Abnormal cardiac sensory innervation associated with experimentally induced, electrocardiographic long QT intervals in chick embryos.

Abstract

Prolongation of the QT interval in the ECG can be induced in d 17 chick embryos by ablating the nodose placode on the right side on d 1 of development. The nodose placode contains the precursor cells which form the neurons of the nodose (inferior vagal) ganglion. Neurons in this ganglion provide sensory innervation to the heart and other viscera. In this study, we measured ganglion volume and neuron size and number in the right and left nodose ganglia in d 17 experimental and control embryos from whom electrocardiograms had been obtained. A significant reduction in the number of neurons present in the right nodose ganglion, relative to the left ganglion, was evident in all embryos with abnormally prolonged QT intervals. Embryos with prolonged QT, as well as lesioned embryos who demonstrated normal.QT on d 17, also had abnormally small neurons in both right and left nodose ganglia, indicating an additional nonspecific, perhaps permissive, effect of the lesion. These results suggest that abnormal development of the sensory innervation of the heart may be an important link in the chain of events leading to the developmental long QT syndrome expressed by these embryos.