Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1987-11-19
pubmed:abstractText
Although 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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
912-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Stimulation of the caudal ventrolateral medulla decreases total lung resistance in dogs.
pubmed:affiliation
Department of Physiology, University of Texas Southwestern Medical School, Dallas 75235.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't