[Effect of internal iliac artery ligation on the bladder wall circulation (author's transl)].

Abstract

The present study was undertaken to determine if internal iliac artery ligation causes changes in the bladder wall circulation sufficient to control hemorrhage by shutting off the blood flow in urologic surgery. Such study is prerequisite for a better understanding of the internal iliac artery ligation widely used as a means of hemostasis in urologic surgery.Twenty-two dogs weighing 7 to 31 kg were used in the present study. Dogs were anesthetized with thiamylal-Na and the aorta, the internal iliac artery and the bladder were exposed transperitoneally. One male patient with bladder carcinoma was anesthetized epidurally and his bladder was exposed by a median incision at the lower abdomen.The bladder wall PO2, an index of blood flow, was continuously measured by the Yagi's polarographic O2 electrode of an enameled copper wire 300μ in diameter implanted in the muscular layers of bilateral and posterior bladder walls, respectively.In the patient with bladder carcinoma the electrode was implanted in the posterior bladder wall.In four dogs, the electrode was also placed in the abdominal aorta to measure arterical PO2. Changes in the polarographic amplitudes after artery ligation were expressed as percent of the level obtained before ligation.In the experiments with ligations of internal iliac artery and abdominal aorta ligation, both arterial and bladder wall PO2 were monitored during 100% O2 breathing and the increment of the bladder wall PO2 and the response time to O2 breathing were measured.The following results were obtained:1) Before ligation, the bladder wall PO2 increased up to 141-174 during O2 breathing.2) After internal iliac artery ligation, the bladder wall PO2 decreased to 76-79% and the PO2 increments (28-45) were significantly lower than the control values (41-74) (P<0.01). The response time to O2 breathing was significantly greater in the ligation (20-25sec) than the control (8-10sec). After ligation PO2 decreased initially but it showed an increase in 14 out of 46 areas of the bladder later, the mean increment was 11% and it occurred 204 seconds after the ligation on the average.3) The bladder wall PO2 during ligation of the aorta was 59-70% which was lower than that of internal iliac artery ligation and that of 11 areas did not respond at all to O2 breathing. The increment of PO2 during O2 breathing was 12-20 which was lower than that seen in the internal iliac artery ligation (p<0.05). The response time to O2 breathing was significantly prolonged (40-51sec). These results indicate that the ligation of the aorta causes a profound decrease in the bladder wall blood flow.4) In the patient with bladder carcinoma the bladder wall PO2 increased markedly (193). After internal iliac artery ligation, it decreased to 79% but again increased to 114 by O2 breathing. The response time to O2 breathing before internal iliac atery ligation was 6sec and 12sec after ligation. This finding suggests that like in the dog the internal iliac artery ligation does not reduce bladder wall blood flow sufficiently to produce ischemia in humans.In conclusion, a significant fraction of the bladder wall circulation (71-76%) can be maintained agter internal iliac artery ligation and collateral circulation can also occur in about 200 seconds. The results of these studies indicate that clinically effective hemostasis can not be expected by iliac artery ligation alone.