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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a considerable body of evidence to suggest that activation of vasodilator fibers in the parasympathetic facial (VIIn) nerve can increase cerebral blood flow. The changes seen with VIIn stimulation raise the question as to whether they occur independent or in parallel with changes in cerebral metabolism. In these studies cerebral cortical perfusion was monitored continuously using laser Doppler flowmetry (CBFLDF) in the alpha-chloralose anesthetised cat. Cell firing in the region underlying the laser Doppler probe was monitored using tungsten-in-glass microelectrodes whose signals were amplified and filtered, and then monitored on-line by a microcomputer. Thus measures of both blood flow and local functional activity could be obtained that were continuous and contemporaneous. The VIIn was electrically stimulated through a craniotomy after isolation from the brainstem. CBFLDF and cell firing were monitored during several physiological manoeuvres. Hypercapnia produced the expected increase in CBFLDF that was brisk and stimulus locked. Cell firing did not alter except for a brief increase that was seen at the initiation of the hypercapnia and not maintained. The CBFLDF signal autoregulated to a level of 50-60 mmHg with no change in cellular activity. To determine if classical dynamic flow/metabolism coupling was present bicuculline, a GABAA receptor antagonist was superfused over the cortex. This led to increases in both CBFLDF and cell firing that were tightly and clearly linked. Stimulation of the VIIn led to a marked increase in the CBFLDF signal (47 +/- 7%) that was not accompanied by changes in cell firing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral blood flow is not coupled to neuronal activity during stimulation of the facial nerve vasodilator system. 792 95

1. We investigated the neural mechanisms of the increases in blood flow produced by synaptic activity using the parallel fiber (PF) system of the cerebellum as a model. The midline cerebellum was exposed in anesthetized rats and the PFs were stimulated with tungsten microelectrodes. Cerebellar blood flow (BFcrb) was recorded using a laser-Doppler probe, whereas field potentials were recorded using glass micropipettes. PF stimulation produced increases in BFcrb that were related to the frequency and intensity of stimulation (+60 +/- 9%, mean +/- SE, at 100 microA and 30 Hz; n = 6). The greatest increases were confined to a band stretching along the major axis of the stimulated folium and corresponding to the beam of activated PFs. The increase in evoked by PF stimulation was associated with a corresponding increase in glucose utilization, assessed by the 2-deoxyglucose method. The increases in BFcrb and the field potentials evoked by PF stimulation were abolished by tetrodotoxin (1 microM; n = 6). Ringer solution containing 12 mM Mg2+ and 0 mM Ca2+ blocked synaptic activity in the PFs and abolished the increases in flow (P > 0.05 from baseline; n = 5). The broad-spectrum glutamate receptor antagonist kynurenate (5 mM) prevented depolarization of Purkinje cells and interneurons and abolished the increase in BFcrb evoked by PF stimulation (P > 0.05; n = 6). Treatment with tetrodotoxin, Mg2+, or kynurenate did not affect the increase in BFcrb elicited by systemic hypercapnia or by topical application of the nitric oxide donor 3-morpholino sydnonimine (P > 0.05 from Ringer solution). We conclude that the increases in flow produced by synaptic activity are linked to glutamate-induced depolarization of Purkinje cells and interneurons. These findings provide evidence that activation of glutamate receptors participates in the mechanisms of functional hyperemia, and they support the validity of the PF system as a model for study of the relationship between synaptic activity and blood flow in the CNS.
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PMID:Neural mechanisms of blood flow regulation during synaptic activity in cerebellar cortex. 871 66

The genioglossus (GG) is considered the principle protrudor muscle of the human tongue. Unlike most skeletal muscles, GG electromyographic (EMG) activities are robustly preserved in sleep and thus may fulfill a critical role in preserving airway patency. Previous studies in human subjects also confirm that the GG EMG increases in response to chemoreceptor and mechanoreceptor stimulation. This increase occurs secondary to the recruitment of previously inactive motor units (MUs) and/or an increase in firing rate of already active MUs. Which strategy the nervous system uses when the synaptic drive onto GG motoneurons increases is not known. Here we report on GG whole muscle and tonic MU activities under conditions that mimic sleep, i.e., mild-moderate elevations in CO(2) (3% inspired CO(2) or the addition of a 1.0 l dead space) and elevated airway resistance. Based on previous work in rat, we hypothesized that mild hypercapnia would increase the firing rates of tonic MUs and that these effects would be further potentiated by a modest increase in airway resistance. Fine wire and tungsten microelectrodes were inserted into the GG to record whole muscle and single MU activities in 21 subjects (13 women, 8 men; 20-55 yr). Either 3% inspired CO(2) or added dead space resulted in a 200-300% increase in the amplitude of both tonic and phasic components of the whole muscle GG EMG and a doubling of minute ventilation. Despite these changes, recordings obtained from a total of 84 tonically discharging GG single MUs provide no evidence of a change in firing rate under any of the conditions. On this basis we conclude that in healthy adults, the increase in the tonic component of the whole muscle GG EMG secondary to mild hypercapnia is due almost exclusively to the recruitment of previously inactive MUs.
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PMID:Tonically discharging genioglossus motor units show no evidence of rate coding with hypercapnia. 2005 47