[Establishment and evaluation of a new method for determining hemodynamics of pulmonary hypertension rats].

Objective: By evaluating the hemodynamic parameters such as cardiac output (CO), right ventricular pressure (RVP), pulmonary artery pressure (PAP) and total pulmonary resistance index (TPRI) in pulmonary hypertension rat model, we established a more comprehensive hemodynamic evaluation system, which objectively evaluated the severity of disease and exercise tolerance in rats with pulmonary hypertension. Methods: SD rats were randomly divided into a control group and a model group with 5 rats in each group. The model group was intraperitoneally injected with SU5416 (20 mg/kg) and placed in an oxygen chamber at a 10% oxygen concentration for 21 days and then placed in a normoxic environment for 14 days. After modeling, rats were anesthetized and mechanically ventilated. The operator cut the skin along the right paraxial line, detached and ligated the intercostal artery, and then cut off the 3 and 4 ribs, exposing the heart and freeing aortic root about 0.2 cm. The flowmeter probe was set in the dissected aortic segment, and real-time recording time, blood flow waveforms, cardiac output were calculated accordingly. Then the needle attached to the baroreceptor was inserted into the right ventricle and the system acquired the right ventricular time-pressure waveform. After the waveform stabilized for about 30 seconds, the end of the cannula was sent to the pulmonary artery trunk through the entrance of the pulmonary artery to record the time-pressure curve of the pulmonary artery. Results: RVSP, PASP, PADP and mPAP in the model group were significantly higher than those of the control group [ RVSP(23.4±5.4) mmHg, 1 mmHg=0.133 kPa vs (56.4±13.0) mmHg, PASP (22.8±4.4) mmHg vs (58.5±14.9) mmHg, PADP (9.7±1.9) mmHg vs (30.3±7.0) mmHg, mPAP (14.1±2.7) mmHg vs (41.9±8.0) mmHg, all P<0.05 ]. Compared with the control group, the cardiac index in the model group was significantly lower [ CI (0.54±0.08) ml·min(-1)·g(-1) vs (0.40±0.09) ml·min(-1)·g(-1,) P=0.02 ]. Furthermore, compared with the control group, pulmonary vascular resistance index was significantly increased in the model group[PVRI (0.27±0.03) mmHg·ml(-1)·min(-1)·kg(-1) vs (0.06±0.01) mmHg·ml(-1)·min(-1)·kg(-1,) P<0.05]. The pathological results also showed that the middle part of pulmonary arterioles in the model group had muscular hypertrophy and muscular pulmonary arterioles, and even plexiform lesions. Conclusion: In this study, we established a new method that simultaneously determined several hemodynamic parameters such as RVSP, PASP, PADP, CO, CI and PVRI, which provided a more comprehensive assessment of hemodynamic changes in pulmonary hypertension rat models.

[Method for recording tension changes of small pulmonary artery and vein using the isolated vessel tension measurement system].

Objective: To establish a standardized method for isolated pulmonary artery and vein rings with different diameter, pressure and length, which could provide a more scientific method for in vitro study of pulmonary vessel diseases. Methods: Male SD rats were anesthetized, and the right ventricular systolic pressure were measured. Small pulmonary artery and vein rings with 200-400 µm in diameter and 2 mm in length were prepared by dissecting pulmonary arteries and veins. The pulmonary vessel rings were mounted in the organ bath by 2 stainless steel wires with diameter of 40 µm. Then the internal circumference of the vessel rings was increased gradually with 100 µm per step. At the same time the vascular tension was recorded by the Myograph System and Acknowledgement data acquisition system, and subsequently the passive length-tension exponential curve was made. The initial tension of the rings was set, equilibrated for another 30 min, and then stimulated with 60 mmol/L KCl 3 times, and the best contractile reactivity was achieved. The contractile reactivity of pulmonary artery rings and endothelial integrity were detected by exposure to 1 µmol/L phenylephrine(PE) and 10 µmol/L acetylcholine(Ach), while the contractile reactivity of pulmonary vein rings was detected by exposure to 1 µmol/L U46619 and 10 µmol/L papaverine. Results: The contraction and relaxation effects of the pulmonary artery rings reached 0.39 mg and 92% when they were stimulated by 1 µmol/L PE and 10 µmol/L Ach. The contraction and relaxation effects of pulmonary vein rings were up to 0.13 mg and 84% when they were exposed to 1 µmol/L U46619 and 10 µmol/L papaverine, respectively. Conclusion: Pulmonary artery and vein rings with appropriate basal tension and optimal vasodilator activity were prepared, and a standardized method of tension experiment for isolated pulmonary artery and vein rings established.