INTRODUCTION: Corporal veno-occlusive dysfunction (CVOD), which usually is associated with a loss of smooth muscle cells (SMC) and an increase in fibrosis within the corpora cavernosa, can be induced by an injury to the cavernosal nerves. The corporal tissue expresses inducible nitric oxide synthase (iNOS), presumably as an antifibrotic and SMC-protective response. AIMS: We studied the temporal relationship in the corpora between the expression of iNOS, other histological and biochemical changes, and the development of CVOD, after bilateral cavernosal nerve resection (BCNR) in the rat. METHODS: Rats underwent either BCNR or sham operation. Cavernosometry was performed 1, 3, 7, 15, 30, and 45 days (N = 8/groups) after surgery. Penile tissue sections were subjected to Masson trichrome staining for SMC and collagen, and immunodetection for alpha smooth muscle actin, iNOS, neuronal NOS (nNOS), endothelial NOS (eNOS), proliferating cell nuclear antigen (PCNA), and terminal transferase dUTP nick end labeling (TUNEL). Quantitative western blot analysis was done in homogenates. MAIN OUTCOME MEASURES: Time course on the development of fibrosis and CVOD. RESULTS: Following BCNR, CVOD was detectable 30 days later, and it became more pronounced by 45 days. In contrast, the SMC/collagen ratio in the BCNR corpora was reduced at 7 days and bottomed at 30 and 45 days, due in part to the reduction of SMC, presumably caused by an increase in apoptosis peaking at 3 days. PCNA also peaked at 3 days, but then decayed. nNOS was reduced early (3-7 days) and disappeared at 30 days, whereas eNOS was not affected. iNOS was induced at day 3, and steadily increased peaking at 30 days. CONCLUSIONS: CVOD develops in the BCNR rat as a result of the early loss of corporal SMC by the neuropraxia-induced apoptosis, which the initial cell replication response cannot counteract, followed by fibrosis. The time course of iNOS induction supports the antifibrotic role of iNOS.
INTRODUCTION: Corporal veno-occlusive dysfunction (CVOD), which usually is associated with a loss of smooth muscle cells (SMC) and an increase in fibrosis within the corpora cavernosa, can be induced by an injury to the cavernosal nerves. The corporal tissue expresses inducible nitric oxide synthase (iNOS), presumably as an antifibrotic and SMC-protective response. AIMS: We studied the temporal relationship in the corpora between the expression of iNOS, other histological and biochemical changes, and the development of CVOD, after bilateral cavernosal nerve resection (BCNR) in the rat. METHODS:Rats underwent either BCNR or sham operation. Cavernosometry was performed 1, 3, 7, 15, 30, and 45 days (N = 8/groups) after surgery. Penile tissue sections were subjected to Masson trichrome staining for SMC and collagen, and immunodetection for alpha smooth muscle actin, iNOS, neuronal NOS (nNOS), endothelial NOS (eNOS), proliferating cell nuclear antigen (PCNA), and terminal transferase dUTP nick end labeling (TUNEL). Quantitative western blot analysis was done in homogenates. MAIN OUTCOME MEASURES: Time course on the development of fibrosis and CVOD. RESULTS: Following BCNR, CVOD was detectable 30 days later, and it became more pronounced by 45 days. In contrast, the SMC/collagen ratio in the BCNR corpora was reduced at 7 days and bottomed at 30 and 45 days, due in part to the reduction of SMC, presumably caused by an increase in apoptosis peaking at 3 days. PCNA also peaked at 3 days, but then decayed. nNOS was reduced early (3-7 days) and disappeared at 30 days, whereas eNOS was not affected. iNOS was induced at day 3, and steadily increased peaking at 30 days. CONCLUSIONS: CVOD develops in the BCNR rat as a result of the early loss of corporal SMC by the neuropraxia-induced apoptosis, which the initial cell replication response cannot counteract, followed by fibrosis. The time course of iNOS induction supports the antifibrotic role of iNOS.
Authors: Gaby Nolazco; Istvan Kovanecz; Dolores Vernet; Robert A Gelfand; James Tsao; Monica G Ferrini; Thomas Magee; Jacob Rajfer; Nestor F Gonzalez-Cadavid Journal: BJU Int Date: 2008-02-21 Impact factor: 5.588
Authors: Andreas Muhs; Bernd Heublein; Jens Schletter; Andreas Herrmann; Manfred Rüdiger; Matthias Sturm; Andreas Grust; Jochen Malms; Jürgen Schrader; Heiko E von der Leyen Journal: Hum Gene Ther Date: 2003-03-01 Impact factor: 5.695
Authors: Jeffrey J Lysiak; Sang-Kuk Yang; Adam P Klausner; Hwancheol Son; Jeremy B Tuttle; William D Steers Journal: J Urol Date: 2007-12-20 Impact factor: 7.450
Authors: Alberto Briganti; Andrea Salonia; Andrea Gallina; Felix K-H Chun; Pierre I Karakiewicz; Markus Graefen; Hartwig Huland; Patrizio Rigatti; Francesco Montorsi Journal: World J Urol Date: 2007-03-06 Impact factor: 4.226
Authors: Monica G Ferrini; Hugo H Davila; Eliane G A Valente; Nestor F Gonzalez-Cadavid; Jacob Rajfer Journal: Cardiovasc Res Date: 2004-03-01 Impact factor: 10.787
Authors: Guiting Lin; Xuefeng Qiu; Thomas M Fandel; Maarten Albersen; Zhong Wang; Tom F Lue; Ching-Shwun Lin Journal: Urology Date: 2011-08-16 Impact factor: 2.649
Authors: Fara Sirad; Su Hlaing; Istvan Kovanecz; Jorge N Artaza; Leah A Garcia; Jacob Rajfer; Monica G Ferrini Journal: J Sex Med Date: 2011-01-26 Impact factor: 3.802
Authors: Faysal A Yafi; Lawrence Jenkins; Maarten Albersen; Giovanni Corona; Andrea M Isidori; Shari Goldfarb; Mario Maggi; Christian J Nelson; Sharon Parish; Andrea Salonia; Ronny Tan; John P Mulhall; Wayne J G Hellstrom Journal: Nat Rev Dis Primers Date: 2016-02-04 Impact factor: 52.329