Cystometric and in vitro muscle studies of cystoplastic appendiceal segments in the rat.

AIMS: The functional integration of the smooth muscle of enterocystoplasties into the detrusor muscle was investigated in an awake-rat cystometry model and in vitro. METHODS: The upper fourth of the bladder was removed, and a detubularized appendiceal segment (7 x 7 mm), with preserved vasculature, was incorporated into the bladder. After 1 or 3 months, a catheter was fixed to the top of the bladders. After a 3-day recovery, cystometries were performed. In separate experiments, agonist and nerve-induced responses were evaluated on isolated bladder strips. RESULTS: Cystometries revealed reduced basal pressure and micturition pressure in enterocystoplasty (ECP) bladders. Bladder capacity and micturition volume were increased. Threshold pressure (pressure immediately before micturition) was significantly lower at 1 month, but not at 3 months. Bladder compliance was significantly higher in the operated at 1 month but not at 3 months. Threshold tension did not differ between control and corresponding operated groups. Residual urine was significantly higher in the operated groups. ECP strips showed increased maximal contractions to nerve stimulation, to levels similar to those of detrusor strips. Maximal responses to carbachol increased to levels between those of intestine and detrusor. The inhibitory effect of scopolamine on nerve induced contractions increased to levels similar to those for detrusor. Purinergic activation had no effect on intestinal or ECP strips, but contracted detrusor muscle. CONCLUSIONS: The smooth muscle of the bowel segment in rat ECP bladders underwent a partial change in the response to nerve stimulation from that of intestine towards that of detrusor. The cystometry experiments suggested a partial functional integration of the ECP segment into the detrusor.

Comparison of laparoscopic saline infused to dry radio frequency ablation of renal tissue: evolution of histological infarct in the porcine model.

PURPOSE: We investigated and compared the gross and histopathological features of radio frequency (RF) ablated renal tissue using saline infused RF ablation (RFA) vs dry RFA in a porcine model. MATERIALS AND METHODS: Ten porcine kidneys underwent laparoscopic RFA. The lower and upper poles of each right kidney were treated with 1 and 2 cycles of saline augmented (wet) RFA, respectively. The upper pole of each left kidney was RF ablated without saline infusion (dry RFA) and a control lesion was created in the lower pole. The animals were sacrificed immediately after ', 2 and 9 days after (subacute), and 14 and 21 days after (chronic) treatment, respectively. Gross pathological and histological changes caused by the different RF treatments were compared. RESULTS: Mean time to attain target temperature was shorter with wet than with dry RFA. Grossly the lesion sizes achieved were larger using wet RFA but independent of the number of wet RFA treatment cycles. Gross lesion sizes decreased with time for each treatment modality. No histopathological differences were seen between the 2 RFA treatment modalities as well as between 1 vs 2 cycles of wet RFA. In the acute phase hematoxylin and eosin staining of ablated tissue revealed focal areas of alterations in renal tubular histology. However, nicotinamide adenine dinucleotide staining of corresponding areas confirmed the lack of cellular viability except for glomeruli. In the subacute phase there were focal coagulation necrosis and thrombosed blood vessels. Within the necrotic areas the glomeruli were the last structures to lose viability. In the chronic phase fibrosis with decreased lesion size was seen. Nicotinamide adenine dinucleotide staining demonstrated that the cellular kill was permanent during the entire study period. CONCLUSIONS: The effects of RFA of renal tissue has 2 phases, namely initial direct thermal ablation causing acute cell death and a later subacute phase causing subsequent infarction of the distal arterial vascular supply to the ablated region, resulting in more cell death and coagulative necrosis. Glomeruli are the last structures to lose viability in necrotic areas. Most importantly cellular death caused by RFA is permanent.