Abstract
We recorded transmembrane potentials from atrial, AV nodal and ventricular cells in perfused canine and rabbit heart preparations, and from Purkinje cells in superfused canine false tendons. Recording was maintained during perfusion with an aldehyde fixative. Action potential duration was greatly prolonged, and finally repolarization failed when the cells became fixed. After fixation the microelectrodes were withdrawn. Appropriate tissue blocks were embedded in Epon and serially sectioned at 4 μm. In 24 out of 34 attempts, the very cell recorded from was identified under the light microscope. After remounting and resectioning of the 4 μm sections for electron microscopy, the terminal electrode track was found in 12 instances, the very end of the track in six cases. Two main types of atrial action potentials were recorded: with and without a plateau phase. After retrieval of the individual cells we found no basis for a morphological distinction between different cell types. In the AV node, electrotonic contact between two cells was established for distances up to 320 μm by delivering current pulses to one of two microelectrodes which were simultaneously in an intracellular position. Both “N” and “NH” types of action potentials could originate in the proximal atrioventricular bundle. Possibly the N-type in this location was induced by hypoxia. Impalements of Purkinje fibres and ventricular myocardial cells extended the observations on details of microelectrode penetration and impalement damage. The most conspicuous disorder observed in all cells impaled by a microelectrode was a local or universal hypercontraction of myofibrils. In all cases where stable recordings were obtained, the microelectrode tip was found close to the cell membrane opposite to the site of entrance.
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