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Testis torsion-induced aspermatogenesis is not necessarily due to permanent loss of blood flow nor to dysfunctional Leydig cells or Sertoli cells. This investigation was undertaken to gain further insight into the mechanism underlying torsion-induced germ cell loss. Male rats were subjected to 1-h or 2-h ischemia-inducing torsion, and testes were examined at either 1, 2, 4, 24, or 48 h after torsion, depending on the study. Testes were examined for evidence of 1) in situ apoptosis by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP)-biotin nick-end labeling (TUNEL) technique, 2) apoptosis by the DNA "laddering" technique, 3) leukocyte margination and diapedesis in testicular vessels by immunocytochemical and histological techniques, and 4) testicular lipid peroxidation by the thiobarbituric acid reactive substances assay. The first TUNEL evidence for torsion-induced apoptosis was at 4 h after repair of 1-h torsion. Induction of apoptosis was confirmed by the electrophoretic laddering of DNA fragments. It was hypothesized that apoptosis was induced by reactive oxygen species arising from reperfusing leukocytes. A significant increase in both leukocyte margination and diapedesis occurred 4 h after torsion repair as did a significant increase in intratesticular lipid peroxidation products. These events were contemporaneous with the first appearance of apoptosis and consistent with the hypothesis that post-torsion, germ cell-specific apoptosis is induced by reactive oxygen species.

Of 131 patients with hypertension and renal arterial stenosis, 99 were treated either by nephrectomy or revascularization operations and 32 were treated medically. Anti-hypertensive effects of surgical treatment were analyzed in 76 patients in whom operations had been performed 1 to 6 years before. Of the remaining 23, 10 died in the immediate postoperative period; in 11, operative treatment was incomplete at the time of review; and, in 2, who did not have sustained diastolic hypertension, operation was performed only to conserve renal function. Diastolic hypertension remitted in 47 patients (62 per cent); in 12 (16 per cent) arterial pressure was much reduced but not to normal levels, and in 17 (22 per cent) it was unchanged. The antihypertensive effects of surgical treatment could not be predicted preoperatively. In general, patients less than 21 years of age did not respond with as much blood pressure reduction as did those older, and patients hypertensive for longer than 5 years responded less well than those hypertensive for less than 1 year. Results of function tests of individual kidneys were not helpful in prediction. Surgical treatment seemed contraindicated in 32 patients because of diffuse atherosclerosis, azotemia from severe nephrosclerosis, unsustained diastolic hypertension or because lesions had not caused disparity in function of the two kidneys. In three of these patients diastolic hypertension remitted spontaneously and in 11 arterial pressure was controlled at near normal levels with antihypertensive drugs. Eighteen patients have persistent diastolic hypertension; 13 of these have been inadequately treated with drugs. In the group treated surgically, there were 10 immediate postoperative deaths, seven of which were due to atherosclerotic complications. Twelve patients died later, and 11 deaths were due to atherosclerosis. Most of the patients who died had no blood pressure reduction following operation. Ten of the medically treated group have died of atherosclerosis. The mortality was 50 per cent in the patients with ineffective treatment and poor blood pressure control and only 7 per cent in those with good blood pressure control.

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