Bilateral asynchronous perinatal torsion is an uncommon but serious event. In our experience torsion of the contralateral gonad was not associated with signs or symptoms of acute torsion. Observation and serial examinations are then a challenging proposition. Due to the consistently poor outcome from bilateral asynchronous torsion, we continue to recommend early exploration and empiric contralateral orchiopexy for all cases of perinatal torsion. Parents must be counseled regarding the relative risks of exploration and anesthesia versus observation.

The potentiation of LPS-induced pulmonary hypertension following NAME infusion suggests that inhibition of nitric oxide synthase may have a limited role in the treatment of septic shock.

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The results of early studies suggest that nitric oxide (NO) synthesis inhibition may be therapeutic in sepsis, but recent data indicate that NO inhibition may be harmful. This study investigates the effects of NO synthesis inhibition with N-nitro-L-arginine methyl ester (NAME) on regional blood flow following endotoxemia. Anesthetized, instrumented swine were randomly divided into four groups. Controls received normal saline resuscitation (NSR) at 1 cc/kg/min beginning at T0. The lipopolysaccharide group (LPS) received NSR and Escherichia coli LPS, 200 micrograms/kg at T0. The LPS+NAME group received NSR and LPS at T0, plus NAME (50 micrograms/kg/min) starting at T1. The NAME group received only NSR and NAME. Hemodynamic data, regional blood flow, and gastric intramucosal pH (pHi) were measured hourly. LPS increased renal and carotid blood flow consistent with a hyperdynamic state. Mesenteric blood flow was decreased. Treatment of endotoxic animals with NAME decreased renal and carotid blood flow. Mesenteric blood flow and gastric pHi were improved by NAME. NO inhibition in endotoxic shock results in decreased carotid and renal blood flow, by decreasing cardiac output. Mesenteric blood flow and perfusion were improved; however, this requires further study for validation.

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We administered the diuretics furosemide and ethacrynic acid to conscious freshwater turtles to assess changes in renal function and plasma renin activity (PRA) in an animal which lacks a loop of Henle. Furosemide (2 and 5 mg/kg) produced no changes in blood pressure, hematocrit, plasma electrolytes, glomerular filtration rate (GFR), or PRA. Furosemide doubled urine volume while sodium excretion increased 20-fold and chloride and potassium excretion increased 12-fold (P less than 0.05 in each case). Net potassium secretion was observed. Ethacrynic acid (2 and 5 mg/kg) also produced no changes in blood pressure, hematocrit, plasma electrolytes, or PRA. At the lower dose GFR increased by 40% and urine volume nearly doubled (P Less than 0.05 in each case). Sodium, chloride, and potassium excretion increased roughly 10-fold (P less than 0.05 in each case). At the higher dose, GFR increased by 80% and urine volume more than doubled (P Less than 0.05 in each case). Sodium excretion rose 40-fold, chloride excretion rose 25-fold, and potassium excretion rose 10-fold (P less than 0.05 in each case). At both doses net potassium secretion occurred. The results demonstrate that both drugs inhibit tubular reabsorption in the turtle, acting primarily on distal segments of the nephron. The failure of either drug to alter PRA suggests that the turtle lacks a tubular mechanism for altering renin release.

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