{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T07:14:14Z","timestamp":1783494854485,"version":"3.55.0"},"reference-count":0,"publisher":"J-SciMed Central, LLC","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Subst Abuse Alcohol"],"abstract":"<jats:p>Carfentanil exposure could cause severe ventilatory depression associated with \nmuscle stiffness, hypoxemia\/hypercapnia (due to hypoventilation) and hypothermia; \nhowever, its effect on inspiratory motor drive alone (without these associated effects) \nhas not been investigated. This, along with the inhibitory impact of opioids on hypoxic \nand hypercapnic ventilation, allows us to determine the impacts of carfentanil on the \nphrenic nerve (PN) activities before and during hypoxia and hypercapnia in this study. \nTwo groups of anesthetized and spontaneously breathing rats were initially exposed \nto aerosolized vehicle (Ctrl) and carfentanil (1.7 mg\/m3) for 10 min. After vagotomy, \nparalysis and artificial ventilation, the peak and frequency of integrative PN activity \n(\u0283PN and fR\n), minute PN (MPN = \u0283PN \u00d7 fR\n), arterial blood pressure (ABP) and heart rate \n(HR) were recorded before and during hypoxia (10% O2\n for 1 min) and hypercapnia \n(10% CO2\n for 3 min). Our results showed that: 1) carfentanil significantly reduced MPN \nand \u0283PN by ~50% and led to hypertension without change in fR\n and HR; 2) hypoxia \nenhanced MPN, \u0283PN and fR\n and decreased ABP and hypercapnia brought about \nsimilar PN responses with HR decreased in the Ctrl rats; and 3) carfentanil strikingly \nattenuated the MPN, fR\n and \u0283PN during both chemical challenges and exacerbated \nthe hypotension during hypoxia and the bradycardia during hypercapnia. Our results \nsuggest that carfentanil greatly suppresses the inspiratory motor drive, at least \npartially, via attenuating the chemoreflexes to substantially contribute to carfentanil\ninduced ventilatory depression and failure.<\/jats:p>","DOI":"10.47739\/substanceabuse.1111","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T06:31:07Z","timestamp":1783492267000},"page":"1-8","source":"Crossref","is-referenced-by-count":0,"title":["Carfentanil Depresses Inspiratory Motor Drive"],"prefix":"10.47739","volume":"13","author":[{"given":"Jianguo","family":"Zhuang","sequence":"first","affiliation":[{"name":"Department of Physiology, Lovelace Biomedical Research Institute, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiuping","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Physiology, Lovelace Biomedical Research Institute, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shan","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Physiology, Lovelace Biomedical Research Institute, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fadi","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Physiology, Lovelace Biomedical Research Institute, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"14791","published-online":{"date-parts":[[2026,6,3]]},"container-title":["Journal of Substance Abuse and Alcoholism"],"original-title":[],"deposited":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T06:31:08Z","timestamp":1783492268000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.jscimedcentral.com\/jounal-article-pdf\/Journal-of-Substance-Abuse-and-Alcoholism\/substanceabuse-13-1111.pdf"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,6,3]]},"references-count":0,"journal-issue":{"issue":"2","published-online":{"date-parts":[[2026,6,3]]}},"URL":"https:\/\/doi.org\/10.47739\/substanceabuse.1111","relation":{},"ISSN":["2373-9363"],"issn-type":[{"value":"2373-9363","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,6,3]]}}}