Caudal midline medulla mediates behaviourally-coupled but not baroreceptor-mediated vasodepression
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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2008, NeuroscienceCitation Excerpt :Consistent with this conclusion are earlier findings that microinjection into the CMM of either local anesthetic (lignocaine) or a synaptic blocker (cobalt chloride) respectively either blocked, or delayed and attenuated, hemorrhage-evoked decompensation (Henderson et al., 1998a, 2000, 2002; Heslop et al., 2002). Strikingly, such blockade of the CMM altered neither resting AP nor heart rate, nor did it affect cardiovascular reflexes triggered by either baroreceptor-loading (i.v. phenylephrine) or activation of 5-HT3-sensitive cardiopulmonary afferents (i.v. phenylbiguanide or 5-HT) (Henderson et al., 2000). In this context the dramatic effects on hemorrhage-evoked decompensation suggest that CMM neurons are recruited only under special circumstances (i.e. injury-related/life-threatening challenges), the adaptive responses to which require more than basic homeostatic cardiovascular adjustments (see also Johansson, 1962).
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