Autonomic neuroscience : basic & clinical
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The antihypertensive drugs moxonidine and clonidine are α2-adrenoceptor and imidazoline (I1) agonists. Previous results from our laboratory have shown that moxonidine can act in the commissural nucleus of the solitary tract (commNTS). In addition, some studies have shown that GABA or glutamate receptor blockade in the RVLM blunted the hypotension produced by these antihypertensive agents in spontaneously hypertensive rats. ⋯ Injection of the GABAA antagonist bicuculline (25 pmol/50 nL) into the commNTS reduced the hypotension as well as the sympathoinhibition elicited by moxonidine. Prior injection of the glutamate receptor antagonist kynurenic acid (2.5 nmol/50 nL) into the commNTS was not effective in reducing the hypotension and sympathoinhibition elicited by moxonidine. Therefore, we conclude that the hypotensive and sympathoinhibitory effects elicited by microinjection of moxonidine into the commNTS are dependent on GABA receptors, but not ionotropic glutamate receptors.
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Paroxysmal sympathetic hyperactivity (PSH) is a condition in which there is extreme autonomic dysregulation leading to multiple episodes of sympathetic hyperactivity. Its occurrence after traumatic brain injury (TBI) in pediatric population is a neglected scenario. In our series, all pediatric patients with moderate and severe head injuries were studied and those patients who developed PSH were monitored for the PSH episodes. ⋯ Admission GCS of 3 children were 4/15 and 1 child was 6/15 and each of them had an ICU stay of more than 2weeks and a poor DRS score at discharge. The presence of PSH is known to produce poorer outcome in terms of overall mortality, time needed for recovery, chances of developing infections, etc. which was also seen in these cases presented here. Though some studies have provided guidelines for the management of PSH like symptomatic management and use of drugs like clonidine, bromocriptine, benzodiazepines, and gabapentin, strict management guidelines are not established and exact incidence in pediatric population is not determined.
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Pupillary unrest is a chaotic fluctuation in pupil size that is observed in darkness with the onset of drowsiness, and in ambient light. The mechanism of pupillary unrest in darkness as well as in ambient light is unknown but studies suggest that it is caused by fluctuating activity in the Edinger-Westphal (E. W.) nucleus. ⋯ Recovery from the drug effect was observed. Based upon the data from this study we propose that pupillary unrest in light originates within oscillating inhibitory neurons that intermittently depress the E. W. nucleus.
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We speculated that stroke volume would be higher and heart rate would be lower when the head and upper trunk were mainly upright in the Fowler's position. We therefore analyzed the effects of three trunk postures in Fowler's position on heart rate, blood pressure and circulatory volume. Heart rate (HR), blood pressure (BP), stroke volume (SV), cardiac output (Q), systemic vascular resistance (SVR), ejection time (ET) and pre-ejection period (PEP) were measured in 10 healthy male volunteers (mean age ± SEM, 20.7 ± 0.5 y; range, 19-23 y) while in three trunk postures in Fowler's position. ⋯ None of Q, SVR and BP significantly differed among the three conditions (p > 0.05). These findings suggested that SV and preload are higher when the upper trunk is upright (UT60°) than when the entire trunk is upright (WT60°) while in Fowler's position. In addition, Q might be maintained without increasing HR through vagal withdrawal when only the upper trunk is upright in healthy young males in Fowler's position.
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A transient decrease in G protein-coupled receptor kinase 2 (GRK2) in nociceptors can produce long-lasting neuroplastic changes in nociceptor function, eventually enhancing and prolonging inflammatory hyperalgesia. Here, we investigated the effects of selective α2-adrenoceptor agonist dexmedetomidine (DMED) on GRK2 expression in superior cervical ganglion (SCG) in a rat model of complex regional pain syndrome type I (CRPS-I). The ipsilateral 50% paw withdrawal thresholds (PWTs) to mechanical stimuli decreased significantly starting from 24 h after ischemia-reperfusion (I/R) injury, and lasted for over 3 weeks; the ipsilateral cold allodynia scores, GRK2 protein and mRNA levels in SCGs all increased significantly. ⋯ Following daily injection of 10 μg/kg of DMED for a maximum of 7 days, the ipsilateral PWTs on days 1, 2, 7, 14, and 21 after DMED administration were significantly higher than those in control group; the GRK2 protein and mRNA expressions in the ipsilateral SCGs were also significantly upregulated; the ipsilateral cold allodynia scores were significantly reduced. No significant differences were found in the contralateral 50%PWTs, cold allodynia scores, and GRK2 protein level except GRK2 mRNA levels increased significantly on days 1 to 7 after DMED administration. Therefore, a transient decrease of GRK2 expression in SCG neurons might be involved in the development and maintenance of allodynia in CRPS-I and DMED might alleviate this allodynia through GRK2 upregulation in SCG neurons.