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Ganglionic blockade alters behavioral and cerebral metabolic responses to corticotropin releasing factor in the rat.
No full text
Effects of anesthesia and recovery from ketamine racemate and enantiomers on regional cerebral glucose metabolism in rats
Full text linkBackground: Unlike most anesthetics, ketamine racemate
(S,R()-ketamine) induces heterogenous changes in cerebral metabolism. S,R()-ketamine is an equimolar mixture of two enantiomers, S()-ketamine and R()-ketamine, which differ in affinity for neuroreceptors and pharmacologic activities.
This study investigated comparatively the effects of ketamine
racemate and enantiomers on cerebral metabolism.
Methods: Regional cerebral metabolic rates for glucose
(rCMRglc) were determined with the quantitative, autoradio-
graphic [14C]2-deoxy-D-glucose technique in 40 brain regions of Fischer-344 rats. rCMRglc were measured in three groups of rats during equimolar anesthesia, 10 min after intraperitoneal injection of 170 mg/kg S,R()-ketamine, S()-ketamine, or R()-ketamine; in three groups of rats during recovery from equivalent anesthesia, 20 min after intravenous injection of 20, 12.5, and 30 mg/kg S,R()-ketamine, S()-ketamine, or R()-ketamine; and in two groups of sa line-injected control rats.
Results: S,R()-ketamine and S()-ketamine induced a sus-tained anesthesia; deep rCMRglc decreases in 22 and 14 cortical, thalamic, cerebellar, and brainstem regions; and rCMRglc in-creases in two limbic regions (average decreases, 23 and 15%).
R()-ketamine determined a shorter anesthesia, lesser rCMRglc decreases in 11 brain areas, and marked rCMRglc increases in 14 basal ganglia and limbic regions (average decrease, 4%).
S,R()-ketamine, S()-ketamine, and R()-ketamine all produced postanesthetic behavioral activation; widespread rCMRglc in-creases in 28, 16, and 20 cortical, thalamic, basal ganglia, limbic, and brainstem regions; and rCMRglc decreases in few auditory and limbic regions (average increases, 35, 13, and 20%).
Conclusions: S,R()-ketamine and S()-ketamine anesthesia but not R()-ketamine anesthesia induced widespread rCMRglc reductions that were unreported but are typical of gaseous and intravenous general anesthetics. Postanesthetic recovery led to divergent, sharp behavioral and rCMRglc activations. The relation to dose of behavioral and rCMRglc effects differs from those of aminergic agents and resembles those of N-methyl-D-aspartate receptor antagonists, suggesting that ketamine racemate and enantiomers may preferentially interact with this
receptor type
Bronchoscope-guided intubation through a Laryngeal Mask Airway Supreme in a patient with a difficult-to-manage airway.
No full textWe report a case of an obese patient who presented with
laryngeal edema and diffi cult ventilation after failed attempts
to intubate. A Laryngeal Mask Airway Supreme (LMA
Supreme) reestablished the ventilation and allowed broncho-
scope-guided intubation of the trachea. The case suggests that
the LMA Supreme may be useful in patients with a diffi cult
airway
Cerebral metabolic effects of acetyl-L-carnitine in rats during aging
No full textThe aim of the present study was to investigate the neuronal structure sthat mediate the
Antiaging properties of acetyl-l-carnitine(ALCAR). The regional cerebral metabolic rates for
Glucose (rCMRglc) have been determined with the quantitative autoradiographic [14C]2-
Deoxyglucose procedure at different times after i.v. administration of saline or ALCAR
500mg/kg to naïve, non pretreated 3-, 12-and24-month-old rats and to24-month-old rats
pretreated with ALCAR (100 mg/kg/day, for 3 months). rCMRglc increased maximally at
30 min after ALCAR in 3-, 12-and 24-month old rats (14, 15 and 15 areas affected, 19, 24
and 22% mean increments). Peak metabolic activations occorre with similar magnitude
in motor, visual, limbic and talamic areas in all age rats and with large
rmagnitude in hippocamp al and talami areas in aged rats. Cerebral metabolic activations subsided by
60 min after ALCAR in 3-month rats (3 brain regions affected, 4% decrease) and persisted
by that time in12- and24-month-oldrats (14 and12 regions affected, 15 and 20%
increases). Cerebral activations were enhanced in aged rats after chronic treatment
with ALCAR (24 brain region saffected, 20% mean increase). Hence, duringaging, metabolic
responsività to ALCAR is maintained in most brain areas and increate in limbic and
thalamic regions. Increased responsivity to ALCAR may result from undetermined
pharmacokinetic factors and/or from a higher sensitività and contribute to the aging
reversal properties of ALCAR
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