Changes of urodynamic findings after radical retropubic prostatectomy.

OBJECTIVES: We wanted to evaluate the urodynamic changes of radical retropubic prostatectomy in patients with localized prostate cancer and identify specific factors that could influence the postoperative continence status. METHODS: Sixty-six consecutive patients (mean age 68 years) were studied urodynamically within 1 week before surgery, and 44 of them at a mean 7.6 months after radical intervention. RESULTS: Complete urinary continence was achieved in 37/44 men (84. 1%) after 6 months and in 43/44 patients (97.7%) 1 year after surgery. Stress incontinence of varying degree improved with time. Seven patients demonstrated a moderate incontinence 4 months after radical prostatectomy and 1/7 was still incontinent after 1 year. Mean flow rate, maximum detrusor pressure, maximum urethral closure pressure (at rest and voluntary contraction of the sphincter) and functional urethral length showed significant changes after surgery. Detrusor instability, which was present in 31.8% of the 66 patients preoperatively, was not responsible for any case of postoperative incontinence. The urethral pressure profile was significantly reduced in all patients after surgery. CONCLUSIONS: The present study indicates that there are no preoperative alterations in bladder function such as detrusor instability to identify patients at risk for postoperative incontinence. Postoperative incontinence seems to depend upon sphincteric deficiency as expressed by the reduced pressures in the sphincteric mechanism.

Experience with the Mainz modification of ureterosigmoidostomy.

BACKGROUND: The purpose of this study was to report experience with the revived surgical concept of ureterosigmoidostomy in its low pressure modification and to discuss its value within the current spectrum of urinary diversion. METHODS: Between February 1992 and September 1997 modified ureterosigmoidostomy (rectosigmoid pouch; Mainz pouch II) was performed in 34 patients aged 1.9-76.9 (mean 55.8) years as a primary urinary diversion after radical cystectomy for bladder cancer (n = 30) and benign conditions (bladder exstrophy, three patients; intractable urinary incontinence, one). All patients were followed prospectively according to a standard protocol including assessment of continence, renal function and acid-base balance. RESULTS: There were no perioperative deaths. In one patient dislocation of a ureteral stent in the early postoperative course required insertion of a percutaneous nephrostomy. All patients were continent during the day. One patient experienced night-time incontinence but rejected a conversion procedure. In one case ureterosigmoidostomy was replaced by an ileal conduit after several episodes of septicaemia. One nephrectomy was performed for ureterointestinal obstruction. Mild hyperchloraemic acidosis was seen in two patients. CONCLUSION: Bowel frequency and urge incontinence, the major weaknesses of classical ureterosigmoidostomy, can be overcome by detubularization of the rectum. As the modified procedure is quick, safe and easy to perform with highly satisfactory results, the rectosigmoid pouch has potential in reconstructive urology.

Faster ribosome synthesis induced by elevated aortic pressure in rat heart.

An increase in aortic pressure from 60 to 120 mmHg accelerated ribosomal protein synthesis in rat hearts during 1 or 2 h of labeling with 0.4 mM [3H]phenylalanine. When hearts were perfused with buffer that contained 20 mM glucose and normal plasma concentrations of 19 other amino acids without added insulin, ribosomal protein synthesis relative to the rate of total protein synthesis increased from approximately 0.22 to 0.36 and 0.30 as aortic pressure was raised from 60 to 120 mmHg during 1 or 2 h of labeling, respectively. With the addition of insulin, the relative rate of ribosomal protein synthesis averaged 0.33 at an aortic pressure of 60 mmHg and increased to 0.42 when aortic pressure was raised to 120 mmHg. These results indicate that elevation of aortic pressure has a preferential effect on synthesis of new ribosomes. This response appears to be an early and physiologically significant event in cardiac hypertrophy.

Effect of redox potential on protein degradation in perfused rat heart.

The effect of redox potential on protein degradation was assessed in rat hearts supplied either glucose or pyruvate, and the correlation between redox state and proteolysis was examined after the addition of insulin and leucine. In hearts supplied glucose as the sole energy source, the inhibition of protein degradation by a range of concentrations of insulin was associated with increased ratios of perfusate lactate to pyruvate and intracellular lactate to pyruvate, malate to pyruvate, and NADH to NAD. However, the extent of inhibition did not correlate with the redox state. The inhibitory effect of leucine on protein degradation was not accompanied by any change in redox state of the hearts. In hearts provided with pyruvate, rates of protein degradation continued to be inhibited by insulin even though the perfusate lactate to pyruvate was decreased by 14-fold and the calculated cytosolic NADH-to-NAD ratios were only 3% of those seen in hearts supplied glucose. These results indicated that a correlation between redox state and protein degradation was not apparent in myocardium under the experimental conditions examined.

Differential effects of cysteine on protein and coenzyme A synthesis in rat heart.

The effect of cysteine availability on protein and coenzyme A (CoA) synthesis in perfused rat heart was incompletely evaluated in earlier experiments because rapid conversion of cysteine to cystine occurred when the perfusion buffer was oxygenated. This conversion was minimized by addition of an excess of reducing agents such as dithiothreitol or mercaptodextran or by provision of bathocuproine disulfonate, a copper chelator. Dithiothreitol was not a suitable protective agent because it reduced ATP and creatine phosphate contents. Perfusion of hearts with [35S]cystine or [35S]cysteine in the presence of mercaptodextran resulted in a 22-fold or 5-fold increase, respectively, in incorporation of [35S] into protein and a 5-fold or 8-fold increase, respectively, in incorporation into CoA compared with hearts supplied [35S]cystine or [35S]cysteine without the reducing agent. When compared with hearts perfused at an aortic pressure of 90 mmHg with bicarbonate buffer that contained 15 mM glucose, 25 mU insulin/ml, 0.4 mM [14C]phenylalanine, no cysteine and plasma levels of other amino acids, provision of 0.09 or 0.2 mM cysteine alone or in the presence of mercaptodextran, or bathocuproine disulfonate enhanced rates of protein synthesis 16-35%. When 0.2 mM cysteine was added to bicarbonate buffer containing 7 microM pantothenic acid, supplementation with mercaptodextran or bathocuproine disulfonate was required to raise CoA content. These results indicated that an exogenous supply of cysteine was needed to maintain maximal rates of protein and CoA synthesis in the perfused rat heart. Protective compounds were required to obtain the cysteine effect on CoA but not on protein synthesis.