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Biomedical subjects

J W Manning

Publications and source records attributed to J W Manning.

35 records · Page 2Linked to original sources
PubMed1976

Central nervous system control of cardiac rhythm.

Stimulation of sites in the midbrain reticular formation and in the posterior hypothalamus of the cat resulted in a large to modest rise of arterial pressure and the induction of cardiac dysrhythmias. Most frequently, these arrhythmias developed upon cessation of brain stem stimulation but also occurred during the stimulus period in 5 of 23 cats studied. The arrhythmias disappeared upon cooling and reappeared upon rewarming the vagus nerves. The ventricular dysrhythmias also were abolished by methylscopolamine, by bilateral vagatomy, or by extirpation of the stellate ganglia. Simultaneous stimulation of both distal end of the cut right vagus nerve and the decentralized right stellate ganglion caused arrhythmias similar to those observed after diencephalic stimulation. These data are interpreted to indicate that the cardiac arrhythmias evoked by brain stem stimulation result from the interplay of both sympathetic and parasympathetic influences on the heart. The response patterns of a population of medullary neurons activated by carotid sinus nerve stimulation were modified by condition stimuli to posterior hypothalamic sites. From studies on unit activity of brain stem areas known to participate in cardiovascular adjustment, a schema is proposed of hypothalamic-medulla interaction as a central mechanism that may account for the development of ventricular arrhythmias.

Animals↗
PubMed1975

Hypothalamic modulation of baroreceptor afferent unit activity.

Unit responses to sinus nerve stimulation were recorded in the medulla. A conditioning stimulus to the posterior hypothalamus produced inhibition of 65% of unit responses to sinus nerve stimulation as early as 7 ms and extending as long as 790 ms after conditioning; 50% recovered after 300 ms. Unit responses to hypothalamic stimulation alone were also recorded in the medulla, some in the same loci as other unit responses to sinus nerve stimulation. They could be activated by contralateral as well as ipsilateral hypothalmic stimulation and showed recurrent bursts of firing over a 1,000-ms poststimulus interval. Evoked potentials and unit responses were recorded in the posterior hypothalamus, some occurring within 10--20 ms poststimulation of the sinus nerve, indicating that baroreceptor information is ascending in a time sufficiently short to involve the hypothalamus in reflex regulation of blood pressure as well as more generalized homeostatic responses which include the cardiovascular system.

Animals↗
PubMedDate not supplied

The median preoptic area in cardiovascular reflex activity.

Two examples are used to illustrate the flexibility within the central servocontrol system that regulates blood volume and blood pressure. The variations are seen in the modification of components directed both towards short-term and long-term control. The preferential circuit used in the servocontrol system can and does change. The interaction of baromechanisms with cerebellar-fastigial activation selectively engages sympathetic output to the kidney resulting in an enhanced release of renin that is disproportional to the rise in renal vascular resistance. The cerebellar component adds a feature to the reduction in vascular conductance that when fully developed increases vascular volume. The permissive role of sites in the anteroventral hypothalamus suggests a neural loop that, when absent, not only allows the sympathetic activity to run unabated but fails to prevent a tachycardia state or to develop a bradycardia in response to a rise in arterial pressure. The latter may be a transient feature not persisting for more than a day. However, when compared to the normal responses of the paired sham controls, such a change is taken as an example of dynamic shift in preferential pathways.

Afferent Pathways↗
PubMedDate not supplied

Paradoxical cardiovascular response to visceral afferent stimulation in the established spontaneously hypertensive rat.

Afferent splanchnic nerve stimulation with different frequencies in Wistar Kyoto rats caused depressor and pressor responses depending on the frequency employed. Similar visceral afferent activation in spontaneously hypertensive rats caused depressor responses at all frequencies of stimulation. It is suggested that the central integrated mechanisms for activating a cardiovascular state change as evoked by visceral afferents may differ in the established hypertensive rat from that of the normotensive.

Afferent Pathways↗