In vivo changes in canine ventricular cardiac conduction during halothane anesthesia.

Changes in the ventricular conduction system associated with halothane anesthesia were investigated by direct methods of His bundle recording, pacing, and premature stimulation in a canine model. In eight animals a change from 1.5% to 2.4% halothane concentrations was associated with significant prolongation of epicardial activation times by an average of 2.4 and 2.9 msec during atrial and His bundle paced rhythms, respectively. Ventricular functional refractory periods decreased significantly by an average of 7.3 msec, the effective refractory period of the ventricular conduction system did not system did not change, and epicardial conduction delays at the effective refractory period decreased. In six other animals the addition of 1.5% halothane to basal thipental anesthesia was not associated with prolongation of epicardial activation times or decreased ventricular functional refractory periods. However, the effective refractory period of the ventricular conduction system significantly decreased by an average of 9.1 msec, and epicardial conduction delays at the effective refractory period significantly increased by an average of 9.6 msec. A change in halothane concentrations from 1.5% to 2.4% is associated with depression of ventricular conduction and shortened duration of refractory periods in the ventricular conduction system in vivo in a manner consistent with the reported actions of halothane on Purkinje fibers in vitro.

Reflex effects of thoracic sympathetic afferent nerve stimulation on the kidney.

Thoracic sympathetic afferents may play a role in the reflex control of renal vascular resistance during hypotension. Mongrel dogs were anesthetized with ketamine hydrochloride and maintained on a 50-50, O2-N2O mixture supplemented with 0.5%-1.0% halothane. Systemic arterial blood pressure was lowered to 50 mmHg with use of a constant pressure hemorrhage technique. The renal circulation was perfused with a constant-flow perfusion system. Low-frequency (3 Hz) stimulation of thoracic sympathetic afferents produced renal vasodilation. A reduction of renal vascular resistance was measured as a decrease in constant-flow perfusion pressure. Vagotomy accentuated the dilator response to stimulation. High-frequency (30 Hz) afferent stimulation produced renal vasoconstriction. Renal efferent nerve activity and renal blood flow responded to afferent stimulation (3 Hz) by transient inhibition of efferent activity and increases in renal blood flow. Afferent stimulation (30 Hz) caused increases in renal efferent nerve activity and decreases in renal blood flow. The thoracic sympathetic afferents carry information from cardiopulmonary structures that alter renal efferent nerve activity and renal hemodynamics during hypotension.

Sympathetic afferent nerve activity of right heart origin.

Six mongrel dogs anesthetized with sodium pentobarbital and paralyzed with gallamine triethiodide were studied on total cardiopulmonary bypass. This study verified the existence of right heart mechanoreceptors whose afferent nerves traverse the upper thoracic white rami communicantes. these mechanoreceptors were studied by observing changes in average maximum, and total nerve spike frequency when right atrial and right ventricular systolic and diastolic pressures were altered by means of intracardiac balloons. Receptors that responded to volume and pressure changes were found in both the right atrium and right ventricle. Nerve activity in these afferents increased with increasing right atrial and right ventricular pressures. These mechanoreceptors were more responsive in the upper physiological ranges of right heart pressures. In most nerve fibers studied, maximum activity occurred during both right atrial and right ventricular diastole.