Evaluation of corporal fibrosis in cadaveric pericardium and vein grafts for tunica albuginea substitution in rats

<abstract>Abstract Aim: To evaluate the degree of corporal fibrosis in rats with cadaveric pericardium or vein as grafting materials for tunica albuginea substitution. Materials and methods: Thirty male Sprague-Dawley rats (300 g-325 g) were divided at random into 3 groups of 10 animals each: group 1 was the sham-operated controls and groups 2 and 3 underwent wedge excision of tunica albuginea and replacement with cadaveric pericardium and vein grafts, respectively. Four months later, rats were sacrificed and the penis removed to assess the degree of fibrosis using RT PCR technique for TGP-β1 mRNA expression. The tissues were fixed in 10 % formalin, paraffin-embedded and stained with Masson's trichrome and Verhoff's van Giesen for collagen and elastic fibers. Results: Four months after grafting, there was minimal fibrosis surrounding the patch in the vein graft rats and moderate fibrosis in the pericardial graft rats. The degree of penile fibrosis in the pericardial graft rats was significantly higher than that in the controls (P<0.01), but in the vein graft rats it was not significantly different from that of the controls (P>0.05). Conclusion: The degree of penile fibrosis of cadaveric pericardial graft was significantly higher than that of the control group, while in the vein graft group it was comparable to the latter. The authors believe that the vein graft may be a more ideal substance to be used as the tunica albuginea substitute than the pericardial graft in the surgical treatment of Peyronie's disease.

Purinergic contraction of the rat vas deferens in L-NAME-induced hypertension：effect of sildenafil

Hypertension （HTN） is a risk factor for erectile dysfunction, but its effect on vas deferens （VD） contractility and the ejaculatory response has not been delineated. NG-nitro-L-arginine methyl ester （L-NAME）, a nitric oxide synthase inhibitor, was used for induction of nitric oxide （NO）-deficient HTN. Our aim was to evaluate the effects of L-NAME-induced HTN on rat VD contractility and to determine whether sildenafil affects VD contractility. A total of 36 male rats were divided into （1） control, （2）L-NAME-HTN, （3） sildenafil treated L-NAME-HTN groups. Group 2 was treated with L-NAME （40 mg kgI per day） in drinking water for 4 weeks. Group 3 received sildenafil （1.5 mg kg^-1 per day, by oral gavage） concomitantly with L-NAME. The prostatic portion of the VD was subjected to electrical field stimulation （EFS, 1-20 Hz）, and the P2X1 agonist α,β-methylene ATP （α,β meATP, 100 μmol L^-1-1 μmol L-1） and the al-adrenoceptor agonist phenylephrine （Phe, 100 μmol L^-1-1 mmol L^-1） were used to construct concentration-response curves. These experiments were repeated in the presence of P2X receptor antagonist, pyridoxalphosphate-6-azophenyl-2＇,4＇-disulfonic acid （PPADS, 30 μmol L-1）. VD contractions in response to EFS, a,β-meATP and Phe were significantly enhanced by L-NAME. Sildenafil treatment in the L-NAME group improved the contractile response of VD to EFS （20 Hz）. In the presence of PPADS, the enhanced contractile response of VD to EFS and a,β-meATP in hypertensive rats was reversed. In the rat model of chronic NO depletion, the purinergic and adrenergic components and EFS affect VD contractility. The VD contractile response may be mediated more by the purinergic system than the adrenergic system, and sildenafil may alter the ejaculatory response in men with PE.