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Rat model for the study of penile erection: pharmacologic and electrical-stimulation parameters.

We report the use of a modified rat model for the study of the mechanisms of penile erection. In 92 Sprague-Dawley rats, the cavernous nerve was stimulated with different pulse intensities and frequencies, and the intracavernous pressure, time to maximal pressure and total duration of tumescence were measured. A maximal response was elicited at 20 pulses per second (pps) and 1.5 mA. Using this as 100%, we determined the relative pressure responses obtained with other frequencies: 5 pps, 57.3% (p = 0.007), 10 pps, 84.9% (p = 0.043); 30 pps, 99.5% (p = 0.832); 40 pps, 97.8% (p = 0.168); 50 pps, 90.9% (p = 0.021); 100 pps, 76.1% (p < 0.001). The time to maximal pressure varied with different frequencies, but was in all cases significantly different from the 20-pps response. Erection time during continuous cavernous nerve stimulation was significantly longer with frequencies below 20 pps (10 and 5 pps). In 30 rats, the physiologic response to intracavernous injection (0.03 ml) of acetylcholine, atropine, guanethidine, norepinephrine, phenylephrine, papaverine, terbutaline (intravenous also) and phentolamine was measured. Papaverine caused a dose-dependent rise in pressure; acetylcholine, atropine (a parasympathetic blocking agent) and guanethidine all had minimal effects. Phentolamine and norepinephrine increased systemic blood pressure, whereas phenylephrine decreased the intracavernous pressure in response to electrostimulation significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Cyclic guanosine monophosphate mediates penile erection in the rat

Recent in vivo and in vitro studies suggest that nitric oxide or a nitric-oxide-like substance mediates nonadrenergic, noncholinergic relaxation of trabecular smooth muscle through activation of the cyclic guanosine monophosphate (cGMP) pathway. In 60 Sprague-Dawley rats, we investigated the effect of intracavernous administration of different drugs known to act at different levels of the cyclic adenosine monophosphate (cAMP) and cGMP pathways. Neither cAMP nor drugs that stimulate adenylate cyclase activity (vasoactive intestinal peptide, prostaglandin E1, calcitonin gene-related peptide) provoked any change in the basal intracavernous pressure. N-ethylmaleimide, an inhibitor of the enzyme adenylate cyclase, did not modify the response to electrostimulation of the cavernous nerve, indicating that the cAMP pathway does not play a significant role in penile erection in rats. However, intracavernous administration of methylene blue, a guanylate cyclase inhibitor, significantly reduced the response to electrostimulation (p = 0.001). Direct intracavernous injection of cGMP caused a statistically significant, dose-dependent increase in intravenous pressure that was not significantly inhibited by methylene blue. Sodium nitroprusside, a nitric oxide releaser and therefore a guanylate cyclase activator, caused a dose-dependent increase in intracavernous pressure (p < 0.05) that was inhibited almost completely by methylene blue (p = 0.002), supporting the theory that nitric oxide activates the synthesis of cGMP and that cGMP causes cavernous smooth muscle relaxation. Papaverine elicited an intracavernous pressure increase that was not affected by methylene blue or N-ethylmaleimide, indicating that papaverine acts through an independent pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Combined Cavernous Compression Device and Arteriovenous-Cavernous Fistula: A Chronic Canine Model

In 5 dogs studied over a 3-month period, we evaluated the chronic effects of the combination of deep dorsal vein arterialization with implantation of an inflatable venous compression device. The device was placed around the proximal corpora cavernosa, sparing the left dorsal artery. A left-to-right, end-to-side dorsal artery-dorsal vein fistula was fashioned, and the right dorsal vein was anastomosed to the corpus cavernosum as an end-to-side venocorporeal window. From postoperative day 15, the device was activated twice a day for 3 months. Intracavernous pressure (bilateral) and left dorsal artery blood flow were monitored, and the patency of the anastomoses was evaluated by vascular clamping, arteriography, cavernosography and microscopic dissection. The device was well-tolerated, requiring no anesthesia during activation. (A sixth dog developed glanular hyperemia and priapism and was excluded from evaluation). With cuff inflation, the intracavernous pressure was significantly higher on the experimental side (range, 20 to 106 cm. H2O higher; p = 0.028), and arteriography demonstrated contrast flowing in the fistula and window in 3 of 4 dogs in which it was done. Both clamping and microscopic dissection of the specimen showed patency of the anastomoses in all 5 dogs. Histologic examination revealed maintenance of normal cavernous tissue histology.