J Roca, J M Montserrat, R Rodriguez-Roisin, R Guitart, A Torres, A G Agusti, P D Wagner
{"title":"慢性阻塞性肺疾病伴高碳酸血症性呼吸衰竭患者对纳洛酮的气体交换反应。","authors":"J Roca, J M Montserrat, R Rodriguez-Roisin, R Guitart, A Torres, A G Agusti, P D Wagner","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>It has been hypothesized that naloxone may alter the ventilation-perfusion relationship in patients with chronic obstructive pulmonary disease (COPD) with associated respiratory failure, through the release of hypoxic pulmonary vasoconstriction. To investigate the effects of naloxone on gas exchange, seven clinically stable patients with severe COPD (type B) (forced expiratory volume in one second/forced vital capacity (FEV1/FVC) 38.3 +/- 4.0%) with hypoxaemia and hypercapnia (PaO2 7.6 +/- 0.4 kPa; PaCO2 6.4 +/- 0.3; pH 7.37 +/- 0.02), aged 59.0 +/- 4.6 yr, were studied. Breathing patterns, haemodynamic and conventional and inert gas exchange measurements were made while breathing room air before, during and 60 min after i.v. naloxone infusion. Naloxone and catecholamine plasma levels were also determined. In three subjects (protocol A), measurements were made using increasing concentrations of naloxone (cumulative dose: 54 mg), while the remaining four patients were studied (protocol B) at a fixed concentration of naloxone (cumulative dose: 38 mg). Despite high levels of naloxone (up to 150 ng.ml-1), no significant differences from baseline were observed in any of the measurements, during or after infusion. It is concluded that i.v. naloxone given as described has no effects on pulmonary gas exchange in clinically stable COPD patients with chronic respiratory failure.</p>","PeriodicalId":75642,"journal":{"name":"Bulletin europeen de physiopathologie respiratoire","volume":"23 3","pages":"249-54"},"PeriodicalIF":0.0000,"publicationDate":"1987-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Gas exchange response to naloxone in chronic obstructive pulmonary disease with hypercapnic respiratory failure.\",\"authors\":\"J Roca, J M Montserrat, R Rodriguez-Roisin, R Guitart, A Torres, A G Agusti, P D Wagner\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>It has been hypothesized that naloxone may alter the ventilation-perfusion relationship in patients with chronic obstructive pulmonary disease (COPD) with associated respiratory failure, through the release of hypoxic pulmonary vasoconstriction. To investigate the effects of naloxone on gas exchange, seven clinically stable patients with severe COPD (type B) (forced expiratory volume in one second/forced vital capacity (FEV1/FVC) 38.3 +/- 4.0%) with hypoxaemia and hypercapnia (PaO2 7.6 +/- 0.4 kPa; PaCO2 6.4 +/- 0.3; pH 7.37 +/- 0.02), aged 59.0 +/- 4.6 yr, were studied. Breathing patterns, haemodynamic and conventional and inert gas exchange measurements were made while breathing room air before, during and 60 min after i.v. naloxone infusion. Naloxone and catecholamine plasma levels were also determined. In three subjects (protocol A), measurements were made using increasing concentrations of naloxone (cumulative dose: 54 mg), while the remaining four patients were studied (protocol B) at a fixed concentration of naloxone (cumulative dose: 38 mg). Despite high levels of naloxone (up to 150 ng.ml-1), no significant differences from baseline were observed in any of the measurements, during or after infusion. It is concluded that i.v. naloxone given as described has no effects on pulmonary gas exchange in clinically stable COPD patients with chronic respiratory failure.</p>\",\"PeriodicalId\":75642,\"journal\":{\"name\":\"Bulletin europeen de physiopathologie respiratoire\",\"volume\":\"23 3\",\"pages\":\"249-54\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1987-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Bulletin europeen de physiopathologie respiratoire\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bulletin europeen de physiopathologie respiratoire","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Gas exchange response to naloxone in chronic obstructive pulmonary disease with hypercapnic respiratory failure.
It has been hypothesized that naloxone may alter the ventilation-perfusion relationship in patients with chronic obstructive pulmonary disease (COPD) with associated respiratory failure, through the release of hypoxic pulmonary vasoconstriction. To investigate the effects of naloxone on gas exchange, seven clinically stable patients with severe COPD (type B) (forced expiratory volume in one second/forced vital capacity (FEV1/FVC) 38.3 +/- 4.0%) with hypoxaemia and hypercapnia (PaO2 7.6 +/- 0.4 kPa; PaCO2 6.4 +/- 0.3; pH 7.37 +/- 0.02), aged 59.0 +/- 4.6 yr, were studied. Breathing patterns, haemodynamic and conventional and inert gas exchange measurements were made while breathing room air before, during and 60 min after i.v. naloxone infusion. Naloxone and catecholamine plasma levels were also determined. In three subjects (protocol A), measurements were made using increasing concentrations of naloxone (cumulative dose: 54 mg), while the remaining four patients were studied (protocol B) at a fixed concentration of naloxone (cumulative dose: 38 mg). Despite high levels of naloxone (up to 150 ng.ml-1), no significant differences from baseline were observed in any of the measurements, during or after infusion. It is concluded that i.v. naloxone given as described has no effects on pulmonary gas exchange in clinically stable COPD patients with chronic respiratory failure.