Introduction: The ability to genetically engineer specific gene 'knock-out' mice has provided a powerful tool for investigating the various mechanisms that contribute to the pathogenesis of pulmonary arterial hypertension (PAH). Yet, so far there have been no reports describing the measurement of pulmonary arterial pressure (PAP) in the conscious wild type mouse-an essential requirement for monitoring dynamic changes associated with the pathogenesis of PAH. Therefore, in this study we describe a new technique for long-term measurement of PAP in conscious unrestrained mice using telemetry.
Methods: In five male C57BL/6 mice (B.W. 25-30 g), the sensing catheter of a telemetric transmitter was inserted into the right ventricle and advanced into the pulmonary artery. The transmitter body was positioned either within the abdominal cavity or subcutaneously on the back. During recovery from surgery, mean PAP was recorded daily for 1 week. Subsequently, the PAP responses to acute hypoxia (8% O2 for 10 min) and L-NAME (50 mg/kg, s.c.) were tested in three mice.
Results: By 1-week post surgery, all mice had fully recovered from surgery and baseline MPAP was stable at 14.9+/-0.7 mm Hg. Additionally, the pulmonary vascular stimulants acute hypoxia and L-NAME provoked a 63% and 86% increase MPAP, respectively.
Discussion: In summary, this study has demonstrated the ability to accurately measure PAP by telemetry in conscious, unrestrained mice. One important application of this technique for future studies is the possibility to assess the relative contribution of specific genes (using 'knock-out' mice) during the chronic development of pulmonary pathological conditions.