Myocardial microcirculation stereological changes in rats subjected to nitric oxide synthesis inhibition.
This work aims to study stereological changes in intramyocardial blood vessels in rats submitted to nitric oxide (NO) synthesis inhibition within different periods. NO synthesis inhibition was achieved by administration of L-NAME (50 mg/kg/day); control and L-NAME rats were sacrificed 25 and 40 days after experimentation. Light microscopy and stereology [according to references 7, 13 and 14] were used for analyzing the myocardium. Arterial blood pressure and cardiac weight increased by 74.5% and 57.8% after 25 days and by 90.2% and 34.6% after 40 days, respectively. Comparing the L-NAME rats with corresponding controls revealed that the volume density of the vessels decreased by 31.3% after 40 days, and the length density by 53.5% after 25 days and by 25.7% after 40 days. The mean cross-sectional area of the vessels increased by 154.6% after 25 days. In this study on intramyocardial vessels, we observed an important decrease of the length density in L-NAME animals. Likewise, the volume density also decreased significantly in L-NAME animals. The mean cross sectional area of the vessels, which normally increases during cardiac growth between 25 and 40 days, was precociously increased in L-NAME animals at 25 days, suggesting that these animals suffer from a precocious increase of the heart (including blood vessels) due to pressure overload. Stereology of cardiac microvessels revealed remodeling of these vessels in rats under NO synthesis inhibition. Although these changes may be caused by NO inhibition and not by arterial hypertension, further comparative studies on different models of arterial hypertension are needed to confirm this hypothesis.
Pereira
L M
LM
Laboratory of Morphometry and Cardiovascular Morphology, State University of Rio de Janeiro, Brazil. mandarim@uerj.br
Mandarim-De-Lacerda
C A
CA
D000818:Animals; D003326:Coronary Circulation / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D018715:Microscopy, Video; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar
D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester