EFFECT OF INCREASED INTRAVESICAL HYDROSTATIC PRESSURE ON THE BLADDER WALL MICROCIRCULATION IN DOG

Abstract

The rationale of the treatment of bladder carcinomas by a hydrostatic pressure technique has been based on the concept that increased intravesical hydrostatic pressure induces a reduction of blood circulation, thus causing ischemic damage on the carcinoma tissues, without affecting the normal bladder wall. The purpose of this study was to determine if an increased hydrostatic pressure induces a significant reduction of the blood flow within the normal bladder wall. Such a study is prerequisite for a better understanding of the hydrostatic treatment of bladder carcinomas.
Twenty dogs weighing 7 to 31kg were used in this study. Under thiamylal-Na anesthesia, the bladder and abdominal aorta were exposed by a median incision in the lower abdomen. intravesical hydrostatic pressure was increased by saline infusion via a catheter secured through a bladder fistula.
Bladder wall PO₂, an index of blood flow, was continuously measured by the Yagi's polarographic oxygen electrode implanted in the muscular layers of bilateral and posterior bladder walls. Changes in the polarographic amplitudes with the increasing hydrostatic pressure were expressed as percent of the control level obtained from the same but empty bladder.
The results obtained were as follows:
1) The mean increments of the bladder wall PO₂ during 100% oxygen breathing were 90±62% (1 S. D.) in the left lateral wall, 54±42% in the right lateral wall and 80±48% in the posterior wall. Thus, the Yagi's polarographic PO₂ measurement was proved to be a potentially useful tool for monitoring bladder wall PO₂ in situ.
2) During an elevation of intravesical hydrostatic pressure, the bladder wall PO₂ was decreased to 50±19% in the left lateral wall, 49±25% in the right lateral wall and 61±24% in the posterior wall, indicating a marked reduction of the blood flow within the bladder wall. The response of bladder wall PO₂ to 100% oxygen breathing was also markedly reduced, suggesting a total obstruction of blood vessels in the bladder wall.
3) The response time, a time between the beginning of O₂ breathing and the onset of PO₂ elevation was prolonged two to five folds that of the control (empty bladder) by the increased intravesical hydrostatic pressure. This is a further evidence of a marked reduction of blood flow in the bladder wall.
4) The PO₂ levels measured at various sites of the bladder did not significantly differ from one another, suggesting a uniform hydrostatic pressure effect on blood flow in the bladder wall.
5) The bladder wall blood flow was restored by reducing intravesical hydrostatic pressure. This suggests that a reduction in the bladder perfusion is reversible and gives no ischemic damage to normal bladder wall.
These results indicate that the therapeutic effect of hydrostatic treatment is probably due to the ischemic insult selective to the carcinoma tissue which is known to be highly vulnerable to the ischemic condition.