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Published Online:https://doi.org/10.1176/ajp.109.1.27

The immediate effects of ECS on the carotid blood flow, arterial pressure, and cardiac rate were recorded in experiments on a series of 16 unanesthetized dogs. The shock stimulus in terms of milliamperage, voltage, and duration of the electrical current were also recorded.

Blood flow was measured continuously by the use of an electromagnetic blood flow meter. Blood pressure was measured directly and continuously in the femoral artery through the use of a Statham Gage-Brush recorder system.

All operative procedure was carried out under general ether and/or local procaine anesthesia.

The initial responses to ECS were convulsions, respiratory arrest, bradycardia, and reduced carotid blood flow and arterial pressure; the latter 3 responses had a duration of one second. The bradycardia could be prevented by vagotomy. The initial decrement in these entities was followed by a prolonged secondary increase above control levels. Blood flow and arterial pressure reached their highest elevations concomitantly and then, while the convulsions continued and respiration was resumed, they began a gradual decline, until at 10 and 5 minutes, respectively, a majority of the 16 animals had returned to control levels of blood flow and arterial pressure. Cardiac rate did not reach a peak until the respiratory arrest and convulsions had ceased; the peak value was maintained for several seconds followed by a gradual return to control level that was attained by about 5 minutes postshock.

This study offers indirect evidence against the concept that the therapeutic effects of electroconvulsive therapy are due to cerebral ischemia resulting from widespread cerebral vasoconstriction.

Changes in blood flow in the carotid artery of dogs appear to be a passive response to marked changes in systemic pressure.

Whereas convulsions may augment the cardiovascular changes subsequent to electroshock, these changes are independent of the convulsions, per se, since the same patterns of response occur in subconvulsive electroshock. The significance of these cardiovascular changes in ECT has yet to be determined.

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