Simon P M, Pope A, Lahive K, Steinbrook R A, Schwartzstein R M, Weiss J W, Fencl V, Weinberger S E
Charles A. Dana Research Institute, Boston, MA.
Am Rev Respir Dis. 1989 Jan;139(1):134-8. doi: 10.1164/ajrccm/139.1.134.
To assess the role of endogenous opioid peptides in ventilatory control in patients with chronic obstructive lung disease, we measured the ventilatory and mouth occlusion pressure responses to hypercapnia and the compensatory response to an inspiratory resistive load in 11 male patients with COPD before and after intravenous administration of naloxone or placebo on 2 separate days. There were no statistically significant differences between naloxone and placebo administration in any index of ventilatory response to CO2 or resistive loading. When an inspiratory resistive load was added during CO2 rebreathing, minute ventilation at PETCO2 = 50 mm Hg in all 11 patients decreased significantly (p less than 0.05) with placebo and naloxone. In response to the inspiratory resistive load, in eight of the 11 patients mouth occlusion pressure (P0.1) did not increase; these eight subjects were classified as noncompensators. Naloxone did not affect the P0.1 response to inspiratory resistive loading, either in the group as a whole or in the subgroup of eight patients classified as noncompensators. Our study was unable to demonstrate that increased activity of endogenous opioid peptides suppresses the ventilatory response to CO2 or resistive loading in patients with chronic obstructive lung disease.
为评估内源性阿片肽在慢性阻塞性肺疾病患者通气控制中的作用，我们在11例男性慢性阻塞性肺疾病患者中，于静脉注射纳洛酮或安慰剂前后的2个不同日期，测量了对高碳酸血症的通气和口腔阻断压力反应以及对吸气阻力负荷的代偿反应。在对二氧化碳或阻力负荷的通气反应的任何指标上，纳洛酮和安慰剂给药之间均无统计学显著差异。在二氧化碳重复呼吸期间增加吸气阻力负荷时，所有11例患者在呼末二氧化碳分压（PETCO2）=50 mmHg时的分钟通气量，使用安慰剂和纳洛酮时均显著降低（p<0.05）。在11例患者中的8例，对吸气阻力负荷的反应中，口腔阻断压力（P0.1）未增加；这8名受试者被归类为无代偿者。纳洛酮无论是对整个组还是对被归类为无代偿者的8例患者亚组，均未影响P0.1对吸气阻力负荷的反应。我们的研究未能证明内源性阿片肽活性增加会抑制慢性阻塞性肺疾病患者对二氧化碳或阻力负荷的通气反应。
