The right ventricular failure is the most important cause of death in pulmonary arterial hypertension (PAH). Colchicine, a naturally occurring tricyclic alkaloid, protects against inflammatory diseases by favorable modulation of pro-inflammatory cytokine production. In our present work, we aimed to clarify the effects of colchicine treatment in PAH, specifically on right ventricular cardiac myocytes. We examined the effects of colchicine treatment on the pulmonary vasculature and on the right ventricular cardiomyocytes. Pulmonary arterial hypertension was induced in Wistar Kyoto rats by monocrotaline (MCT). Wistar Kyoto (WKY) rats were then treated with colchicine or placebo for two-weeks. Colchicine treatment successfully prevented the development of right ventricular failure in an MCT-induced PAH model. The echocardiographic parameters characterizing right ventricular function improved. The signaling pathways associated with cardiac remodeling showed favorable alterations attributed to colchicine treatment. Consequently, the interstitial collagen deposition was reduced, and the energy supply of right ventricular myocytes was preserved. Colchicine treatment inhibited pulmonary vascular remodeling and reduced the amount of α-smooth muscle actin (α-SMA) and collagen in pulmonary vessel walls. Our results suggest that even a short-term and low-dose colchicine treatment could protect against PAH-induced right ventricular failure. Therefore, colchicine may be a promising therapeutic option in the treatment of PAH.