Carotid baroreceptor reaction after stenting in 2 locations of carotid bulb lesions of different embryologic origin.

BACKGROUND AND PURPOSE: The carotid bulb is innervated by the sinus nerve of Hering, a branch of the glossopharyngeal nerve, derived from the third pharyngeal arch. The aim of this study was to determine the frequency, predictors, and outcome of the carotid BR after carotid stent placement according to the location of the plaque lesion. MATERIALS AND METHODS: Atherosclerotic carotid plaques of apical versus body lesions were prospectively analyzed in 95 consecutive patients who underwent carotid stent placement. Patients with hypertension after stent placement were excluded, and transient (<3 hours) and prolonged (3-24 hours) BR, together with AEs such as strokes and death, were assessed in the 2 lesion locations (apical versus body). Other factors known to affect the carotid baroreceptor were also investigated, and the results were analyzed by χ(2) or Mann-Whitney U tests. RESULTS: Transient BR occurred in 30% of apical lesions in contrast to 70% of body lesions (P = .001). Transient BR showed a significant relationship to lesion location (P = .001), occurring most frequently in body lesions, and to the distance of maximum stenosis from the ICA ostium (P = .001). Hyperperfusion and AE rates (P = .076) in 1 month occurred more frequently in apical lesions. CONCLUSIONS: The frequency of transient BR after carotid stent placement was lower in the apical region of the carotid bulb. Different cardiovascular disturbances after carotid stent placement can be attributed to anatomically different areas of the carotid bulb.

FRS2 alpha 2F/2F mice lack carotid body and exhibit abnormalities of the superior cervical sympathetic ganglion and carotid sinus nerve.

The docking protein FRS2 alpha is an important mediator of fibroblast growth factor (FGF)-induced signal transduction, and functions by linking FGF receptors (FGFRs) to a variety of intracellular signaling pathways. We show that the carotid body is absent in FRS2 alpha(2F/2F) mice, in which the Shp2-binding sites of FRS2 alpha are disrupted. We also show that the carotid body rudiment is not formed in the wall of the third arch artery in mutant embryos. In wild-type mice, the superior cervical ganglion of the sympathetic trunk connects to the carotid body in the carotid bifurcation region, and extends thick nerve bundles into the carotid body. In FRS2 alpha(2F/2F) mice, the superior cervical ganglion was present in the lower cervical region as an elongated feature, but failed to undergo cranio-ventral migration. In addition, few neuronal processes extended from the ganglion into the carotid bifurcation region. The number of carotid sinus nerve fibers that reached the carotid bifurcation region was markedly decreased, and baroreceptor fibers belonging to the glossopharyngeal nerve were absent from the basal part of the internal carotid artery in FRS2 alpha(2F/2F) mutant mice. In some of the mutant mice (5 out of 14), baroreceptors and some glomus cells were distributed in the wall of the common carotid artery, onto which the sympathetic ganglion abutted. We propose that the sympathetic ganglion provides glomus cell precursors into the third arch artery derivative in the presence of sensory fibers of the glossopharyngeal nerve.

Oestrogen augments the fetal ovine hypothalamus- pituitary-adrenal axis in response to hypotension.

In the fetal sheep, parturition is triggered by an increase in the activity of the fetal hypothalamus- pituitary-adrenal (HPA) axis which, in turn, augments the biosynthesis of oestrogen by the placenta. Parturition can be prevented or delayed by destruction of the paraventricular nucleus (PVN), pituitary or adrenal, or stimulated by infusions of adrenocorticotropin (ACTH) or glucocorticoids. We have previously reported that physiological increases in fetal plasma concentrations of oestradiol have a neuroendocrine effect to increase both basal and hypotension-stimulated ACTH secretion. The present study was performed to test the effect of oestradiol on the central baroreceptor and chemoreceptor reflex pathways. We used immunohistological techniques to identify various neuroanatomical regions which are activated by hypotension and, subsequently, those areas modified by oestrogen's action and baroreceptor and chemoreceptor denervation. We assessed cellular activation in these brain regions by immunostaining for Fos, the protein product of c-fos, an immediate early response gene. We found that oestradiol increased Fos abundance in nucleus tractus solitarius (NTS), rostral ventrolateral medulla (RVLM), and PVN, and augmented the increase in Fos in these regions in response to a 10 min period of brachiocephalic arterial occlusion (BCO). Carotid sinus denervation blocked the Fos response to BCO, but not to oestrogen alone, in these regions. In contrast, the hippocampus responded to BCO with increase Fos in intact fetuses, but did not respond to oestrogen treatment. None of the treatments altered Fos expression in cerebral cortex or in cerebellum. We conclude that oestradiol augments the activity of the central baroreceptor and chemoreceptor reflex pathways, and that it may influence fetal ACTH secretion via this site of action.

The action of angiotensin II on the baroreflex response of the conscious ewe and the conscious fetus.

1. In conscious non-pregnant and pregnant ewes and in chronic fetal lamb preparations, the beat by beat relationship between pulse interval and systolic pressure was studied during acute elevations in arterial pressure induced by phenylephrine. Baroreflex sensitivity, which was defined as the slope of the pressure-pulse interval relationship when phenylephrine was used to raise pressure, was abolished by atropine and increased by propranolol. Baroreflex sensitivity was less in pregnant ewes and in foetal lambs compared with non-pregnant ewes. 2. These findings suggest that the vagus nerve is responsible for the reflex bradycardia that occurs in the foetus and the ewe when arterial pressure is increased. 3. In both fetal and adult sheep, actue hypertension due to I.V. injection of angiotensin II was not associated with a consistent and progressive bradycardia, such as was seen with acute hypertension caused by phenylephrine. Angiotensin II has no direct chronotropic effect on heart rate in either the adult or the fetus. 4. No linear relationship between arterial pressure and pulse interval was seen when angiotensin II was used to raise pressure in sheep which were treated with propranolol. Therefore the lack of cardiac slowing with pressor doses of angiotensin II was not due to concomitant activation of the sympathoadrenal system. 5. It is concluded that in both fetal and adult sheep angiotensin II reduces the increase in vagal tone which is responsible for slowing of heart rate in response to acute rises in arterial pressure.

Baroreflex activity in conscious fetal and newborn lambs.

The immediate transient baroreceptor sensitivity was measured in 9 conscious fetal and 7 conscious newborn lambs for periods of at least 35 days following bolus injections of phenylephrine (20-50 mug/kg). Mean sensitivities were unchanged throughout gestation from 105 days at 6.7 +/- 0.4 msec/cm H2O (n = 45) and were insignificantly different from those in the newborn period, 5.9 +/- 0.4 msec/cm H2O (n = 78). In contrast, baroreflex sensitivities were less in 2 fetuses and 2 newborn lambs when pressures were increased by chronically implanted thoracic aortic balloon cuff; they were 3.03 +/- 0.11 (n = 127) and 0.91 +/- 0.11 msec/cm H2O (n =61), respectively. "Steady-state" heart period-arterial pressure curves indicate that the baroreflex operates down to levels of 40 cm H2O in the fetus which is lower than that achieved in the adult of other species, rabbit and man.