Angiogenesis in the latissimus dorsi muscle using different regimens of electrical stimulation and pharmaceutical support

It is our contention that the prevention of ischemia-reperfusion injuries i mmediately after latissimus dorsi muscle (LDM) mobilization and enhancement of angiogenesis will be effective in improving cardiomyoplasty results. Th e investigations were performed on adult sheep. Three hours after LDM mobil ization, various stages of leukocyte-endothelium interaction were revealed: leukocytes binding to the endothelium, leukocyte destruction of endotheliu m, and leukocytes leaving capillaries through gaps in the endothelium. Fift y-six days after mobilization various stages of necrosis were discernible. The area occupied by capillaries was 3.45 +/- 0.26% vs. 3.99 +/- 0.24% in c ontrol muscle; most of the endothelial cells exhibited morphologic degenera tion. Electrical stimulation with 60 CPM actually decreased the capillary d ensity to 2.15 +/- 0.7%, and most of the endothelial cells were damaged, wi th disrupted plasma membranes. Muscle subjected to 15 CPM increased the per cent of capillaries to 5.01 +/- 0.56%, and endothelial cells appeared norma l in ultrastructure. Pharmaceutical support prevented muscle damage and acc elerated revascularization. After 56 days of autologous biological glue (AB G) application, the area occupied by capillaries was 5.57 +/- 0.24%. This i ncreased to 8.47 +/- 0.72% when aprotinin (proteinase inhibitor) was added to ABG, and to 9.40 +/- 1.24% with pyrrolostatin (free radical scavenger). Both ABC application with aprotinin and electrical stimulation at 15 CPM pr event the LDM from postmobilization damage, and increase angiogenic potenti al.