Abstract
We investigated whether magnesium sulfate (MgSO4) mitigated pulmonary hypertension progression in rats. Pulmonary hypertension was induced by a single intraperitoneal injection of monocrotaline (60 mg/kg). MgSO4 (100 mg/kg) was intraperitoneally administered daily for 3 weeks, from the seventh day after monocrotaline injection. Adult male rats were randomized into monocrotaline (MCT) or monocrotaline plus MgSO4 (MM) groups (n = 15 per group); control groups were maintained simultaneously. For analysis, surviving rats were euthanized on the 28th day after receiving monocrotaline. The survival rate was higher in the MM group than in the MCT group (100% versus 73.3%, p = 0.043). Levels of pulmonary artery wall thickening, α-smooth muscle actin upregulation, right ventricular systolic pressure increase, and right ventricular hypertrophy were lower in the MM group than in the MCT group (all p < 0.05). Levels of lipid peroxidation, mitochondrial injury, inflammasomes and cytokine upregulation, and apoptosis in the lungs and right ventricle were lower in the MM group than in the MCT group (all p < 0.05). Notably, the mitigation effects of MgSO4 on pulmonary artery wall thickening and right ventricular hypertrophy were counteracted by exogenous calcium chloride. In conclusion, MgSO4 mitigates pulmonary hypertension progression, possibly by antagonizing calcium.
Highlights
Pulmonary hypertension, characterized by increased pulmonary artery resistance and poor compliance, may cause right ventricular hypertrophy, right heart failure, and even death [1,2]
Analysis revealed that the survival rate in the monocrotaline plus MgSO4 (MM) group was significantly higher than in the MCT group (p = 0.043)
These findings indicate that exogenous calcium counteracted the effects of long-term MgSO4 therapy, reducing pulmonary artery wall thickening and right ventricular hypertrophy induced by monocrotaline
Summary
Pulmonary hypertension, characterized by increased pulmonary artery resistance and poor compliance, may cause right ventricular hypertrophy, right heart failure, and even death [1,2]. Approved pulmonary hypertension medications (such as endothelial receptor antagonists and phosphodiesterase inhibitors) improve pulmonary functional capacity and cardiopulmonary hemodynamics [3,4]. These medications do not improve clinical outcomes [5]. A primary reason is that these medications cannot block the pathogenesis of pulmonary hypertension [3,4,5]. Pulmonary artery remodeling is crucial in mediating the development of pulmonary hypertension and right ventricular hypertrophy [6]. Effective therapy for pulmonary hypertension is not currently available [10,11]
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