[The chronological process of erectile function after low-dose rate prostate brachytherapy for localised prostate cancer]. / Die chronologische Entwicklung der erektilen Funktion nach LDR-Brachytherapie beim lokal begrenzten Prostatakarzinom.

OBJECTIVES: The aim of this study was to evaluate the effect of low-dose rate prostate (LDR) brachytherapy on erectile function in correlation to the time intervals after seed implantation. DESIGN AND METHODS: 32 patients with localised prostate cancer and a median age of 74 years (range 65-83) were treated with permanent seed implantation. Erectile function was assessed by means of a validated questionnaire (IIEF-5) before and at 12, 24 and 36 months after treatment. No patient received supplemental external beam -radiation therapy or antiandrogen therapy. Of the 32 patients, 26 (81%) completed and returned the questionnaire. None of the patients used PDE-5 inhibitors or intracavernousal injection therapy. RESULTS: Before treatment, 15 patients (58%) had no erectile dysfunction (ED) (score 22-25) or mild ED (score 17-21), 11 (42%) moderate or -severe ED (score 0-16). Overall, before seed implantation the mean IIEF score was 14.4. The mean IIEF score decreased by 4.4 points 12 months after treatment, 3.1 points 24 months after treatment and 9.8 points 36 months after treatment (p < 0.05). In the group of no or mild ED, the mean IIEF score dropped by 9.7 points compared to a decrease of 1.4 points in the group of mod-erate or severe ED. CONCLUSIONS: Most of the patients treated with LDR brachytherapy suffered an ED in correlation to the time interval with a significant loss in the third year after treatment. In this study, the most significant loss occured in the groups that had no or only mild erectile dysfunction before treatment.

Centrally bradykinin B2-receptor-induced hypertensive and positive chronotropic effects are mediated via activation of the sympathetic nervous system.

OBJECTIVE: The presence of bradykinin B2 receptors in the cardiovascular regulatory centres of the brain indicates that increase in mean arterial pressure (MAP) and heart rate after intracerebroventricular (i.c.v.) injections of bradykinin is mediated via stimulation of sympathetic nervous system. METHODS: Adult Wistar- Kyoto (WKY) rats were instrumented chronically with an i.c.v. cannula, and the catheters were placed into the femoral artery and vein. Increasing doses of bradykinin (1 -300 pmol) were given i.c.v. and (i) MAP and heart rate, (ii) plasma dopamine, noradrenaline and adrenaline, and (iii) plasma arginine vasopressin (AVP) levels were determined. In addition, following blockade of peripheral alpha1 -adrenoceptors with prazosin (50 and 250 microg/kg i.v.) beta1-adrenoceptors with atenolol (10 mg/kg i.v.) or V1 -receptors with TMe-AVP (Manning compound) (10 microg/kg i.c.v. and 100 microg/kg i.v.) the effects of bradykinin (100 pmol i.c.v.) on MAP and heart rate were determined. RESULTS: Bradykinin increased MAP and heart rate dose-dependently. The pressor effects of 100 pmol bradykinin i.c.v. were completely blocked by pretreatment with the specific B2 receptor antagonist Hoe 140 (3 pmol, i.c.v.). There was no change in plasma dopamine, noradrenaline, adrenaline or AVP levels after increasing doses of bradykinin. However, peripheral blockade of alpha1- and beta1-adrenoceptors reduced the bradykinin-induced increase in MAP and heart rate, whereas central and peripheral V1 receptor blockade did not alter the cardiovascular responses to i.c.v. bradykinin. CONCLUSION: Our data suggest that the hypertensive and positive chronotropic effects induced by i.c.v. bradykinin are due to stimulation of sympathoneuronal rather than sympathoadrenal pathway in vivo.