Depriming effect of the cerebral cortex (predominantly of zones 1 and 2 of viscerosomatic sensitivity) on transmission of the cardiac afferent signals with a subcortical nociceptive component, which were provoked by electrical stimulation of the sinoatrial node of the heart conduction system, was established in experiments on cats. The agonist of opiate M-receptors morphine considerably potentiated the effect of cortical stimulation, while opiate receptor blocker naloxone antagonized it.Key Words: cerebral cortex; descending control; nociception; heart Clinical practice and physiological experiments demonstrated the important role of the cerebral cortex (CC) in perception and regulation of pain [2,10]. One of the components of cortical antinociceptive mechanism is descending inhibition of the nociceptive traffic from cutaneous or pulpal afferent somatic nerves in the spinal cord and supraspinal structures [1,2,10].Our aim was to study cortical effect on transmission of visceral nociceptive signals and to elucidate the role of opiatergic mechanisms in this process. The source of afferent signals was the sinoatrial node (SAN) of the cardiac conducting system.
MATERIALS AND METHODSExperiments were. carried out on cats weighing 2.5-3.7 kg, which were narcotized intraperitoneally with chloralose (30-60 mg/kg), paralyzed with gallamine triethiodide, and artificially ventilated. Electrical stimulation was applied to SAN innervated by spinal afferent system of the heart [3,4,11]. Bipolar silver stimulating electrodes had contact area of 0.1 mm 2. the distance between electrodes was 0.5 mm. SAN was