Magnesium sulfate protects the heart against carbon monoxide-induced cardiotoxicity in rats

Abstract

Carbon monoxide (CO), a toxic gas produced via incomplete fossil fuel combustion, has several poisonous effects in the heart including induction of necrosis, apoptosis, and electrocardiogram (ECG) changes. Magnesium sulfate (MS) is a drug with cardioprotective effects especially when used after ischemia/reperfusion. In the current study, we aimed to evaluate MS cardioprotective effects following CO poisoning. Animals were exposed to CO 3000 ppm for 1 h and immediately after the exposure period and on the next 4 days (a total of 5 consecutive doses given on a daily basis), MS (75, 150 and 300 mg/kg) was injected intraperitoneally (i.p.) and ECG was recorded focusing on ST-segment, T-wave, and Q-pathologic wave changes. On day 5, animals were sacrificed and their heart was excised for determination of BAX, BCL2 and Akt expression level using western blot analysis and necrosis investigations. The results showed that MS significantly decreased necrosis and BAX/BCL2 ratio (P < 0.001) while pro-survival protein Akt was significantly increased (P < 0.001). Moreover, CO-induced ST-segment depression, T-wave inversion, and atrioventricular block (AV-block) were decreased following treatment with MS. In conclusion, our results showed that MS could decrease cardiac deleterious effects of CO poisoning including necrosis and apoptosis while increased the expression of Akt, as a cell survival protein.

Magnesium sulfate ameliorates carbon monoxide‑induced cerebral injury in male rats

“…In the current study, we demonstrated that MS decreased brain cell necrosis, apoptosis and oxidative stress, while it increased pro-survival Akt protein levels in a dose-dependent manner. Previously, we reported several neuroprotective and cardioprotective substances, which may be used to decrease CO poisoning consequences, in animal models (2,33,36,37,42,44–46). More specifically, in a recent study from our group, MS administration was found to exert positive effects against the cardiotoxicity of CO in rats (33).…”