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Article: Isoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteries

TitleIsoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteries
Authors
Issue Date1987
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.org
Citation
Anesthesiology, 1987, v. 67 n. 4, p. 513-517 How to Cite?
AbstractThe authors sought to determine if isoflurane would attenuate effects of three different types of vasoconstrictors on isolated segments of canine epicardial coronary arteries removed from healthy dogs. As the endothelium has a major role in regulating epicardial coronary artery tone, and as it modulates the effect of many vasoactive substances, experiments were conducted both on normal rings and on rings whose endothelium had been mechanically removed. In addition, the endothelium is thought to be damaged in human atherosclerosis. Rings were suspended in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% oxygen and 5% carbon dioxide, and connected to strain gauges for the measurement of isometric tension. Isoflurane 2.3% (1.5 MAC in the dog) was added to the aerating gas mixture in half the preparations, while the other rings served as control. The vasoconstrictors serotonin, phenylephrine, or prostaglandin F(2α) were added in increasing concentrations to the bath solution. In the presence of endothelium, vasoconstrictor evoked contractions were attenuated by isoflurane. Maximal tension generated by prostaglandin F(2α) in untreated rings was 114 ± 18% (mean ± SEM) of a reference contraction, while, following isoflurane, it was 46 ± 8% (P<0.005). In the absence of endothelium, isoflurane attenuated neither prostaglandin F(2α) nor serotonin evoked contraction, and had decreased effectiveness against phenylephrine mediated contraction (P<0.001). It is concluded that isoflurane attenuates vasoconstrictor-evoked contraction of isolated canine epicardial coronary arteries, and that this effect is mediated by the endothelium.
Persistent Identifierhttp://hdl.handle.net/10722/170857
ISSN
2015 Impact Factor: 5.264
2015 SCImago Journal Rankings: 2.162
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBlaise, Gen_US
dc.contributor.authorSill, JCen_US
dc.contributor.authorNugent, Men_US
dc.contributor.authorVan Dyke, RAen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:08Z-
dc.date.available2012-10-30T06:11:08Z-
dc.date.issued1987en_US
dc.identifier.citationAnesthesiology, 1987, v. 67 n. 4, p. 513-517en_US
dc.identifier.issn0003-3022en_US
dc.identifier.urihttp://hdl.handle.net/10722/170857-
dc.description.abstractThe authors sought to determine if isoflurane would attenuate effects of three different types of vasoconstrictors on isolated segments of canine epicardial coronary arteries removed from healthy dogs. As the endothelium has a major role in regulating epicardial coronary artery tone, and as it modulates the effect of many vasoactive substances, experiments were conducted both on normal rings and on rings whose endothelium had been mechanically removed. In addition, the endothelium is thought to be damaged in human atherosclerosis. Rings were suspended in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% oxygen and 5% carbon dioxide, and connected to strain gauges for the measurement of isometric tension. Isoflurane 2.3% (1.5 MAC in the dog) was added to the aerating gas mixture in half the preparations, while the other rings served as control. The vasoconstrictors serotonin, phenylephrine, or prostaglandin F(2α) were added in increasing concentrations to the bath solution. In the presence of endothelium, vasoconstrictor evoked contractions were attenuated by isoflurane. Maximal tension generated by prostaglandin F(2α) in untreated rings was 114 ± 18% (mean ± SEM) of a reference contraction, while, following isoflurane, it was 46 ± 8% (P<0.005). In the absence of endothelium, isoflurane attenuated neither prostaglandin F(2α) nor serotonin evoked contraction, and had decreased effectiveness against phenylephrine mediated contraction (P<0.001). It is concluded that isoflurane attenuates vasoconstrictor-evoked contraction of isolated canine epicardial coronary arteries, and that this effect is mediated by the endothelium.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.anesthesiology.orgen_US
dc.relation.ispartofAnesthesiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshIsoflurane - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshVasoconstrictor Agents - Antagonists & Inhibitorsen_US
dc.titleIsoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteriesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00000542-198710000-00012-
dc.identifier.pmid3662080-
dc.identifier.scopuseid_2-s2.0-0023550347en_US
dc.identifier.volume67en_US
dc.identifier.issue4en_US
dc.identifier.spage513en_US
dc.identifier.epage517en_US
dc.identifier.isiWOS:A1987K280900011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridBlaise, G=7005522049en_US
dc.identifier.scopusauthoridSill, JC=7003810915en_US
dc.identifier.scopusauthoridNugent, M=7007070457en_US
dc.identifier.scopusauthoridVan Dyke, RA=7005816060en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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