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Department of Drug Safety Evaluation, Developmental Research Laboratories, Shionogi & Co., Ltd., Toyonaka, Osaka 561-0825, Japan
We investigated the possible
contribution of inducible nitric oxide synthase (iNOS) to postischemic
heart dysfunction and injuries in stroke-prone spontaneously
hypertensive rats (SHRSP). SHRSP, 13-14 wk of age, had
significantly higher systolic blood pressure and greater heart weight
than age-matched Wistar-Kyoto rats (WKY). Permanent occlusion of the
left anterior descending coronary artery (LAD) caused significant and
long-lasting increases in the activity and mRNA expression of
myocardial iNOS in SHRSP compared with WKY. However, there was no
significant difference in the LAD occlusion-induced expression of
interleukin-1
mRNA between SHRSP and WKY. Hemodynamic deterioration
and myocardial fibrosis were also observed in SHRSP at 4 wk after LAD
occlusion. Continuous administration of
2-amino-5,6-dihydro-6-methyl-4H-1,2-thiazin (AMT)
completely blocked the LAD occlusion-induced increase in the
myocardial iNOS activity of SHRSP. Moreover, postischemic heart
dysfunction and injuries were also significantly ameliorated by
2-amino-5,6-dihydro-6-methyl-4H-1,2-thiazin (AMT). These
results suggest that the increased activity of myocardial iNOS plays a pivotal role in the development of postischemic cardiac dysfunction and
injuries in SHRSP with the hypertensive and hypertrophic heart.
cardiac hypertrophy; left anterior descending coronary artery occlusion; 2-amino-5,6-dihydro-6-methyl-4H-1,2-thiazin
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