A new application of electrical stimulation to inhibit detrusor activity has been used in 15 patients with a variety of neural lesions. The results were astonishingly good and the device was well tolerated. In patients treated successfully for detrusor instability an absence of urgency occurred as a by-product of electrical stimulation. Therefore, stimulation was used to treat uncomfortable bladder urgency without detrusor instability and was successful in the majority of patients.

Urinary stress incontinence associated with poor urethral sphincter function and indicated by a urethral pressure of less than 10 cm. water was treated in 52 cases with a pubovaginal autogenous fascial sling. No urethral sphincter function could be measured in 7 patients. Of these 52 patients 42 had undergone a previous operation for stress incontinence. The uninhibited detrusor dysfunction that accompanied the stress incontinence in 29 cases ceased after operation in 20 but persisted in 9. Postoperative urethral pressure measurements indicated that while the sling increased urethral pressure it did not cause an obstruction during voiding, since there was a measurable decrease in urethral pressure during a detrusor contraction. Urodynamic determination were useful in patient selection, in the adjustment of sling tension at operation and in the assessment of reasons for failure. A satisfactory result with good urinary control was obtained in 50 cases and the procedure was a failure in 2.

Preoperative urodynamic testing for the identification of specific types of urinary incontinence was found useful to select an appropriate operative procedure. Failure of the operation to relieve stress incontinence was unusual in 346 patients followed for a minimum of 2 years. Of the total group of patients with stress incontinence 27 per cent also had detrusor instability identified urodynamically preoperatively. However, identification of the syndrome is of limited prognostic significance since the majority of these patients had no difficulty with the syndrome postoperatively and some other patients appeared to have the syndrome only postoperatively.

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Although a number of manipulations prior to or during the initiation phase of an acute renal injury will modify the degree of functional impairment, agents administered after the acute insult usually have been ineffective. In the present study, adenine nucleotides (AMP, ADP, or ATP) combined with magnesium chloride were infused after an ischemic renal injury. Twenty-four hours later: (1) rats that received no infusion or one of the components of the mixture alone had reduced CIn (355 +/- 40 microliter/min/100 g of body wt vs. 977 +/- 40 control value), decreased RBF (3550 +/- 205 microliter/min/100 g of body wt vs. 5095 +/- 171 control value), elevated FENa (0.65 +/- 0.10% vs. 0.17 +/- 0.04 control value), and diminished UOsm (862 +/- 110 mOsm/kg vs. 1425 +/- 132 control value); (2) rats given dopamine or phenoxybenzamine maintained low CIn (365 +/- 50) despite improved RBF (4678 +/- 222); (3) rats infused with either AMP, ADP, or ATP combined with magnesium chloride had markedly improved CIn (594 +/- 44, P < 0.01), increased RBF (4269 +/- 223, P < 0.01); normalized FENa (0.18 +/- 0.07%, P < 0.01), and improved UOsm (1201 +/- 106 mOsm/kg, P < 0.05). In animals given no infusion or only magnesium chloride, ultrastructural studies demonstrated focal cellular necrosis and marked generalized tubular cell and mitochondrial swelling, whereas rats infused with ATP and magnesium chloride had fewer ultrastructural changes with better preservation of cellular morphology. Rats treated with ATP and magnesium chloride had improved CIn despite ischemic periods of 30, 45, and 60- min; and the degree of improvement was directly related to the quantity of ATP and magnesium chloride administered. The cellular content of exogenously administered ATP was 2.5 times greater in previously ischemic kidneys than in nonischemic kidneys. The data indicate that adenine nucleotides combined with magnesium chloride when infused after the initiation of acute renal failure significantly improve both CIn and tubular function and suggest that these agents effectively enhance recovery following an ischemc renal insult.