Santiago T V, Remolina C, Scoles V, Edelman N H
N Engl J Med. 1981 May 14;304(20):1190-5. doi: 10.1056/NEJM198105143042002.
Since narcotic drugs profoundly depress breathing, we tested whether endogenous opioids influenced control of breathing in chronic obstructive pulmonary disease (COPD), reasoning that the stress of chronic dyspnea might cause elaboration of "endorphins." In 14 patients with COPD (but without respiratory failure) and eight normal controls, we measured ventilation, mechanical lung function, respiratory sensitivity to carbon dioxide, and the increase in respiratory effort elicited by an increase in resistance to breathing; each measurement was performed before and after administration of the opiate antagonist naloxone. Before naloxone, increased resistance to breathing enhanced respiratory effort in all controls, but seven of 14 patients with COPD had no response. After naloxone, these seven patients had load responses. Furthermore, the respiratory effort elicited by the resistance also increased after the drug was given to the patients who had had a response. These data suggest that endorphin elaboration minimizes the stress of chronic airway obstruction.
由于麻醉药物会严重抑制呼吸,我们推测内源性阿片类物质是否会影响慢性阻塞性肺疾病(COPD)患者的呼吸控制,理由是慢性呼吸困难的应激可能会导致“内啡肽”的分泌增加。我们对14例COPD患者(无呼吸衰竭)和8名正常对照者进行了研究,测量了通气、肺机械功能、对二氧化碳的呼吸敏感性以及呼吸阻力增加引起的呼吸努力增加情况;每项测量均在给予阿片拮抗剂纳洛酮前后进行。在给予纳洛酮之前,所有对照者呼吸阻力增加时呼吸努力均增强,但14例COPD患者中有7例无反应。给予纳洛酮后,这7例患者出现了负荷反应。此外,给予纳洛酮后,原本有反应的患者呼吸阻力引起的呼吸努力也增加了。这些数据表明,内啡肽的分泌可减轻慢性气道阻塞的应激。