Document Detail


Total peripheral resistance during cardiac tamponade: adrenergic and angiotensin roles.
MedLine Citation:
PMID:  3022609     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During progressive cardiac tamponade in conscious dogs, cardiac output falls continuously while arterial blood pressure is maintained until cardiovascular decompensation by increases in total peripheral resistance (TPR). Plasma renin activity (PRA) is known to increase at decompensation. We hypothesized that the increase in TPR during cardiac tamponade was mediated by alpha-adrenergic and renin-angiotensin mechanisms. Twelve adult dogs were instrumented to measure cardiac output (electromagnetic flow probe), aortic and right atrial blood pressures, and intrapericardial pressure (IPP). TPR was calculated as the conscious euvolemic animals underwent cardiac tamponade induced by intrapericardial saline infusion at 20 ml/min. Six dogs underwent cardiac tamponade in the control condition (no medications) and during independent alpha- and beta-adrenergic and angiotensin-converting enzyme (ACE) inhibition. PRA and angiotensin II (ANG II) were measured during control tamponade. We found that TPR increased continuously to levels of greater than 200% of base line as IPP rose during cardiac tamponade (P less than 0.01). This increase in TPR was unaffected by beta-adrenergic or ACE blockade but was blunted by alpha-adrenergic blockade. PRA and ANG II increased only at decompensated tamponade (P less than 0.05) when arterial blood pressure had fallen by 30%. These changes in PRA and ANG II during tamponade were not altered by beta-blockade in six separate animals. We conclude that cardiac tamponade stimulates renin release and ANG II generation by a non-beta-receptor-mediated mechanism. The increase in TPR during cardiac tamponade is primarily dependent on alpha-adrenergic mechanisms, with a limited late contribution from the renin-angiotensin system.
Authors:
T L Cogswell; G A Bernath; H Raff; R G Hoffmann; H S Klopfenstein
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  251     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1986 Nov 
Date Detail:
Created Date:  1986-12-15     Completed Date:  1986-12-15     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  R916-22     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / blood,  physiology*
Angiotensin-Converting Enzyme Inhibitors
Animals
Cardiac Tamponade / blood,  physiopathology*
Dogs
Female
Male
Pericardium / physiopathology
Receptors, Adrenergic / physiology*
Renin / blood
Vascular Resistance*
Grant Support
ID/Acronym/Agency:
HL-27615/HL/NHLBI NIH HHS; HL-32228/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Receptors, Adrenergic; 11128-99-7/Angiotensin II; EC 3.4.23.15/Renin

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