Vasculogenic impotence was evaluated by high-resolution sonography and quantitative Doppler spectrum analysis in 21 patients and two normal volunteers. Erection was induced by intracorporeal injection of papaverine, and B-scan imaging and Doppler analysis were performed with the penis flaccid and erect. The corpora cavernosa and its deep arteries, median septum, and corpus spongiosum were clearly displayed in every subject, with the dorsal vein and dorsal artery seen ventral to the corpora cavernosa. In the flaccid state, in all subjects, Doppler analysis demonstrated flow in the dorsal arteries but not in the deep arteries. During erection, the B-mode image showed varying degrees of enlargement of the corpora cavernosa, with increased tissue echogenicity, as well as a hypoechoic area in the peri-arterial region. The diameter of the penile arteries and flow within them also increased by varying degrees. Quantification of blood flow through all deep and dorsal arteries is feasible with this technique.
Being able to induce controlled erection in dogs and monkeys, we investigated the hemodynamics and mechanism of penile erection. 'Chronic' monkey models, having had electrodes implanted around the cavernous nerves for electroerection, were studied to evaluate the details of the hemodynamic changes. The studies included: 1) arterial blood flow, 2) corporeal pressure, 3) blood gases, 4) venous flow and 5) radiography. Tumescence of the corpora cavernosa was found to be a result of: 1) active relaxation of the sinusoidal spaces, 2) active arteriolar dilatation and 3) active venous outflow constriction. At full erection there is adequate but reduced blood flow into and out of the corpora cavernosa for metabolic exchange.
Objective
To find a means of bladder augmentation that would avoid the complications encountered with the use of bowel segments, using a newly developed acellular biomaterial, the bladder acellular matrix graft (BAMG), as a homologous graft.
Materials and methods
Thirty‐four rats underwent a partial cystectomy (40–50%) and grafting with a BAMG of equal size. Eleven rats died within the first 72 h, probably from urinary leakage caused by obstruction of the bladder neck with stones or coagula; the surviving 23 were killed at varying intervals after cystectomy and examined.
Results
After providing initial bladder enlargement, the graft was progressively infiltrated by the vessels and smooth muscle cells of the host; furthermore, the mucosal lining was complete within 10 days. After 4 weeks, all bladder wall components were evident histologically in the graft. The ingrowth was complete after 8 weeks, except for neural regeneration, which was only partial. At 12 weeks, the bladder wall muscle structure in the graft was so well developed that it was difficult to delineate the junction between host bladder and BAMG. Neural regeneration continued to improve. Normal bladder capacities were maintained throughout the study.
Conclusion
The BAMG appears to serve, without rejection, as a framework of collagen and elastin for the ingrowth of all bladder wall components. The reason for the better acceptance of the BAMG than of other bladder augmentation grafts requires further investigation.
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