Laparoscopic Management of a Complex Adrenal Cyst.

Adrenal cysts are rare, and their clinical management remains controversial. We report a case involving an adrenal cyst with a complicated appearance on radiological studies. Unenhanced computed tomography revealed a unilocular, noncalcified, hypoattenuating mass with a thin wall in the left adrenal gland. The lesion gradually increased in size from 10 to 50 mm at two-year follow-up. On contrast-enhanced magnetic resonance imaging, a mural nodule with contrast enhancement was observed. The entire adrenal gland was excised en bloc via a lateral transperitoneal laparoscopic approach without violating the principles of surgical oncology. The pathological diagnosis was an adrenal pseudocyst. Laparoscopic adrenalectomy is a safe option for the treatment of complex adrenal cysts, while maintaining the benefits of minimal invasiveness.

A causative factor of copulatory disorder in rats following social stress.

PURPOSE: We investigated the causative role of testosterone in copulatory disorder and the expression of c-fos messenger (m)RNA in the medial preoptic area in rats after social stress. MATERIALS AND METHODS: To generate copulatory disorder rats in the experimental defeated group were attacked by residents for 10 minutes daily for 7 consecutive days (social stress). We then investigated the effect of repeat defeat on the frequency of mounting behavior and plasma testosterone levels. The effects of testosterone replacement and/or apomorphine (100 microg./kg. subcutaneously), a dopamine receptor agonist, on the frequency of mounting behavior were also studied. After experiencing social stress the brain area within the medial preoptic area was removed for analysis of c-fos and androgen receptor mRNA expression. Real-time reverse transcription-polymerase chain reaction was done to analyze gene expression. RESULTS: Rats in the defeated group showed a reduced frequency of mounting behavior and a decrease in plasma testosterone levels compared with values in control rats (p <0.01). After testosterone replacement the frequency of mounting behavior became significantly higher than that of socially stressed rat (p <0.05) but did not achieve control levels. The frequency of mounting behavior by socially stressed rats after apomorphine treatment was significantly higher than that of vehicle treated rats (p <0.05) but the frequency produced by the combination of testosterone replacement and apomorphine injection did not achieve control levels. After the social stress experience c-fos mRNA expression was significantly increased compared with that in control rats (p <0.05). The expression of androgen receptor mRNA was not affected by social stress. Testosterone replacement significantly reduced the expression of c-fos mRNA in the medial preoptic area (p <0.05). CONCLUSIONS: Our results indicate that a reduction in plasma testosterone may have a causative role in copulatory disorder induced by social stress. Changes in c-fos mRNA expression in the medial preoptic area correlated with copulatory disorder and, thus, they are suitable for monitoring that disorder.

Contribution of cerebral nitric oxide to bladder overactivity after cerebral infarction in rats.

PURPOSE: We investigated the contribution of cerebral nitric oxide to neurogenic voiding dysfunction after cerebral infarction. MATERIALS AND METHODS: The left mid cerebral artery in female Sprague-Dawley rats was occluded with 4-zero monofilament nylon thread. Bladder activity was monitored during infusion cystometrography. Time or dose dependent effects of intracerebral ventricular administration of the nonselective nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), were investigated in conscious, sham operated and cerebral infarcted rats. The selective neuronal nitric oxide synthase inhibitor 1-(2-trifluoromethylphenyl) imidazole was also administered to determine the participation of nitric oxide synthase subtypes. Cross-sectional infarct area was measured and infarct volume was calculated 12 hours after mid cerebral artery occlusion. RESULTS: Bladder capacity was reduced by 54% 30 minutes after mid cerebral artery occlusion. L-NAME significantly increased bladder capacity in a dose and time dependent manner in cerebral infarcted rats but had no effect on sham operated rats. L-NAME (50 microg./kg.) administered 3 or 5 hours after occlusion significantly increased bladder capacity. This effect of L-NAME was reversed by injecting 250 microg. L-arginine per rat, which alone did not produce any significant change in bladder capacity in cerebral infarcted rats. Administration of 1-(2-trifluoromethylphenyl) imidazole also significantly increased bladder capacity in these rats. On the other hand, 5 microg. of the nitric oxide donor FK-409 per rat reduced bladder capacity for 10 to 15 minutes. None of the drugs affected infarct volume. CONCLUSIONS: These results indicate that supraspinal nitric oxide has an important role in bladder overactivity after cerebral infarction but it does not affect normal micturition in rats. This finding suggests a central mechanism sensitive to nitric oxide for bladder overactivity after cerebral infarction.