A modulation of vesicourethral function with naloxone in traumatic paraplegics during the spinal shock phase: preliminary report.
Experimental studies have suggested that endorphins released in response to spinal injury might play a part in the pathogenesis of spinal shock and that an interaction might occur between the endorphin systems and central parasympathetic centres in such circumstances. To investigate the role of endorphins in the causation of detrusor areflexia during spinal shock, the effect of intravenous administration of 10 mg of naloxone upon vesicourethral function was studied in eight traumatic paraplegics during the spinal shock phase. Naloxone caused a significant rise in detrusor pressure during bladder distension in the post-naloxone cystometrogram. The compliance decreased in six patients. Voiding occurred in one patient although it was transient and did not result in complete emptying of the bladder. An increase in the sphincter electromyographic activity in response to bulbocavernosus stimulation was observed after naloxone in three patients. In conclusion, the significant increase observed in detrusor pressure in traumatic paraplegics during the spinal shock phase subsequent to naloxone (10 mg intravenously) provides evidence for the role of endorphins in the causation of detrusor areflexia in spinal shock.
D000328:Adult; D004723:Endorphins / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009270:Naloxone; D010264:Paraplegia / Q000209:etiology / Q000503:physiopathology*; D011312:Pressure; D013119:Spinal Cord Injuries / Q000150:complications*; D014521:Urethra / Q000503:physiopathology*; D001743:Urinary Bladder / Q000503:physiopathology*
D004723:Endorphins; D009270:Naloxone