ABSTRACT
Rapid eye movement (REM) sleep is characterized by periods of profound cardiac autonomic activation evident in heart rate surges in humans and canines. Our goals were to determine whether or not the heart rate surge phenomenon occurs in cats and to characterize concurrent central nervous system activity. Cortical and hippocampal electroencephalogram, electromyogram, electrooculogram, pontogeniculooccipital (PGO) waves, subcutaneous electrocardiogram, and respiration were recorded. Bouts of sinus tachycardia lasting >/=3.5 s achieved a rate of 210 beats/min and were present predominantly during REM sleep. Heart rate during the surges rose an average of 26.4% from 132.5 +/- 2.0 beats/min before the surge to 167.5 +/- 2.6 beats/min (P < 0.001) and returned to 130.7 +/- 2.6 beats/min (P < 0.001). The heart rate surges were invariably accompanied by increased incidence and frequency of hippocampal theta waves and increased PGO wave frequency and incidence of PGO wave clusters and eye movement clusters. The occurrence of surges was dramatically reduced from 0.11 +/- 0.03 to 0.01 +/- 0.01/15 s of REM sleep (P = 0.02) by atenolol (0.6 mg/kg iv), indicating that the phenomenon is beta(1)-adrenergically mediated. These findings suggest a coupling between central activation of cardiac sympathetic nerves and the generation of hippocampal theta waves and PGO activity.
Subject(s)
Heart Rate/physiology , Hippocampus/physiology , Sleep, REM/physiology , Animals , Cats , ElectroencephalographyABSTRACT
Rapid eye movement (REM) sleep results in profound state-dependent alterations in heart rate. The present study describes a novel phenomenon of a primary deceleration in heart rate that is not preceded or followed by increases in heart rate or arterial blood pressure and occurs primarily during tonic REM sleep. The goals were to characterize the primary decelerations and to provide insights on the underlying central and peripheral autonomic mechanisms. Cats were chronically implanted with electrodes to record electroencephalogram, pontogeniculooccipital wave activity in lateral geniculate nucleus, hippocampal theta rhythm, electromyogram, electrooculogram, respiration (diaphragm), and electrocardiogram. Arterial blood pressure was monitored from a carotid artery catheter. R-R interval fluctuations were continuously tracked using customized software. The muscarinic blocking agent glycopyrrolate (0.1 mg/kg i.v.) and the beta-adrenergic blocking agent atenolol (0.3 mg/kg i.v.) were administered in alternating sequence with a 90- to 120-min interval. Glycopyrrolate immediately eliminated the decelerations during REM sleep. Atenolol alone had no effect on their frequency. These findings suggest that a change in the centrally induced pattern of autonomic activity to the heart is responsible for the primary decelerations, namely, a bursting of cardiac vagal efferent fiber activity.