Document Detail

Ischemic dysfunction and impaired recovery in hypertensive hypertrophied hearts is associated with exaggerated intracellular sodium accumulation.
MedLine Citation:
PMID:  7986466     Owner:  NLM     Status:  MEDLINE    
The primary objectives of this study were to determine if hypertrophied spontaneously hypertensive rat (SHR) hearts exhibited a greater increase in intracellular sodium (Na+i) compared with Wistar-Kyoto (WKY) control rats during low flow ischemia, and to determine whether Na+i accumulation in these hearts was associated with greater ischemic dysfunction and damage. In addition, intracellular pH and high energy phosphates were monitored to assess the relationships between changes in these variables and changes in Na+i. Interleaved 31P and 23Na spectra were acquired in perfused hearts from 8- to 10-month-old rats during low flow ischemia and reperfusion, while left ventricular pressures were monitored continuously. The majority of SHR (n = 13) exhibited an increase in Na+ similar to that for WKY and did not demonstrate exaggerated ischemic dysfunction or damage. However, a subgroup of SHR (n = 7) exhibited exaggerated Na+i accumulation during ischemia, compared with WKY, that was associated with contractile failure and a greater increase in left ventricular end diastolic pressure during ischemia, and slower recovery of developed pressure during reperfusion. Greater Na+i accumulation in this SHR subgroup preceded significantly greater depletion of high energy phosphates compared with WKY. In conclusion, increased Na+i accumulation was observed in all hypertrophied hearts with greater ischemic dysfunction compared with WKY. These results suggest that impaired Na+i handling may indeed contribute to the greater susceptibility of hypertrophied hearts to ischemic dysfunction and damage.
A L Golden; J M Bright; G M Pohost; M M Pike
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of hypertension     Volume:  7     ISSN:  0895-7061     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  1994 Aug 
Date Detail:
Created Date:  1995-01-12     Completed Date:  1995-01-12     Revised Date:  2009-02-24    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  745-54     Citation Subset:  IM    
Cardiovascular Research Laboratory, University of Tennessee College of Veterinary Medicine, Knoxville.
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MeSH Terms
Adenosine Triphosphate / metabolism
Cardiomegaly / complications,  metabolism*,  physiopathology
Hydrogen-Ion Concentration
Hypertension / complications,  metabolism*,  physiopathology
Lactates / metabolism
Lactic Acid
Magnetic Resonance Spectroscopy
Myocardial Ischemia / complications,  metabolism*,  physiopathology
Myocardial Reperfusion Injury / metabolism*,  physiopathology
Phosphates / metabolism
Rats, Inbred SHR
Rats, Inbred WKY
Sodium / metabolism*
Ventricular Function, Left / physiology
Reg. No./Substance:
0/Lactates; 0/Phosphates; 50-21-5/Lactic Acid; 56-65-5/Adenosine Triphosphate; 7440-23-5/Sodium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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