Intravital microscopic assessment of pressure induced microcirculatory changes after enterocystoplasty in rats

Chronic over distention may lead to enterocystoplasty rupture. It is hypothesized that pressure induced microvascular derangement and subsequent ischemia of the enterocystoplasty intestinal patch may have a role in this process. We describe distention induced microcirculatory alterations in a chronic rat model of enterocystoplasty using intravital video microscopy.

Microcirculation in the muscle layer of the intact bladder and intestine, and in the enterocystoplasty 90 days after surgery were examined at greater and less than urethral sphincter closure pressure. Microcirculatory changes were recorded during stepwise increments of intraluminal pressure up to 80 mm. Hg or when 20 mm. Hg was continuously maintained for 60 minutes.

The enterocystoplasty components of intestine and bladder displayed baseline microcirculatory characteristics similar to those observed in the intact organs. As evidenced by microcirculatory flow and functional capillary density measurements in the intact intestine and the ileal portion of enterocystoplasty, intraluminal pressure elevation to greater than 25 or 30 mm. Hg significantly compromised capillary perfusion by approximately 50% and 75%, respectively. Lower intraluminal pressure did not cause microcirculatory disturbance even when maintained for a longer period. In the intact bladder and bladder portion of enterocystoplasty only pressure increases to greater than 80 mm. Hg affected tissue perfusion.

Intravital microscopy in the augmented rat bladder is a sensitive and suitable means of assessing clinically relevant microcirculatory changes. These experiments demonstrate the significance of distention induced microcirculatory impairment in the intact bowel and the intestinal site of enterocystoplasty even at less than urethral closure pressure.