Persistence of the cardio‐inhibitory response to brain stem ischaemia after destruction of the area postrema and the dorsal vagal nuclei

Abstract

SUMMARY1. In anaesthetized cats, in which the carotid arterial bifurcation had been denervated and the spinal cord transacted at the cervical level, reversible bradyeardia mediated by the vagus nerves was elicited by temporary arrest of the cranial circulation. Methoxamine was infused intravenously to maintain peripheral vascular resistance, and artificial ventilation was given to avert systemic asphyxia.2. The bradycardia persisted in cats subjected to one or more of the following acute surgical procedures: left vagotomy, mid-collicular decerebration, decerebellation, bulbar transactions at the acoustic striae and inferior fovea, and destruction of the area postrema and the underlying dorsal vagal nuclei. Ischaemia-induced bradycardia was invariably abolished after bilateral vagotomy or the administration of atropine.3. Bradycardia could not be elicited by electrical stimulation of the dorsal vagal nuclei, but was evoked by stimulation of deep structures in the vicinity of the nucleus ambiguus even after destruction of the dorsal vagal nuclei.4. Simultaneous application of ischaemia and electrical stimulation of the medullary cardio-decelerator locus produced convergent occlusion of the vagal response. The effect of ischaemia was inhibited by stimulation of a neighbouring region in the medial reticular formation. These interactions indicate that an interneuronal link is involved in the mechanism of ischaemia-induced bradycardia. 5. It is concluded that the cardio-decelerator response to ischaemia is initiated upstream to the primary efferent vagal motor neurones and that the cardio-inhibitory fibres do not originate in the dorsal vagal nuclei.

Central neural mechanisms of the cerebral ischemic response. Characterization, effect of brainstem and cranial nerve transections, and simulation by electrical stimulation of restricted regions of medulla oblongata in rabbit.

“…This study has confirmed and elaborated upon the long-standing observations that the primary response to cerebral ischemia consists of arterial hypertension (McDowell, 1933;Guyton, 1948;Sagawa et al, 1961;Downing et al, 1963;Miyakawa, 1966), bradycardia (McDowell, 1933Levy et al, 1968;Borison and Domjan, 1970), and apnea (Guyton, 1948;Levy et al, 1968) and that the rise in arterial pressure is due to increased peripheral resistance caused by intense vasoconstriction (Downing et al, 1963;Shimizu and Miyakawa, 1968). The vasoconstriction is primarily neurogenic and is mediated by a-adrenergic receptors.…”

“…THE CEREBRAL ischemic response consists of an elevation of arterial pressure (McDowell, 1933;Guyton, 1948;Sagawa et al, 1961;Downing et al, 1963;Miyakawa, 1966), bradycardia (Anrep and Segall, 1926;McDowell, 1933;Guyton, 1948;Miyakawa, 1966;Levy et al, 1968;Borison and Domjan, 1970), and apnea (Guyton, 1948;Levy et al, 1968) elicited by interruption of the blood supply to the head. In the past, most investigations of the response have focused on its cardiovascular components (Anrep and Segall, 1926;McDowell, 1933;Guyton, 1948;Sagawa et al, 1961;Downing et al, 1963;Miyakawa, 1966;Levy et al, 1968;Borison and Domjan, 1970).…”

“…In the past, most investigations of the response have focused on its cardiovascular components (Anrep and Segall, 1926;McDowell, 1933;Guyton, 1948;Sagawa et al, 1961;Downing et al, 1963;Miyakawa, 1966;Levy et al, 1968;Borison and Domjan, 1970). Beyond the demonstration that the response persists after pontomedullary transection (Takeuchi et al, 1969), little is known of the central neural mechanisms required for its expression.…”

Open‐loop comparison of carotid sinus reflex respiratory and circulatory effects in cats.

“…The inspiratory gating mechanism was shown to operate also in the presence of brain stem ischaemia, at which time electrical stimulation of'the medullary inspiratory centre reversed the hypoxia-induced bradycardia (Borison & Domjan, 1970). This places the neuronal interaction of respiratory and cardiomotor control mechanisms downstream to the nucleus of the solitary tract, very probably in the reticular formation (Biscoe & Sampson, 1970).…”

“…An outstanding example of centrally co-ordinated cardiorespiratory behaviour is the generation of sinus arrhythmia whereby the act of inspiration silences vagal discharge to the heart (Eckberg, Kifle & Roberts, 1980;Spyer, 1981). The inspiratory gating mechanism was shown to operate also in the presence of brain stem ischaemia, at which time electrical stimulation of'the medullary inspiratory centre reversed the hypoxia-induced bradycardia (Borison & Domjan, 1970). This places the neuronal interaction of respiratory and cardiomotor control mechanisms downstream to the nucleus of the solitary tract, very probably in the reticular formation (Biscoe & Sampson, 1970).…”