Vaidyanathan S, Rao M S, Chary K S, Sharpa P L
Ann Clin Res. 1982 Apr;14(2):98-102.
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.
实验研究表明，脊髓损伤后释放的内啡肽可能在脊髓休克的发病机制中起作用，且在这种情况下内啡肽系统与中枢副交感神经中枢之间可能会发生相互作用。为了研究内啡肽在脊髓休克期间逼尿肌无反射病因中的作用，对8名处于脊髓休克期的创伤性截瘫患者静脉注射10毫克纳洛酮后，观察其对膀胱尿道功能的影响。纳洛酮注射后膀胱测压图显示，膀胱充盈时逼尿肌压力显著升高。6名患者的顺应性降低。1名患者出现排尿，但为一过性，未导致膀胱完全排空。3名患者在注射纳洛酮后，球海绵体肌刺激引起的括约肌肌电图活动增强。总之，在创伤性截瘫患者脊髓休克期静脉注射10毫克纳洛酮后，逼尿肌压力显著升高，这为内啡肽在脊髓休克时逼尿肌无反射病因中的作用提供了证据。
