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pubmed-article:3308819pubmed:abstractTextAlthough the role played by the caudal ventrolateral medulla in the regulation of the cardiovascular system has been extensively investigated, little is known about the role played by this area in the regulation of airway caliber. Therefore, in alpha-chloralose-anesthetized dogs, we used both electrical and chemical means to stimulate the caudal ventrolateral medulla while we monitored changes in total lung resistance breath by breath. We found that electrical stimulation (25 microA) of 26 sites in this area significantly decreased total lung resistance from 7.1 +/- 0.4 to 5.7 +/- 0.3 cmH2O.1-1.s (P less than 0.001). The bronchodilation evoked by electrical stimulation was unaffected by beta-adrenergic blockade but was abolished by cholinergic blockade. In addition, chemical stimulation of seven sites in the caudal ventrolateral medulla with microinjections of DL-homocysteic acid (0.2 M; 66 nl), which stimulates cell bodies but not fibers of passage, also decreased total lung resistance from 8.3 +/- 1.1 to 6.5 +/- 0.8 cmH2O.l-1.s (P less than 0.01). In contrast, microinjections of DL-homocysteic acid into the nucleus ambiguus (n = 6) increased total lung resistance from 7.5 +/- 0.5 to 9.2 +/- 0.4 cmH2O.l-1.s (P less than 0.05). We conclude that the caudal ventrolateral medulla contains a pool of cell bodies whose excitation causes bronchodilation by withdrawing cholinergic input to airway smooth muscle.lld:pubmed
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pubmed-article:3308819pubmed:authorpubmed-author:KaufmanM PMPlld:pubmed
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pubmed-article:3308819pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:3308819pubmed:year1987lld:pubmed
pubmed-article:3308819pubmed:articleTitleStimulation of the caudal ventrolateral medulla decreases total lung resistance in dogs.lld:pubmed
pubmed-article:3308819pubmed:affiliationDepartment of Physiology, University of Texas Southwestern Medical School, Dallas 75235.lld:pubmed
pubmed-article:3308819pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3308819pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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