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Jun Jiang, Yanzheng He, Rui Jiang, Ultrastructural Changes of Penile Cavernous Tissue in Multiple Sclerotic Rats, The Journal of Sexual Medicine, Volume 6, Issue 8, August 2009, Pages 2206–2214, https://doi.org/10.1111/j.1743-6109.2009.01310.x
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ABSTRACT
Multiple sclerosis (MS) is one of the important risk factors resulting in erectile dysfunction (ED). The ultrastructure of corpus cavernous of the penis have an important role in the mechanism of erection.
It is suggested that different medical conditions produce similar degenerative tissue responses. We investigated the ultrastructural changes of penile cavernous tissue and its association with ED in multiple sclerotic rats.
After induction of multiple sclerosis in rat, maximum intracavernosal pressure/mean arterial pressure (ICPmax/MAP) in the severity multiple sclerotic rats (group A),moderate multiple sclerotic rats (group C), and age-matched control rat (group B) were observed and compared. The ultrastructure of the penile cavernous tissue was studied by transmission electron microscope. Expression of neuronal nitric oxide synthase (nNOS) in penile tissue were examined immunohistochemically.
Severity MS (score 3) not only significantly decrease the ICPmax/MAP × 100 and the expression of nNOS, but also might affect the ultrastructure of the penis.
The ICPmax/MAP × 100 in group A was significantly less than in group B and group C at 3 V (5.65 ± 1.78, 20.49 ± 5.84, and 12.78 ± 5.76, respectively) and at 5 V (6.70 ± 1.39, 23.66 ± 5.19, and 16.95 ± 3.31, respectively) stimulation voltage, respectively (P < 0.05). Significant ultrastructral pathological changes characterized by degeneration and demyelination singularly in Schwann cells without significant ultrastructural change of smooth muscle cells and endothelium cells were observed in penile cavernous tissue of group A rats.
The function of penile erection is affected by MS, and the ultrastructural pathological changes of the penile cavernous tissue may be one of the important mechanisms of ED caused by severity MS.
