Why the study?
Does acute right ventricular overload induce intracellular action potential changes in the ventricles of rats?
Does acute right ventricular overload induce intracellular action potential changes in the ventricles of rats?
Acute right ventricular overload induces significant diastolic depolarisation of right ventricular muscle cells, which may contribute to peripheral ECG changes.
May underlie ECG changes in acute RV overload; hypothesis-generating for human arrhythmia risk.
Eleven open chest, artificially ventilated rats were used to observe and compare the intracellular potential changes induced in the right and left ventricles by an acute right ventricular overload. Graded right ventricular hypertension was produced by external constriction of the main pulmonary artery. Transmembrane potentials were obtained using floating glass microelectrodes filled with 3 mol X litre-1 KCl and connected to a cathode follower through a silverchloride-silver junction. Following right ventricular overload, the level of resting potential was depolarised by 20% on the right ventricle and by 4% on the left (P less than 0.001). The repolarisation was not significantly affected. A significant correlation (P less than 0.01) was observed between the increase of right ventricular pressure and the depolarisation of resting right ventricular potential. The right ventricular distension which occurs in our experimental model thus induces a diastolic depolarisation of right ventricular muscle cells which cannot be neglected in the interpretation of the peripheral ECG changes.
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Boland et al. (1980) studied this question.
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