Tehran University Medical Journal

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Background: Post-transplant erythrocytosis (PTE) is characterized by persistent hematocrit level above 51% that develops in 10-20% of kidney recipients, mostly 2 years after kidney transplantation. PTE is self limited in 25% of the patients but can be persistent in other patients with an increased susceptibility for thrombosis. The purpose of this study was to identify the risk factors for development of PTE in our center

Methods: We selected 45 patients who were transplanted at least 3 months before selection (minimum time required for detection of PTE) and were referred to the kidney transplantation clinic during 5 years (1998-2003) as the case group. At the same time, we considered 2 patients without erythrocytosis as control for each patient in the case group among kidney transplant recipients who were referred to the same clinic during 5 years (1998-2003). In total we had selected 135 patients, 45 patients with erythrocytosis as the case group and 90 patients without erythrocytosis as the control group. Patients who were affected by high hematocrit before transplantation (HC>51%),overt pulmonary disorder, and polycytemia Vera were excluded from this study. We collected basic information by using old charts and complementary information was added through phone conversations and physical examination in the clinic. All the information was entered in the digital questionnaire and was analyzed by the SPSS statistical package.

Results: There was no significant difference between the case and control group for age, history of hypertension, diabetes, pretransplant hematocrit, pretransplant transfusions, function of graft and source of kidney. A significantly higher proportion of PTE patients were male, also the case group had a significantly higher frequency for personal history of polycystic kidney disease , glomerulonephritis and higher frequency of azathioparine, prednisolone and cyclosporine regimen.

Conclusion: PTE is an important complication of kidney transplantation that can be fatal. There are multiple risk factors that should be addressed to prevent this complication.

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Background: Relaxation of the corpus cavernosum plays a major role in penile erection. Nitric oxide (NO) is known to be the most important factor mediating relaxation of corpus cavernosum, which is mainly derived from nonadrenergic noncholinergic (NANC) nerves. The aim of the present study was to investigate the effect of biliary cirrhosis on nonadrenergic noncholinergic (NANC)-mediated relaxation of rat corpus cavernosum as well as the possible relevant roles of endocannabinoid and nitric oxide systems.

Methods: Corporal strips from sham-operated and biliary cirrhotic rats were mounted under tension in a standard oxygenated organ bath with guanethidine sulfate (5 µM) and atropine (1 µM) to induce adrenergic and cholinergic blockade. The strips were precontracted with phenylephrine hydrochloride (7.5 µM) and electrical field stimulation was applied at different frequencies (2, 5, 10, 15 Hz) to obtain NANC-mediated relaxation. In separate precontracted strips of the sham and cirrhotic groups, the concentration-dependent relaxant responses to sodium nitroprusside (10 nM-1mM), as an NO donor, were assessed.  

Results: The NANC-mediated relaxation was significantly enhanced in cirrhotic animals (P<0.01). Anandamide potentiated the relaxations in both groups (P<0.05). The cannabinoid CB1 receptor antagonist AM251 (10 µM) and the vanilloid receptor antagonist capsazepine (10 µM) each significantly prevented the enhanced relaxations in cirrhotic rats (P<0.01). The CB2 receptor antagonist AM630 had no effect on relaxations in the cirrhotic group. In a concentration-dependent manner, L-NAME (30-1000 nM) inhibited relaxations in both the sham and cirrhotic groups, although cirrhotic groups were more resistant to the inhibitory effects of L-NAME. The degree of relaxation induced by sodium nitroprusside (10 nM-1 mM) was similar in the two groups.

Conclusions: Biliary cirrhosis enhances the neurogenic relaxation in rat corpus cavernosum probably via the NO pathway and cannabinoid CB1 and vanilloid VR1 receptors.

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Background: It is well known that erectile dysfunction is most commonly associated with diabetes, affecting 35% to 75% of men with diabetes mellitus. Several studies have been carried out to find appropriate strategies for treatment of diabetes-induced erectile dysfunction. The aim of the present study was to investigate the ability of acute administration of the endogenous cannabinoid anandamide in vitro to alter the NANC-mediated relaxation of corpus cavernosum from diabetic rats and the possible role of nitric oxide in this manner.

Methods: Diabetes was induced by the administration of streptozotocin for eight weeks. Corpora cavernosa were isolated in organ baths for measurement of agonist-evoked or electrical field stimulation (EFS)-evoked smooth muscle tensions.

Results: The neurogenic relaxation of phenylephrine (7.5 µM) precontracted isolated corporal strips was impaired in diabetic animals. Anandamide (0.3, 1 and 3 µM) enhanced the relaxant responses to EFS in diabetic strips in a dose-dependent manner. This effect was antagonized by either the selective cannabinoid CB1 receptor antagonist AM251 (1 µM) or the selective vanilloid receptor antagonist capsazepine (3 µM). Concurrent administration of partially effective doses of L-arginine (10 µM) and anandamide (0.3 µM) exerted a synergistic improvement in EFS-induced relaxation of diabetic strips (p<0.001). The relaxant responses to the nitric oxide donor sodium nitroprusside of the subjects in the diabetic and control groups were similar.

Conclusion: For the first time, we demonstrated that acute administration of an endogenous cannabinoid, alone or in combination with L-arginine could improve the NO-mediated relaxation of cavernosal smooth muscle in diabetic rats and this effect was mediated by cannabinoid CB1 and vanilloid VR1 receptors within the tissue.