The effect of hyperbaric oxygen therapy on erectile function recovery in a rat cavernous nerve injury model.
BACKGROUND
Cavernosal oxygenation appears to be important for preservation of erectile tissue health. Hyperbaric oxygen therapy (HBOT) has been shown to improve tissue oxygenation and has neuromodulatory effects.


OBJECTIVE
This study was designed to define the effects of HBOT on erectile function (EF) and cavernosal tissue in the rat cavernous nerve (CN) injury model.


METHODS
Four groups of Sprague-Dawley rats were studied: rats with bilateral CN crush, HBOT treated (Crush+/HBOT+); bilateral CN-crush/no HBOT (C+/H-); no crush/no HBOT (C-/H-); and no crush/HBOT (C-/H+). HBOT was delivered daily for 90 minutes at three atmospheres for 10 days commencing the day of CN crush.


METHODS
Ten days after CN injury, the animals underwent CN stimulation measuring the maximal intracavernosal pressure/mean arterial pressure (ICP/MAP) ratios. Corporal tissue was harvested pre-sacrifice, and immunohistochemically stained for nerve growth factor (NGF), endothelial nitric oxide synthase (eNOS), and cluster of differentiation molecule (CD31). Histologic analysis was performed for Masson's trichrome to assess the smooth muscle-collagen ratio. Terminal deoxynucleotidyl transferase Biotin-dUTP Nick End Labeling assay was used to define apoptotic indices (AIs).


RESULTS
The C+/H- group had significantly lower ICP/MAP ratios compared with C-/H- rats, (31% vs. 70%, P < 0.001). C+/H+ rats had significantly higher ICP/MAP ratio recovery compared with the C+/H- group (55% vs. 31%, P = 0.005). NGF and eNOS staining densities were higher in C+/H+ rats compared with C+/H- rats (P < 0.05 and P < 0.001, respectively). No difference was seen in CD31 expression. Staining density for MT displayed a trend toward higher smooth muscle preservation after HBOT. AIs were significantly increased by HBOT (P < 0.05).


CONCLUSIONS
HBOT following a CN injury improved EF preservation in this model, supporting the cavernosal oxygenation concept as protective mechanism for EF. The effects appear to be mediated via preservation of neurotrophic and endothelial factor expression.
Müller
Alexander
A
Department of Urology, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA.
Tal
Raanan
R
Donohue
John F
JF
Akin-Olugbade
Yemi
Y
Kobylarz
Keith
K
Paduch
Darius
D
Cutter
Suzanne C
SC
Mehrara
Babak J
BJ
Scardino
Peter T
PT
Mulhall
John P
JP
D000818:Animals; D004195:Disease Models, Animal; D007172:Erectile Dysfunction / Q000473:pathology / Q000628:therapy*; D006931:Hyperbaric Oxygenation; D007150:Immunohistochemistry; D008297:Male; D009409:Nerve Crush; D020932:Nerve Growth Factor / Q000378:metabolism; D009416:Nerve Regeneration; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D010413:Penis / Q000293:injuries / Q000294:innervation* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley
D020932:Nerve Growth Factor; D052250:Nitric Oxide Synthase Type III