The effect of cardiac arrest on the blood-testis barrier to albumin, tumornecrosis factor-alpha, pituitary adenylate cyclase activating polypeptide,sucrose, and verapamil in the mouse

Impotence commonly occurs after events such as acute myocardial infarction, coronary bypass, head trauma, and cerebral bleeding, including subarachnoi d hemorrhage. We hypothesize that the hypoxia accompanying these events cou ld damage the blood-testis barrier (BTB) and so cause testicular dysfunctio n, a possible cause of impotence. We examined the effect of cardiac arrest in mice on testis weight and various aspects of BTB function. Testis weight was decreased by about 24% 12 hours after cardiac arrest but had recovered fully by day 7. The testis/serum ratio for albumin was increased 12 hours after arrest, showing a disruption in the vascular BTB with recovery by 24 hours. The testis/serum ratio for sucrose was not consistently elevated, sh owing that the Sertoli cell BTB remained intact. The testis/serum ratio for verapamil was increased on day 3 of cardiac arrest, suggesting impaired fu nction of the BTB's p-glycoprotein efflux transporter. Transporters for pit uitary adenylate cyclase activating polypeptide and tumor necrosis factor-a lpha were not affected by cardiac arrest. These results show that cardiac a rrest affects testis weight and some aspects of BTB function. Such changes might have long-term effects on testicular function.