Hemodynamic and cardiac functions in rats exposed tolead toxicity, the possible effect of vitamin C (ascorbic acid)Ramadan A. Saad, Mohamed H. El_Sayed

摘要

Background:Lead is one of the environmental pollutants of high risk to public health. In this study we tried to find if there is a relationship between blood lead level and cardiac function after myocardial ischemia reperfusion injury. In addition, this study tried to evaluate the effect of ascorbic acid [vitamin C (VC)] on cardiovascular parameters in the lead-exposed rats. Methods: Twenty four Wister male rats (initially weighing 150 to 170 gm) were divided into three groups; Group I (Control rats) was given distilled water every day. Group II (lead-exposed rats) received orally lead acetate solution (60mg/kg body weight), once daily. Group III (lead-exposed + VC-treated rats) received lead acetate 60 mg /kg, once daily and concurrently supplemented with Vitamin C, 40mg/kg, every other day. Water, lead and vitamin C were all administered by using intra-gastric intubation for 8 weeks. All rats were subjected to an in vivo measurement of arterial blood pressure, ECG recording, blood samples collection for determination of lead content in the blood, blood picture, plasma total cholesterol, and HDL, in addition, atherogenic index was calculated. In vitro study of isolated hearts to record the intrinsic activity of the heart under baseline condition, responses of the heart to ischemia and reperfusion and determination of cardiac weights. Also glutathione peroxidase activity, and malondialdehyde level were measured in the cardiac tissue. Results: Lead exposure increased the concentration of lead in the blood from the pre-exposure level of 2.07 ±0.52μg/dl to 25.24 ±1.86 μg/dl after 8 weeks of exposure in lead-exposed rats. In addition, plasma total cholesterol was significantly increased together with reduction in plasma HDL, both values nearly reversed with the administration of vitamin C. Also decreased level of the MDA and increasing glutathione peroxidase activity in cardiac tissue were observed in lead exposed group. RBCs count, hemoglobin content, Haematocrite value, mean corpuscle volume (MCV), mean corpuscle hemoglobin (MCH), of lead exposed animals were significantly decreased, as compared to control rats. Vitamin C attenuated these hematological changes. ECG showed shortened the QT interval with significant increase in QRS voltage in lead exposed rats. Significant elevation of arterial blood pressure was observed in lead exposed rats as compared to control rats, As regards isolated heart perfusion, baseline chronotropy and inotropy were increased, but myocardial flow rate decreased in lead exposed rats. Vitamin C administration diminished the cardiac toxicity of lead as it normalized the mean arterial pressure, QT interval, as well as, HR regarding the baseline values and after 30 minutes of ischemia reperfusion. Conclusion: chronic Lead exposure has toxic effects which disturb the heart function, while natural antioxidant (Vitamin C) may be preferable in reducing Lead toxicity in the exposed rats, suggesting that lead chelating agents having antioxidant properties are preferred in treating cardiovascular disorders accompanying lead toxicity.