Abstract
Background: Preeclampsia was thought to be caused by oxidative stress. Where there was an increased in lipoperoxidation products and nitric oxide synthase (NOS) and decreased antioxidants. L-Arginine through the nitric oxide line inhibit nitrite oxide synthase inhibitor causing vascular vasodilation. This study aimed to analyze the effect L-Arginine to repair endothelial damage: thickness and diameter of the coronary arteries in the heart of the mice preeclampsia model.
Methods: Experimental, 30 pregnant mice were randomly divided into three groups, in normal 10 (N), preeclampsia 10 (PE) and preeclampsia with L-Arginine 10 (PE-L) . Preeclampsia mice were made by injecting anti-Qa2 10 ng ip on day 1 to 4th day of pregnancy. L-Arginine was administered at a dose of 200 mg / kgbw from day 7 to day 15. Termination in 16th day, observation the histologic changes of the thickness and diameter coronary arteries. Statistics were used Kruskall Wallis test, followed by Mann Whitney's test.
Results: Mean coronary artery diameter of normal group was 1098,12 μm, preeclampsia 821,58 μm with p=0,004 and preeclampsia with L-Arginine 991,27 μm with p=0,01 9 . Mean coronary artery diameter was normal 1098,12 μm compared to coronary artery diameter of preeclampsia with L- Arginine 991,27 μm with p=0,326 . Mean coronary artery thickness of normal group 178,13 μm, preeclampsia 235,29 μm with p=0,009. Mean thickness of the coronary arteries of normal 178,13 μm, compared to coronary artery thickness of preeclampsia with L-Arginine 169,96 μm with p=0,669. Mean coronary artery thickness was 235,29 μm preeclampsia compared to coronary artery thickness of preeclampsia with L-Arginine 169,96 μm with p=0,002 (p <0,05).
Conclusions: L-Arginine effects of reducing coronary artery wall thickness and expanding diameter of heart coronary artery of preeclampsia mice model .
