Gamble G D, Milne R J
Department of Physiology, University of Auckland, New Zealand.
Brain Res. 1990 Apr 30;514(2):198-205. doi: 10.1016/0006-8993(90)91416-e.
Hypoventilation produces hypercapnia which can elevate pain thresholds. Hypercapnia is a potent stressor which releases catecholamines and activates the sympathetic nervous system. Some stressors produce analgesia by releasing endogenous opioids. To determine the roles of endogenous opioids and catecholamines in hypercapnic analgesia, we administered CO2 in the inspired gas mixture to conscious rats. CO2 in the range 5-10% elevated tail flick and leg flexion latencies 2- to 3-fold in both intact and spinalised animals. The effects on reflex latencies but not on paCO2 or pHa were blocked by naloxone (2 mg/kg), and were not present in morphine-tolerant animals. The effects were reduced by dexamethasone but were not changed either by adrenalectomy or by systemic guanethidine, propanolol or phentolamine. Hypercapnia delayed the onset of the late phase of behavioural responses to formalin injected into the plantar surface of the hindpaw. We conclude that moderate hypercapnia powerfully depresses flexor withdrawal responses to noxious stimuli, by a mechanism involving release of endogenous opioids but not systemic catecholamines. This effect may account in part for the elevation in pain threshold during hypoventilation.
通气不足会导致高碳酸血症，而高碳酸血症会提高痛阈。高碳酸血症是一种强大的应激源，可释放儿茶酚胺并激活交感神经系统。一些应激源通过释放内源性阿片类物质产生镇痛作用。为了确定内源性阿片类物质和儿茶酚胺在高碳酸血症镇痛中的作用，我们将吸入气体混合物中的二氧化碳给予清醒大鼠。在完整动物和脊髓损伤动物中，5%至10%范围内的二氧化碳使甩尾和屈腿潜伏期延长2至3倍。纳洛酮（2mg/kg）可阻断对反射潜伏期的影响，但对动脉血二氧化碳分压（PaCO2）或动脉血pH值（pHa）无影响，且在吗啡耐受动物中不存在这种影响。地塞米松可降低这种作用，但肾上腺切除术、全身应用胍乙啶、普萘洛尔或酚妥拉明均不改变这种作用。高碳酸血症延迟了后爪足底注射福尔马林后行为反应晚期的发作。我们得出结论，中度高碳酸血症通过一种涉及内源性阿片类物质释放而非全身儿茶酚胺的机制，强烈抑制对有害刺激的屈肌退缩反应。这种作用可能部分解释了通气不足期间痛阈的升高。
