Elsevier

Neuroscience

Volume 98, Issue 4, July 2000, Pages 779-792
Neuroscience

Caudal midline medulla mediates behaviourally-coupled but not baroreceptor-mediated vasodepression

https://doi.org/10.1016/S0306-4522(00)00117-2Get rights and content

Abstract

Within the caudal medulla there are two regions whose activation leads to vasodepression and bradycardia, the caudal ventrolateral medulla and a discrete region of the caudal midline medulla. This study investigated, in the halothane anaesthetized rat, the contribution of these two vasodepressor regions to “homeostatic” and “behaviourally-coupled” cardiovascular regulation. In an initial set of experiments the contribution of each of these two regions to the hypotension and bradycardia evoked by acute hypovolaemia (15% haemorrhage) was investigated. It was found that inactivation of the caudal midline medulla significantly attenuated (cobalt chloride) or completely blunted (lignocaine) the hypotension and bradycardia evoked by acute hypovolaemia. In contrast, inactivation of the caudal ventrolateral medulla using cobalt chloride, although attenuating the magnitude of the hypotension and completely blocking the bradycardia, did not delay the onset of the hypotension evoked by acute hypovolaemia. The caudal ventrolateral medulla is known to be critical in homeostatic cardiovascular control through the expression of the “baroreceptor reflex” and the hypotension and bradycardia evoked by activation of cardiopulmonary afferents. In a second series of experiments we found inactivation of the caudal midline medulla played no role in baroreflex-evoked bradycardia (i.v. phenylephrine) or the hypotension and bradycardia evoked by cardiopulmonary afferent activation (i.v. 5-hydroxytryptamine).

These data suggest that the caudal midline medulla and caudal ventrolateral medulla play different roles in cardiovascular control. The caudal ventrolateral medulla is involved in mediating cardiovascular changes associated with a variety of stimuli including “homeostatic” and “behaviourally-coupled” cardiovascular changes, whereas the caudal midline medulla is critical for mediating “behaviourally-coupled” changes in arterial pressure and heart rate.

Section snippets

Caudal midline medulla inactivation

Two methods of CMM inactivation were utilized in this study. In initial experiments microinjection of the local anaesthetic agent, lignocaine, was used to block neural activity. Because lignocaine acts non-selectively on fibres and cells,52 the effects of microinjections of the specific synaptic blocker, cobalt chloride, were examined only if prior lignocaine blockade was effective.

Hypotensive haemorrhage

Experiments were performed on 33 male Sprague–Dawley rats (mean weight 349 g; range 284–470 g). Following induction

Effects of caudal midline medulla inactivation

As illustrated in Fig. 2, the tips of the micropipettes for each injection of lignocaine or cobalt chloride were located within a region previously defined as the CMM vasodepressor region (Fig. 2, shaded area). This region, which includes parts of both raphe obscurus and raphe pallidus, extends from the obex rostrally for approximately 1.5 mm, with a mediolateral spread of about 0.5 mm.16 The maximum spread of lignocaine or cobalt, as indicated by the markers, was approximately 0.5 mm

Discussion

The main findings of this study were that CMM inactivation: (i) delayed the onset and either blocked (lignocaine) or attenuated (cobalt chloride) haemorrhage-evoked hypotension; (ii) abolished (lignocaine or cobalt chloride) haemorrhage-evoked bradycardia; but (iii) was without effect (lignocaine) on either the reflex bradycardia evoked by baroreceptor loading (i.v. PE injection), or the vasodepressor response to activation of 5-HT sensitive cardiopulmonary vagal afferents. In contrast,

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