An experimental model was developed to investigate the effects of glycemic control and pentoxifylline administration on microvascular anastomotic patency rates in streptozotocin-induced diabetic rats. Diabetes was confirmed by blood glucose levels of more than 300 mg/dl prior to administering insulin and/or pentoxifylline. Microvascular anastomoses of the femoral artery and vein were performed 4 weeks after induction of diabetes. Subsequently, the comparative rates of anastomotic thrombosis in diabetic and nondiabetic groups with or without insulin or pentoxifylline administration were assessed by direct visualization of the anastomotic sites after 4 days. The results suggest that hyperglycemia impairs the post-operative patency of microvascular venous anastomoses. The diabetic animals maintained under insulin regimens that tightly controlled their serum glucose levels (100 to 200 mg/dl) experienced patency rates similar to those of nondiabetic controls (p < 0.05). Pentoxifylline improved microvenous patency at all levels of hyperglycemia studied, suggesting a possible hemorrheologic mechanism for microvascular venous anastomotic thrombus formation in diabetic animals.
The study addresses the histopathology of end-to-end microanastomosis in the rat inferior vena cava. The vessels were harvested in 4 hours and 1, 3, 7, 14, and 30 days after the operation and were evaluated using light, scanning, and transmission electron microscopy. The endothelium was completely restored within 7 days after the surgical procedure. Endovasal structures at the microsuture site and intramural endothelial channels opening into the vena cava lumen developed as a result of endothelialization and parallel substitution of the three-dimensional fibrin framework of the mural microthrombus with connective tissue. By 1 month, aggregates of platelets, fibrin, and adhering leukocytes were observed in the intramural channel mouths. Administration of heparin and Trental for 1 week after the operation reduced the number of intramural channels and prevented the formation of endovasal structures at the site of microvenous anastomosis.
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