The great resistance of muscle to
ischemia was used to study blood flow-dependent phenomena produced by
anesthetic drugs in this condition. A short reperfusion period was used in order to favor metabolic changes indicative of an effect of
chlorpromazine (CPZ) on blood flow. Gracilis muscles of dogs were submitted to 5 h of
ischemia and 30 min of reperfusion. CPZ-treated animals were injected I.V. (2 mg/kg) 10 min before the beginning of
ischemia. Biopsies provided the material for tissue measurements.
Lactate content and pH were determined in blood samples collected from a muscle efferent vein. In both the CPZ-treated and nontreated groups,
ischemia induced a decline in muscle
glycogen content, with a corresponding increase in muscle
lactate and a decrease in mitochondrial respiratory control ratio. After 30 min of reperfusion, tissue levels of
lactate did not attain preischemic values but showed a clear decline in the two experimental groups, evidencing the reversible state of the muscle. All other metabolic parameters remained unchanged. Mitochondrial respiratory control remained functional during
ischemia and reperfusion. Blood pH displayed similar changes in both groups. There was no metabolic indication that the
drug affected blood flow during early reperfusion and/or of a greater sensitivity of muscle endothelial cells to
anesthetic drugs.