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Department of Pharmacology and Toxicology, The University of Western Ontario, London, Ontario, Canada N6A 5C1
We
investigated the effect of sodium/hydrogen exchange inhibition (NHE-1)
on hypertrophy and heart failure after coronary artery ligation (CAL)
in the rat. Animals were subjected to occlusion (or sham) of the left
main coronary artery and immediately administered a control diet or one
consisting of the NHE-1 inhibitor cariporide for 13-15 wk. Hearts
were separated by small [
30% of left ventricle (LV)] and large
(>30% of LV) infarcts. CAL depressed change in left ventricular
increase in pressure over time (LV +dP/dt) in small and
large infarct groups by 18.8% (P < 0.05) and 34%
(P < 0.01), respectively, whereas comparative values
for the cariporide groups were 8.7% (not significant) and 23.1%
(P < 0.01), respectively. LV end-diastolic pressure
was increased by 1,225% in the control large infarct group but was
significantly reduced to 447% with cariporide. Cariporide also
significantly reduced the degree of LV dilation in animals with large
infarcts. Hypertrophy, defined by tissue weights and cell size, was
reduced by cariporide, and shortening of surviving myocytes was
preserved. Infarct sizes were unaffected by cariporide, and the drug
had no influence on either blood pressure or the depressed inotropic
response of infarcted hearts to dobutamine. These results suggest an
important role for NHE-1 in the progression of heart failure after
myocardial infarction.
cariporide; cellular remodeling
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