Revascularization and function of pancreatic islet isografts in diabetic rats following transplantation.

In pancreatic islet transplantation, revascularization is crucial for the graft's survival and function. In this study, the endothelium of isolated islets and revascularization and function of islet isografts in diabetic rat were investigated. Islets were isolated from Lewis rats by collagenase digestion method and were examined using immunohistochemistry (CD31 stain) on days 0, 1, 3, and 7 after isolation. The number of CD31-positive cells in these isolated islets was counted (mean +/- SD %). Isografts (freshly isolated islets: group A, and islets cultured for 7 days: group B) transplanted in the renal subcapsule of streptozotocin-induced diabetic Lewis rats were examined using immunohistochemistry (CD31 stain) on days 3, 5, and 7 after transplantation. Intravenous glucose tolerance tests (IVGTT) were performed on days 3 and 7 after transplantation. The number of CD31-positive cells in the isolated islets on days 0, 1, 3, and 7 after isolation were: 17.3 +/- 4.1%, 8.2 +/- 0.7%, 2.1 +/- 0.8%, and 0.8 +/- 0.5%, respectively (p < 0.05). On day 5 after transplantation, CD31-positive cells were not detected in group A and B grafts, but were detected in both groups in periphery of the islets. On day 7, CD31-positive microvessels were present throughout the entire graft. IVGTT values in groups A and B on days 3 and 7 after transplantation did not show significant differences. In renal subcapsular isografts in diabetic rats, revascularization into islet grafts occurs from the surrounding host tissue 5 days after transplantation, but has no influence on the response to glucose during this period.

[Treatment for the ruptured bilateral vertebral dissecting aneurysms].

We report a case of a bilateral vertebral dissecting aneurysm associated with subarachnoid hemorrhage. Proximal ligation of the vertebral artery on the ruptured side combined with wrapping of the contralateral dissection failed to prevent fatal rebleeding. Since enlargement of the contralateral dissection was observed by postoperative angiography, rupture of the growing contralateral dissecting aneurysm may have caused rebleeding. Hemodynamic changes following the occlusion of one vertebral artery might have led to enlargement and subsequent rupture of the contralateral dissection. Direct wrapping was unable to prevent enlargement of the dissection, so radical surgery including bilateral vertebral artery occlusion combined with vascular reconstruction may be the treatment of choice for this type of lesion.