{'fraction_non_alphanumeric': 0.02386002120890774, 'fraction_numerical': 0.007423117709437964, 'mean_word_length': 6.202290076335878, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Intrinsic neuromuscular defects in the neurogenic bladder. VI. Myofiber ultrastructure in the somatically denervated male feline rhabdosphincter

Ordinary somatic striated muscle with purely somatomotor innervation undergoes atrophy with fibrosis when completely denervated. On this basis, it has been suggested that vesical outlet “obstruction” in voiding dysfunction resulting from lower‐motor neural lesions is due to fibrosis of a denervated rhabdosphincter. We have shown previously that: (1) this sphincter has natural triple somatomotor/autonomic, cholinergic/autonomic adrenergic innervation of its myofibers; and (2) following its somatomotor denervation by bilateral sacral ventral rhizotomy, its myofibers lose somatomotor innervation and eventually acquires a purely autonomic innervation that includes autonomic re‐innervation of their sole plates. The present study was conducted in 16 adult male cats to define the structural changes in myofibers of the somatically denervated rhabdosphincter. Samples of the sphincter, obtained 1, 2, 4, 6, and 10 weeks after bilaterial sacral ventral rhizotomy, were processed and studied by electron microscopy. In all samples, there was a combination of ultrastructurally normal, degenerative, and regenerative myofiber profiles. Degenerative profiles were most frequent in the 1‐week, and regenerative profiles in the 6–10 weeks samples. No atrophic myofibers or interstitial fibrosis were observed in any sample. It is concluded that the somatically denervated male feline rhabdosphincter, unlike ordinary somatic striated muscle, maintains its structural integrity through myofiber regeneration and by not undergoing fibrosis. The somatically denervated rhabdosphincter, with its eventual purely autonomic re‐innervation, therefore, can play an important role in lowermotor neurogenic dysfunctions that needs further investigation.