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PubMed · 8450633

[Etomidate--propofol].

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A Doenicke. 1993. [Etomidate--propofol].. https://pubmed.ncbi.nlm.nih.gov/8450633/

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Beta and gamma oscillations in the olfactory system of the urethane-anesthetized rat.

Fast oscillations in the beta (15-40 Hz in awake rats) and gamma (50-100 Hz) frequency ranges are prominent in field potentials induced by odorants in the mammalian olfactory bulb (OB) and piriform cortex (PC). Whereas the gamma oscillation has been studied for >50 yr, the beta oscillation has attracted attention only recently, and its origin, mechanism, and relationship to gamma are unknown. To address these questions, we have examined responses induced by odorants in the urethane-anesthetized rat-a preparation well-suited for the analysis of mechanisms. We found that both oscillations could be induced by odorants in a concentration-dependent manner. Analysis with a concentration series and spectral methods revealed that the beta and gamma oscillations were distinct and not harmonically related, indicating generation by independent mechanisms. The beta oscillation was synchronous at sites < or =4 mm apart in the OB, the greatest distance tested. In contrast, the gamma oscillation was synchronous in some experiments and asynchronous in others (frequency differed slightly at different sites, resulting in progressive phase shifts). Current source-density analysis indicated that, for both oscillations, the field potentials in the OB were generated by synaptic currents in granule cells. The two oscillations were differently affected by surgical interruption of the lateral olfactory tract. This lesion abolished the beta oscillation, whereas the gamma oscillation was still induced in the OB. Our results confirm previous reports that the gamma oscillation is generated within the OB but indicate that the beta oscillation requires the participation of PC.

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The effect of infusions of adrenaline, noradrenaline and dopamine on cerebral autoregulation under propofol anaesthesia in an ovine model.

OBJECTIVE: To compare the effects of infusions of adrenaline, noradrenaline and dopamine on cerebral autoregulation under steady-state propofol anaesthesia with the awake state. DESIGN: Prospective, randomised, interventional animal study. SETTING: University laboratory. SUBJECTS: Six studies in two cohorts of adult ewes: awake and steady-state propofol anaesthesia (15 mg/min). INTERVENTIONS: In random order, each animal received ramped infusions of adrenaline, noradrenaline (0-40 microg/min) and dopamine (0-40 microg/kg per min). MEASUREMENTS AND RESULTS: Cerebral blood flow (CBF) was measured continuously from changes in Doppler velocities in the sagittal sinus and normalised to a PaCO(2) 35 mmHg. Propofol decreased CBF by 55% relative to pre-anaesthesia values (p=0.0001). All three catecholamines significantly and equivalently increased mean arterial pressure (MAP) from baseline in a dose-dependent manner in both awake and propofol cohorts. Adrenaline significantly increased CBF from baseline in both awake sheep (p<0.01) and during propofol anaesthesia (p<0.001); noradrenaline and dopamine did not statistically increase CBF. When comparing the effects of individual catecholamines with each other within each cohort, no statistically significant difference between the catecholamines was demonstrated. (p>0.05). Using linear regression analysis, normalised CBF was correlated against associated changes in MAP. No significant differences were demonstrated between the slopes of regression lines for adrenaline, noradrenaline and dopamine in either cohort (ANCOVA). There was a statistically significant difference between the intercepts of the awake and propofol cohorts (p<0.0001), but no difference between the slopes (p=0.69). CONCLUSIONS: Over a specific dose range, catecholamine-induced hypertension caused increased CBF during steady-state propofol anaesthesia. This effect was offset by an associated reduction in CBF caused by propofol. The concomitant administration of propofol and catecholamines was not associated with altered autoregulatory function compared to the awake state.

Anesthesia, Intravenous↗

Effects of a selective metabotropic glutamate receptor agonist on the micturition reflex pathway in urethane-anesthetized rats.

AIMS: To determine a possible role of metabotropic glutamate receptors in the spinobulbospinal micturition reflex pathway in the rat. MATERIALS AND METHODS: A selective metabotropic glutamate receptor agonist, trans-(+/-)-1-amino1,3-cyclopentanedicarboxylic acid (trans-ACPD) was administered to the lumbosacral spinal cord via an intrathecal catheter in urethane anesthetized rats. Amplitude of reflex bladder contractions evoked by bladder distension under isovolumetric condition as well as amplitude of bladder contractions elicited by electrical stimulation of the pontine micturition center (PMC) were examined before and after administration of trans-ACPD. The effect of trans-ACPD on the urethral activity during isovolumetric bladder contractions was also examined by monitoring urethral perfusion pressure and electromyography of the external urethral sphincter (EUS-EMG). RESULTS: Trans-ACPD (3-10 microg) completely inhibited reflex bladder contractions evoked by bladder distension and the duration of inhibition was dose dependent (3 microg: 11.4 +/- 2.8 min, 5 microg: 13.2 +/- 1.3 min, 10 microg: 36.2 +/- 2.4 min). The mean amplitude of bladder contractions evoked by electrical stimulation of the PMC was reduced to 12.6 +/- 2.3% of control by 10 microg of trans-ACPD. In addition, bursting activity of EUS-EMG and corresponding high frequency oscillations of urethral pressure during isovolumetric bladder contractions were completely abolished by 10 microg of trans-ACPD. CONCLUSIONS: These results indicate that intrathecal administration of a selective metabotropic glutamate receptor agonist to the lumbosacral spinal cord has an inhibitory effect on the spinobulbospinal micturition reflex pathway in urethane-anesthetized rats. This pharmacological action is attributed at least to the inhibitory effect on the descending pathway from the PMC to the lumbosacral spinal cord.

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