| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
* To whom correspondence should be addressed. E-mail: whellst{at}tulane.edu.
The aim of this study was to evaluate erectile function in monocrotaline (MCT) treated rats with pulmonary hypertension (PH). Forty rats were divided into control (n=20) and MCT-treated groups (n=20). Rats were treated with MCT (60 mg/kg s.c) for 3 weeks to induce PH. Mean pulmonary arterial pressure (mPAP), medial hypertrophy index (percentage of wall thickness [% WT] of pulmonary artery), and right ventricular hypertrophy (RV/ left ventricle [LV] + septum [S] weight ratio) were evaluated. In vivo erectile responses were assessed by measurement of intracavernosal pressure (ICP)/mean arterial pressure (MAP) and total ICP (area under the curve). In vitro organ bath studies with corpus cavernosum smooth muscle (CCSM) strips were performed under both normoxic (95% O2/5% CO2) and hypoxic (by changing gas mixture to 95% N2/5% CO2) conditions. Erectile tissue was processed for immunohistochemistry. The MCT-treated group was associated with an increase in mPAP, medial hypertrophy index, and RV hypertrophy. MCT induced PH rats had significantly reduced erectile responses compared to controls. Nitrergic, endothelium-dependent relaxations, and alpha-adrenergic contractile responses were significantly reduced in the corpus cavernosum (CC) of MCT-rats. The functional responses during prolonged periods of hypoxia were similar to those observed in MCT-treated tissues. PH rats showed enhanced iNOS protein localization, but eNOS and nNOS were unchanged. These results suggest changes in cavernosal physiology are caused by MCT acting on the penile tissues and the systemic vasculature.
Key words: Erectile Dysfunction
Penis
Reactive Oxygen
Pulmonary hypertension
electrical stimulation
erectile dysfunction
hypoxia
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |