Endothelium-dependent vasodilatation in Sprague-Dawley rats with postinfarction hypertrophy: Lack of endothelial dysfunction in vitro

The hypothesis was tested whether postinfarction hypertrophy/congestive hea rt failure in rats is associated with endothelial dysfunction and increased vascular generation of reduced oxygen species. Myocardial infarction was i nduced in Sprague-Dawley rats by ligation of the left coronary artery. Afte r 16 weeks, endothelium-dependent (with acetylcholine) and -independent (wi th sodium nitro-prusside) relaxations were studied in isolated aortic rings , and isolated rings from the femoral and mesenteric arteries. The generati on of superoxide, hydrogenperoxide, and peroxynitrite was measured in arter ies using lucigenin- and luminol-enhanced chemiluminescence techniques. Sys tolic blood pressure decreased over the 16 week study period as compared to sham-operated control rats; organ weights (lungs, right and left ventricle s) significantly increased in coronary artery ligated rats indicating devel opment of congestive heart failure. Surprisingly concentration response cur ves with acetylcholine and sodium nitroprusside were almost identical in my ocardial infarction rats as compared to control animals, irrespective of wh ich type of vessel was studied (aorta, femoral or mesenteric arteries). In addition, no differences in the production of reduced radical species were found in aortic tissue from heart failure rats as compared to control rats.