on myocardial metabolic pattern of local complete and incomplete ischemia.

After local complete ischemia at normothermia of 60, 100, 140, and 180 min duration the status of the adenylic acid-creatine phosphate system in the canine myocardium recovered to 98, 85, 74, and 30 percent of the control values, whereas glycogen was restored even more. In the infarcted myocardium the extent of alterations of the metabolic status was a function of the residual blood flow. Deviations from a regular metabolic status developed if the blood flow dropped below about 35 ml/min/100 gm. This critical flow rate is expected to vary with the energy requirement of the heart, but it is in keeping with results obtained by Rudolph and coworkers (personal communication) who found that patients with a myocardial blood flow below 30 ml/min/100 gm had a life expectancy of less than 1 month. In the nonaffected myocardium, both in experiments with local complete ischemia and in experiments with infarction, the metabolic status was always within normal ranges. This is in contrast to results published by Gudbjarnason (1971/1972) and Gudbjarnason, Puri, and Mathes (1971), who found that in noninfarcted myocardium tissue levels of ATP and creatine phosphate decreased to about 50 percent of the control values and that there was no restoration to normal values within 10 days after infarction.

Metabolic and structural recovery of left ventricular canine myocardium from regional complete ischemia.

The capacity for recovery of the normothermic left ventricular myocardium from a regional complete ischemia (RCI) was investigated using changes in the myocardial metabolic status (ATP, ADP, AMP, creatine phosphate (CrP), free creatine, glycogen, glucose, lactate) and alterations of the morphology as parameters. In dogs, an area of the anterior wall of the left ventricular myocardium was temporarily deprived completely of its blood supply by 5--7 overlapping ligatures extending into the heart cavity. The metabolites of the adenylic acid-CrP system returned to normal tissue levels after 30 and 60 min of RCI within 14 and 35 days of recovery, respectively; restoration averaged 82% after 100 min, 74% after 140 min, and 38% after 180 min of RCI after 5 weeks of recovery. At the same time glycogen amounted to 163% after 100 min, 114% min, and 65% after 180 min of RCI. The biochemical data correlated well with the structural changes in the affected myocardium, especially with the amount of de- and regenerating heart muscle cells. These obviously were functionally defect and were not comparable with normal structured and functioning heart muscle cells.