Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-10-28
pubmed:abstractText
Histamine has a positive inotropic effect on ventricular myocardium and stimulation of histamine H? receptors increases the intracellular cAMP level via Gs protein, as dose stimulation of ?-adrenergic receptors, and worsens heart failure. To test whether a histamine H? receptor blocker had a beneficial effect in addition to ?-adrenergic receptor blockade, we investigated the cardioprotective effect of famotidine, a histamine H? receptor blocker, in dogs receiving a ?-blocker. We induced heart failure in dogs by rapid ventricular pacing (230 beats/min). Animals received no drugs (control group), famotidine (1 mg/kg daily), carvedilol (0.1 mg/kg daily), or carvedilol plus famotidine. Both cardiac catheterization and echocardiography were performed before and 4 weeks after the initiation of pacing. Immunohistochemical studies showed the appearance of mast cells and histamine in the myocardium after 4 weeks of pacing. In the control group, the left ventricular ejection fraction (LVEF) was decreased after 4 weeks compared with before pacing (71 ± 2 vs. 27 ± 2%, p < 0.05) and mean pulmonary capillary wedge pressure (PCWP) was increased (8 ± 1 vs. 19 ± 3 mmHg). Famotidine ameliorated the decrease of LVEF and increase of PCWP, while the combination of carvedilol plus famotidine further improved both parameters compared with the carvedilol groups. These beneficial effects of famotidine were associated with a decrease of the myocardial cAMP level. Histamine H? receptor blockade preserves cardiac systolic function in dogs with pacing-induced heart failure, even in the presence of ?-adrenergic receptor blockade. This finding strengthens the rationale for using histamine H? blockers in the treatment of heart failure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1435-1803
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
787-94
pubmed:meshHeading
pubmed-meshheading:20852875-Adrenergic beta-Antagonists, pubmed-meshheading:20852875-Animals, pubmed-meshheading:20852875-Carbazoles, pubmed-meshheading:20852875-Cardiac Pacing, Artificial, pubmed-meshheading:20852875-Cardiotonic Agents, pubmed-meshheading:20852875-Cyclic AMP, pubmed-meshheading:20852875-Disease Models, Animal, pubmed-meshheading:20852875-Dogs, pubmed-meshheading:20852875-Echocardiography, pubmed-meshheading:20852875-Famotidine, pubmed-meshheading:20852875-Heart Catheterization, pubmed-meshheading:20852875-Heart Failure, pubmed-meshheading:20852875-Histamine, pubmed-meshheading:20852875-Histamine H2 Antagonists, pubmed-meshheading:20852875-Immunohistochemistry, pubmed-meshheading:20852875-Mast Cells, pubmed-meshheading:20852875-Propanolamines, pubmed-meshheading:20852875-Pulmonary Wedge Pressure, pubmed-meshheading:20852875-Stroke Volume, pubmed-meshheading:20852875-Ventricular Function, Left
pubmed:year
2010
pubmed:articleTitle
A histamine H? receptor blocker ameliorates development of heart failure in dogs independently of ?-adrenergic receptor blockade.
pubmed:affiliation
Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, 565-8565, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't