{"title":"囊性纤维化和哮喘患者气道血管活性肠多肽(VIP)结合位点的分布和密度","authors":"R.K. Sharma, B.J. Addis, P.K. Jeffery","doi":"10.1006/pulp.1995.1011","DOIUrl":null,"url":null,"abstract":"<div><p>Summary: The densities of airway binding sites for Vasoactive intestinal polypeptide (VIP) were determined using <sup>125</sup>I-labelled VIP (IVIP) and the technique of autoradiography applied to cryostat sections. Tissue studied included: grossly normal airway tissue taken from lungs resected for bronchial carcinoma (Ca; n=11) and lungs removed at transplant from patients with cystic fibrosis (CF; n=7). Lung tissue obtained at post-mortem in cases of fatal asthma (n=3) or lobes resected for bronchiectasis (n=3) were taken as further disease controls. In the Ca controls there was dense IVIP labelling, of alveolar wall, blood vessels, airway epithelium, submucosal glands, and bronchial smooth muscle: labelling of bronchiolar smooth muscle was sparse. In comparison with the Ca controls, IVIP labelling of all tissue structures in CF, with the exception of bronchial smooth muscle, was reduced (<em>P</em><0.01). The most striking reductions were associated with airway epithelium and alveolar wall. These reductions showed a similar trend in bronchiectasis but did not achieve statistical significance. There was no such change in lung tissue obtained from the cases of fatal asthma where labelling of bronchial smooth muscle and all other structures was similar to that of the Ca controls. It is likely that the reduction of VIP binding sites in CF is secondary to infection and inflammation.</p></div>","PeriodicalId":74618,"journal":{"name":"Pulmonary pharmacology","volume":"8 2","pages":"Pages 91-96"},"PeriodicalIF":0.0000,"publicationDate":"1995-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1006/pulp.1995.1011","citationCount":"18","resultStr":"{\"title\":\"The Distribution and Density of Airway Vasoactive Intestinal Polypeptide (VIP) Binding Sites in Cystic Fibrosis and Asthma\",\"authors\":\"R.K. Sharma, B.J. Addis, P.K. Jeffery\",\"doi\":\"10.1006/pulp.1995.1011\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Summary: The densities of airway binding sites for Vasoactive intestinal polypeptide (VIP) were determined using <sup>125</sup>I-labelled VIP (IVIP) and the technique of autoradiography applied to cryostat sections. Tissue studied included: grossly normal airway tissue taken from lungs resected for bronchial carcinoma (Ca; n=11) and lungs removed at transplant from patients with cystic fibrosis (CF; n=7). Lung tissue obtained at post-mortem in cases of fatal asthma (n=3) or lobes resected for bronchiectasis (n=3) were taken as further disease controls. In the Ca controls there was dense IVIP labelling, of alveolar wall, blood vessels, airway epithelium, submucosal glands, and bronchial smooth muscle: labelling of bronchiolar smooth muscle was sparse. In comparison with the Ca controls, IVIP labelling of all tissue structures in CF, with the exception of bronchial smooth muscle, was reduced (<em>P</em><0.01). The most striking reductions were associated with airway epithelium and alveolar wall. These reductions showed a similar trend in bronchiectasis but did not achieve statistical significance. There was no such change in lung tissue obtained from the cases of fatal asthma where labelling of bronchial smooth muscle and all other structures was similar to that of the Ca controls. It is likely that the reduction of VIP binding sites in CF is secondary to infection and inflammation.</p></div>\",\"PeriodicalId\":74618,\"journal\":{\"name\":\"Pulmonary pharmacology\",\"volume\":\"8 2\",\"pages\":\"Pages 91-96\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1006/pulp.1995.1011\",\"citationCount\":\"18\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pulmonary pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0952060085710113\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pulmonary pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0952060085710113","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The Distribution and Density of Airway Vasoactive Intestinal Polypeptide (VIP) Binding Sites in Cystic Fibrosis and Asthma
Summary: The densities of airway binding sites for Vasoactive intestinal polypeptide (VIP) were determined using 125I-labelled VIP (IVIP) and the technique of autoradiography applied to cryostat sections. Tissue studied included: grossly normal airway tissue taken from lungs resected for bronchial carcinoma (Ca; n=11) and lungs removed at transplant from patients with cystic fibrosis (CF; n=7). Lung tissue obtained at post-mortem in cases of fatal asthma (n=3) or lobes resected for bronchiectasis (n=3) were taken as further disease controls. In the Ca controls there was dense IVIP labelling, of alveolar wall, blood vessels, airway epithelium, submucosal glands, and bronchial smooth muscle: labelling of bronchiolar smooth muscle was sparse. In comparison with the Ca controls, IVIP labelling of all tissue structures in CF, with the exception of bronchial smooth muscle, was reduced (P<0.01). The most striking reductions were associated with airway epithelium and alveolar wall. These reductions showed a similar trend in bronchiectasis but did not achieve statistical significance. There was no such change in lung tissue obtained from the cases of fatal asthma where labelling of bronchial smooth muscle and all other structures was similar to that of the Ca controls. It is likely that the reduction of VIP binding sites in CF is secondary to infection and inflammation.