A refined radio-telemetry technique to monitor right ventricle or pulmonary artery pressures in rats: a useful tool in pulmonary hypertension research

Abstract

Implantable radio-telemetry methodology, allowing for continuous recording of pulmonary haemodynamics, has previously been used to assess effects of therapy on development and treatment of pulmonary hypertension. In the original procedure, rats were subjected to invasive thoracic surgery, which imposes significant stress that may disturb critical aspects of the cardiovascular system and delay recovery. In the present study, we describe and compare the original trans-thoracic approach with a new, simpler trans-diaphragm approach for catheter placement, which avoids the need for surgical invasion of the thorax. Satisfactory overall success rates up to 75% were achieved in both approaches, and right ventricular pressures and heart and respiratory rates normalised within 2 weeks. However, recovery was significantly faster in trans-diaphragm than in trans-thoracic operated animals (6.4+/-0.5 vs 9.5+/-1.1 days, respectively; p<0.05). Stable right ventricular pressures were recorded for more than 4 months, and pressure changes, induced by monocrotaline or pulmonary embolisms, were readily detected. The data demonstrate that right ventricular telemetry is a practicable procedure and a useful tool in pulmonary hypertension research in rats, especially when used in combination with echocardiography. We conclude that the described trans-diaphragm approach should be considered as the method of choice, for it is less invasive and simpler to perform.

Fig. 1

left panel: Live pressure recordings while advancing the pressurecatheter into the pulmonary artery. Notice the stepwise increase in diastolic pressures when manoeuvring the catheter beyond the pulmonary valves (arrow), whereas the systolic pressures remained unchanged. right panel: Live pressure recordings while injecting a bolus injection of microspheres (arrow; 19 μm, 1.5 million/100 g i.v.). Upon embolisation, a significant increase in systolic, diastolic and developed RV pressures was observed. Furthermore, in both recordings, the effect of breathing is noticeable

Fig. 2

Haemodynamic changes during the development of MCT-induced pulmonary hypertension. Four weeks after the rats received MCT, clinical signs of RV heart failure developed. In these 4 weeks, systolic pressures continued to rise, while cardiac output could not be maintained. The presence of RV remodelling was indicated by increased wall thickness and diameter. The pulmonary vascular resistance continued to rise as well, while at 4 weeks, the increase in the RV-power was inadequate to compensate for the dramatically increased afterload. Triangles connected by dashed lines: MCT-treated; squares connected by uninterrupted lines: control group; n = 3 for both groups. All values are in mean ± SEM, Asterisk, p < 0.05; double asterisk, p < 0.01 compared to control (post-hoc analyses). Please note that sometimes the icons conceal the error bars. For explanation of the abbreviations, see corresponding text