The vascular endothelium becomes pro-thrombotic and pro-inflammatory after ischemia/reperfusion, eliciting microcirculatory disturbance and post-ischemic inflammation. First, with mouse model of ischemia/reperfusion, we compared efficacy of cilostazol (n=6), aspirin (n=6) and vehicle (n=6) administered before and after ischemia. Thrombus formation in the injured artery was suppressed in the cilostazol group and aspirin group compared with that in the control group, though all injured arteries were virtually occluded after 150 seconds. Spontaneous recanalization of the thrombosed artery was confirmed at 6 hours. Rolling leukocyte velocity over the microvessels at 24 hours was higher in the cilostazol group than in the aspirin group and control group. The number of adhering leukocytes was lower in the cilostazol group than in the control group, while aspirin did not suppress it significantly. We then confirmed protective effects of cilostazol on human brain microvascular endothelial cells (ECs) against pro-inflammatory changes in vitro. These results suggest that cilostazol suppresses pro-inflammatory changes of ECs and reduces leukocyte rolling and adhesion onto the cerebral microvessels after reperfusion, contributing to its protective effects against reperfusion injury.
We report a case of penile necrosis induced by calciphylaxis associated with chronic renal failure. Calciphylaxis is a rare but life-threatening phenomenon characterized by deposition of calcium within small- and medium-sized blood vessels, with subsequent thrombosis, cutaneous ischemia and necrosis. It is a known complication of chronic renal disease in patients on hemodialysis. The co-morbidity and mortality associated with this disease are extremely high. Secondary hyperparathyroidism and increased serum calcium phosphate are characteristic and require aggressive medical management. Our review suggests that parathyroidectomy may improve survival and that survival is independent of the type of local treatment for the penile lesions. Recently, aggressive medical control with calcimimetics (e.g. cinacalcet) has been considered for secondary hyperparathyroidism.
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