Linked Life Data

6131799

Source:http://linkedlifedata.com/resource/pubmed/id/6131799

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1983-5-27
pubmed:abstractText
The effect of intravenous histamine on intragallbladder pressure (GBp) and subsequent modification of the histamine response by H1- and H2-antagonists was investigated in an awake baboon model. Responses to specific H1- and H2-agonists were also examined in order to further elucidate gallbladder histamine responses. Gallbladder volume (GBv) was arbitrarily set at 60-70% of observed resting GBv, and drugs were then infused intravenously with continuous monitoring of GBp. Histamine administration resulted in a logarithmic dose--response curve with a maximal increase in GBp equal to 31.7 mm Hg at a dose of 0.0625 mg of histamine. Infusion of the H1-antagonist diphenhydramine hydrochloride (Benadryl) resulted in a decreased GBp response to histamine when compared to preblocker response at all doses studied. On the other hand, histamine response following administration of the H2-antagonist metiamide was significantly greater than the preblocker histamine response. Infusion of the H1-agonist 2-pyridylethlamine resulted in a dose-dependent increase in GBp similar to the histamine curve, while infusion of the H2-agonist dimaprit resulted in consistent decreases in GBp. These results extend previous observations in subprimate preparations and demonstrate the presence of both stimulatory H1-receptors and inhibitory H2-receptors in an in situ primate model.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0163-2116
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
353-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Histamine receptors in primate gallbladder.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.