Monocrotaline-induced pulmonary hypertension with sufficient tricuspid regurgitation in a rat model

It is well known that monocrotaline (MCT) induces pulmonary hypertension (PH) in rats. This model is very useful for understanding the physiology of PH and developing treatments for PH. However, it is very difficult to estimate pulmonary artery pressure (PAP) in this model. The purpose of this study is to establish a PH model with sufficient tricuspid regurgitation (TR) to evaluate PAP.

We studied 17 male rats that received 15 injections of 5 mg/kg/day of MCT (PH) or vehicle (control). Three weeks after the first MCT injection, we measured left and right ventricular dimensions, the ratio of acceleration to ejection time in pulmonary flow, and the development of TR using an echocardiograph (SONOS5500) with a s12 probe (frequency: 5-12 MHz, frame rate: 120 Hz).

The right ventricular end-diastolic area in the PH group was significantly larger than that in the control group. The acceleration time/ejection time ratio and velocity time integral of the pulmonary artery in the PH group were smaller than those in the control group. In 78 % of rats in the PH group, sufficient TR was observed and estimated PAP was 75.4 ± 13.8 mmHg. There was a good correlation between PAP estimated by a Doppler method and directly measured right ventricular pressure (r = 0.94, P < 0.0001).

Fifteen injections of 5 mg/kg/day of MCT could induce PH with sufficient TR in rats. Transthoracic echocardiography could be used for monitoring the progress of PH in the rat model.