BNP-32 levels correlate with pulmonary hypertension progression in rats

Objective: Pulmonary hypertension is a progressive disease that leads to right heart failure and eventually death. Brain natriuretic peptide (BNP) has been shown to be a marker for severity of heart failure. In this study, we studied the dynamic changes of BNP during the progression of chemically induced pulmonary hypertension in rats. Methods: Male Sprague Dawley rats (200-250gm) were injected with 60mg/kg/b.wt monocrotaline (MCT) in saline. Control rats received saline alone. The rats were terminated 7, 14 and 21 days after the treatment and their plasma BNP-32 (ng/ml) was determined. There were at least eight in control and 10 rats in MCT group per time point. Results: At the end of 21-day induction of pulmonary hypertension, four male rats died due to right heart failure. The levels of BNP increased significantly with time and differed from control male rats. BNP levels in control rats were 0.45 0.03ng/ml. The data are given in the table below. The levels were 0.82 0.1, 2.47 0.08, and 4.81 0.2ng/ml in rats terminated 7, 14, and 21 days post MCT-treatment. All the levels were significant at at a p-value of 0.001. The rats that died on day 21 had plasma levels of 11.93 0.1ng/ml, 3 times the levels of surviving rats at the same time point. Conclusion: Pulmonary hypertension damages pulmonary vasculature that causes release of vasoconstrictive mediators that leads to right heart failure. This failure results in ventricular hypertrophy and death. The marker of heart failure, BNP-32 is elevated with the progression of disease that could be clinically used to identify the severity of the disease in surgically-induced secondary pulmonary hypertension.