Skip to main content
. 2022 Dec 8;13(6):2369–2382. doi: 10.1016/j.apsb.2022.12.002

Figure 4.

Figure 4

The curative effect of different formulations on the pulmonary hypertension and depressed right ventricle contractility of rats induced by MCT. (A) Schematic flowcharter of animal experiment. (B) Pulmonary arterial pressure was directly reflected by mPAP on Day 35. (C) Fulton's index [RV/(LV + S)] suggested the degree of right ventricular hypertrophy on Day 35. Echocardiographic examination was conducted in MCT-PH rats receiving GlcA-NPplex or GlcA-NPs on Day 33. (D) The representative images of pulmonary arterial blood flow spectral pattern, PAAT, RVID, and TAPSE. (E–J) Quantifying the echocardiographic parameters comprising PAAT, PVR, RVID, TAPSE, CO, LVEF (%). PAAT, PVR, RVID and TAPSE demonstrate RV function. Increasing the mPAP accelerates the PA blood flow and shorts the acceleration time or PAAT. With the PH development, the RV afterload rises and the RVID increases. TAPSE indicates RV systolic function. CO represents cardiac ejection function, while LVEF reflected the systolic function of left ventricle. Data are represented as mean ± SD. ∗P < 0.05, ∗∗∗P < 0.001 compared to MCT group; ns, no significance. n = 6, unless indicated otherwise. CON: controlled rats (normal rats) received intravenous injections of 0.9% saline; MCT: rats received MCT treatment. The MCT-induced rats were dosed with preparations at 0.4 mg/kg PTX and 0.04 mg/kg Cas-3 via the tail vein. PAAT: pulmonary arterial accelerating time; PVR: pulmonary vascular resistance; RVID: right ventricle internal diameter; TAPSE: tricuspid annular plane systolic excursion; CO: cardiac output; LVEF: left ventricle ejection fraction.