Influence of endometriosis on visceromotor and cardiovascular responses induced by vaginal distention in the rat.
This study examined pseudoaffective responses elicited by vaginal distention in urethane-anesthetized rats, and tested hypotheses that responses would be increased by endometriosis (ENDO) and vary with the estrous cycle. Three groups were studied: ENDO, shamENDO, and Naive. ENDO was induced by autotransplanting small pieces of uterine horn (or, for shamENDO, fat) on mesenteric arteries. Ten weeks later, rats in proestrus or metestrus were anesthetized with urethane. Distendable latex balloons were inserted into the vaginal canal. While an increasing series of vaginal distentions was delivered, changes in electromyographic activity of the external oblique musculature (visceromotor response, VMR) and mean arterial pressure (pressor) responses were simultaneously measured. Vaginal distention produced VMR and pressor responses in all groups. These responses were significantly greater in ENDO than in the other groups, and greater in proestrus than metestrus. Although the overall amount of cystic tissue was greater in proestrous than metestrous rats, there was no correlation between these amounts and VMR or pressor responses. Acute spinalization (T8-T9) and bilateral pelvic, but not hypogastric, neurectomy attenuated both VMR and pressor responses, supporting the hypothesis that vaginal nociception involves suprathoracic spinal processing of information conveyed by the pelvic nerve. These effects on VMR and pressor responses to vaginal distention parallel behavioral escape responses to the same stimuli reported previously. The findings encourage continued use of VMR and pressor responses for further investigation of mechanisms underlying pain associated with ENDO and its potential treatment.
Nagabukuro
Hiroshi
H
Program in Neuroscience, Florida State University, Tallahassee, FL 32306-1270, USA.
Berkley
Karen J
KJ
D000009:Abdominal Muscles / Q000294:innervation / Q000502:physiology; D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D017776:Autonomic Pathways / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D004195:Disease Models, Animal; D004715:Endometriosis / Q000150:complications* / Q000503:physiopathology; D005260:Female; D007001:Hypogastric Plexus / Q000503:physiopathology; D009619:Nociceptors / Q000502:physiology; D010147:Pain Measurement; D017699:Pelvic Pain / Q000209:etiology* / Q000503:physiopathology; D010812:Physical Stimulation / Q000009:adverse effects; D011312:Pressure / Q000009:adverse effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012020:Reflex, Abdominal / Q000502:physiology*; D014621:Vagina / Q000294:innervation / Q000503:physiopathology; D017833:Visceral Afferents / Q000503:physiopathology*