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J F Antognini

Publications and source records attributed to J F Antognini.

At least 19 recordsLinked to original sources
PubMed2006

Propofol, more than halothane, depresses electroencephalographic activation resulting from electrical stimulation in reticular formation.

BACKGROUND: Halothane and propofol depress the central nervous system, and this is partly manifested by a decrease in electroencephalographic (EEG) activity. Little work has been performed to determine the differences between these anesthetics with regard to their effects on evoked EEG activity. We examined the effects of halothane and propofol on EEG responses to electrical stimulation of the reticular formation. METHODS: Rats (n= 12) were anesthetized with either halothane or propofol, and EEG responses were recorded before and after electrical stimulation of the reticular formation. Two anesthetic concentrations were used (0.8 and 1.2 times the amount needed to prevent gross, purposeful movement in response to supramaximal noxious stimulation), and both anesthetics were studied in each rat using a cross-over design. RESULTS: Electrical stimulation in the reticular formation increased the spectral edge (SEF) and median edge (MEF) frequencies by approximately 1-2 Hz during halothane anesthesia at low and high concentrations. During propofol anesthesia, MEF increased at the low propofol infusion rate, but SEF was unaffected. At the high propofol infusion rate, SEF and MEF decreased following electrical stimulation in the reticular formation. CONCLUSIONS: At immobilizing concentrations, propofol produces a larger decrease than halothane in EEG responses to reticular formation stimulation, consistent with propofol having a more profound depressant effect on cortical and subcortical structures.

Anesthetics, Inhalation↗
PubMed2005

Nitrous oxide depresses electroencephalographic responses to repetitive noxious stimulation in the rat.

BACKGROUND: Although N(2)O has been widely used as an anaesthetic adjuvant its effect on electroencephalographic (EEG) activity is poorly understood because it is usually studied in the presence of additional anaesthetics, including inhaled anaesthetics. We examined the EEG effects of N(2)O in rats using a hyperbaric chamber that permitted N(2)O to be the sole anaesthetic. METHODS: Rats (n=10) were anaesthetized with isoflurane and EEG activity was recorded from skull screws. The rats were placed into a hyperbaric chamber and mechanically ventilated. Isoflurane was eliminated while the chamber was pressurized with N(2)O. The minimum alveolar concentration (MAC) was determined in five rats by adjusting the chamber pressure and N(2)O concentration, and applying a tetanic noxious stimulus to the tail via an electrical pass-through. EEG responses to noxious stimulation (20 electrical pulses at 40 V applied to the tail at 0.1, 1 and 3 Hz, and 50 Hz tetanic stimulation at 60 mA applied for 30 s) were determined at 1.5 and 2 atm N(2)O. RESULTS: The N(2)O MAC was 1.7+/-0.1 atm. No consistent EEG activation occurred during electrical stimulation at either partial pressure of N(2)O, although spontaneous EEG activation often occurred. Blood pressure increased after the 3 and 50 Hz stimuli. Four other rats anaesthetized with isoflurane had EEG activation with the 3 and 50 Hz stimuli. CONCLUSIONS: These data indicate that N(2)O at peri-MAC partial pressures prevents EEG activation resulting from noxious electrical stimulation. Unlike the situation with isoflurane, stimulus-evoked EEG activation did not occur at peri-MAC anaesthetic concentrations, suggesting that N(2)O potently blocked ascending nociceptive transmission.

Anesthetics, Inhalation↗
PubMed2005

Halothane and propofol differentially affect electroencephalographic responses to noxious stimulation.

BACKGROUND: Anaesthetics blunt neuronal responses to noxious stimulation, including effects on electroencephalographic (EEG) responses. It is unclear how anaesthetics differ in their ability to modulate noxious stimulation-evoked EEG activation. We investigated the actions of propofol and halothane on EEG responses to noxious stimuli, including repetitive electrical C-fibre stimulation, which normally evokes neuronal wind-up. METHODS: Rats were anaesthetized with halothane (n=8) or propofol (n=8), at 0.8x or 1.2x the amount required to produce immobility in response to tail clamping [minimum alveolar concentration (MAC) for halothane and median effective dose (ED(50)) for propofol]. We recorded EEG responses to repetitive electrical stimulus trains (delivered to the tail at 0.1, 1 and 3 Hz) as well as supramaximal noxious tail stimulation (clamp; 50 Hz electrical stimulus, each for 30 s). RESULTS: Under halothane anaesthesia, noxious stimuli evoked an EEG activation response manifested by increased spectral edge frequency (SEF) and median edge frequency (MEF). At 0.8 MAC halothane, the tail clamp increased the MEF from approximately 6 to approximately 8.5 Hz, and the SEF from approximately 25.5 to approximately 27 Hz. At both 0.8 and 1.2 MAC halothane, similar patterns of EEG activation were observed with the 1 Hz, 3 Hz and tetanic stimulus trains, but not with 0.1 Hz stimulation, which does not evoke wind-up. Under propofol anaesthesia, noxious stimuli were generally ineffective in causing EEG activation. At 0.8 ED(50) propofol, only the tail clamp and 1 Hz stimuli increased MEF ( approximately 8 to approximately 10-10.5 Hz). At the higher propofol infusion rate (1.2 ED(50)) the repetitive electrical stimuli did not evoke an EEG response, but the tetanic stimulus and the tail clamp paradoxically decreased SEF (from approximately 23 to approximately 21.5 Hz). CONCLUSIONS: Propofol has a more significant blunting effect on EEG responses to noxious stimulation compared with halothane.

Anesthetics, Inhalation↗
PubMed2005

Application of nucleus pulposus to L5 dorsal root ganglion in rats enhances nociceptive dorsal horn neuronal windup.

Herniation of the nucleus pulposus (NP) from lumbar intervertebral discs commonly results in radiculopathic pain possibly through a neuroinflammatory response. NP sensitizes dorsal horn neuronal responses, but it is unknown whether this reflects a central or peripheral sensitization. To study central sensitization, we tested if NP enhances windup--the progressive increase in the response of a nociceptive spinal neuron to repeated electrical C-fiber stimulation--a phenomenon that may partly account for temporal summation of pain. Single-unit recordings were made from wide dynamic range (WDR; n = 36) or nociceptive-specific (NS; n = 8) L5 dorsal horn neurons in 44 isoflurane-anesthetized rats. Subcutaneous electrodes delivered electrical stimuli (20 pulses, 3 times the C-fiber threshold, 0.5 ms) to the receptive field on the hindpaw. Autologous NP was harvested from a tail disc and placed onto the L5 dorsal root ganglion after recording of baseline responses (n = 22). Controls had saline applied similarly (n = 22). Electrical stimulus trains (0.1, 0.3, and 1 Hz; 5-min interstimulus interval) were repeated every 30 min for 3-6 h after each treatment. The total number of evoked spikes (summed across all 20 stimuli) to 0.1 Hz was enhanced 3 h after NP, mainly in the after-discharge (AD) period (latency > 400 ms). Total responses to 0.3 and 1.0 Hz were also enhanced at > or = 60 min after NP in both the C-fiber (100- to 400-ms latency) and AD periods, whereas the absolute windup (C-fiber + AD - 20 times the initial response) increased at > or = 90 min after treatment. In saline controls, windup was not enhanced at any time after treatment for any stimulus frequency, although there was a trend toward enhancement at 0.3 Hz. These results are consistent with NP-induced central sensitization. Mechanical responses were not significantly enhanced after saline or NP treatment. We speculate that inflammatory agents released from (or recruited by) NP affect the dorsal root ganglion (and/or are transported to cord) to enhance primary afferent excitation of nociceptive dorsal horn neurons.

Action Potentials↗
PubMed2005

Differential effects of halothane and isoflurane on lumbar dorsal horn neuronal windup and excitability.

BACKGROUND: Windup of spinal nociceptive neurones may underlie temporal summation of pain, influencing the minimum alveolar concentration (MAC) of anaesthetics required to prevent movement to supramaximal stimuli. We hypothesized that halothane and isoflurane would differentially affect windup of dorsal horn neurones. METHODS: We recorded 18 nociceptive dorsal horn neurones exhibiting windup to 1 Hz electrical hindpaw stimuli in rats. Effects of 0.8 and 1.2 MAC isoflurane and halothane were recorded in the same neurones (counterbalanced, crossover design). Windup was calculated as the total number of C-fibre (100-400 ms latency) plus afterdischarge (400-1000 ms latency) spikes/20 stimuli (area under curve, AUC) or absolute windup (C-fibre plus afterdischarge-20 x initial response). RESULTS: Increasing isoflurane from 0.8 to 1.2 MAC did not affect AUC, but increased absolute windup from 429 (62) to 618 (84) impulses/20 stimuli (P<0.05) and depressed the initial C-fibre response from 14 (3) to 8 (2) impulses (P<0.05). Increasing halothane from 0.8 to 1.2 MAC depressed AUC from 690 (79) to 537 (65) impulses/20 stimuli (P<0.05) and the initial response from 18 (2) to 13 (2) impulses (P<0.05), but absolute windup was not affected. Absolute windup was 117% greater during 1.2 MAC isoflurane compared with 1.2 MAC halothane. CONCLUSIONS: Windup was significantly greater under isoflurane than halothane anaesthesia at 1.2 MAC, whereas the initial C-fibre response was suppressed more by isoflurane. These findings suggest that these two anaesthetics have mechanistically distinct effects on neuronal windup and excitability.

Action Potentials↗
PubMed2005

Intrathecal picrotoxin minimally alters electro-encephalographic responses to noxious stimulation during halothane and isoflurane anesthesia.

BACKGROUND: Isoflurane and halothane act in the spinal cord to blunt ascending transmission of impulses to the brain resulting from noxious stimulation. Because intrathecal picrotoxin (an antagonist at the gamma-aminobutyric acid-A receptor) partially reverses the immobilizing effect of isoflurane and halothane, we hypothesized that the electroencephalographic response to noxious stimulation would likewise be partially reversed by intrathecal picrotoxin. METHODS: Rats were anesthetized with isoflurane (n = 8) or halothane (n = 8) and a laminectomy performed. Following determination of minimum alveolar concentration (MAC), the electroencephalogram (EEG) was recorded during separate applications of a hindpaw clamp, tail clamp and electrical current to the tail at 0.8 and 1.2 MAC. Picrotoxin was then applied to the exposed spinal cord and the EEG response to noxious stimulation again determined. RESULTS: The EEG was more active during halothane anesthesia than isoflurane (spectral edge frequency for 95% power: 25.6 +/- 2.1 Hz vs. 23.1 +/- 1.6 Hz, P < 0.05). Noxious stimulation usually caused the EEG to shift to higher frequencies (e.g. for 0.8 MAC halothane, median edge frequency for 50% power: from 7.6 +/- 3.1 Hz to 10.7 +/- 2.6 Hz, P < 0.05). Picrotoxin minimally affected this response. CONCLUSIONS: Noxious stimulation evokes an EEG response that is minimally altered by intrathecal picrotoxin. This suggests that isoflurane and halothane do not have GABAergic actions in the spinal cord that indirectly suppress the EEG response.

Anesthetics, Inhalation↗
PubMed2003

Spinal anaesthesia indirectly depresses cortical activity associated with electrical stimulation of the reticular formation.

BACKGROUND: Neuraxial blockade reduces the requirements for sedation and general anaesthesia. We investigated whether lidocaine spinal anaesthesia affected cortical activity as determined by EEG desynchronization that occurs following electrical stimulation of the midbrain reticular formation (MRF). METHODS: Six goats were anaesthetized with isoflurane, and cervical laminectomy performed to permit spinal application of lidocaine. The EEG was recorded before, during and after focal electrical stimulation (0.1, 0.2, 0.3 and 0.4 mA) in the MRF while keeping the isoflurane concentration constant. RESULTS: During lidocaine spinal anaesthesia, the spectral edge frequency (SEF) after MRF electrical stimulation (13.6 (SD 1.0) Hz, averaged across all stimulus currents) was less than the SEF during control and recovery periods (18.6 (3.6) Hz and 17.2 (2.2) Hz, respectively; P<0.05). Bispectral index values were similarly affected: 69 (10) at control compared with 55 (6) during the spinal block (P<0.05). CONCLUSIONS: These results suggest that lidocaine spinal anaesthesia blocks ascending somatosensory transmission to mildly depress the excitability of reticulo-thalamo-cortical arousal mechanisms.

Anesthesia, Spinal↗
PubMed2001

Propofol action in both spinal cord and brain blunts electroencephalographic responses to noxious stimulation in goats.

STUDY OBJECTIVES: Anesthetics, including propofol, depress the electroencephalogram (EEG) and neuronal activity in the midbrain reticular formation (MRF). Because propofol has anesthetic effects in the spinal cord, we hypothesized that it would indirectly depress EEG and MRF neuronal responses to noxious stimulation in part by a spinal cord action. DESIGN: Six goats were anesthetized with isoflurane and the jugular veins and carotid arteries were isolated to permit cranial bypass and differential propofol delivery. A noxious mechanical stimulus was applied to the distal forelimb while recording bifrontal EEG and MRF single-unit activities. Propofol was separately administered to the cranial (0.08 +/- 0.06 mg/kg) and torso circulations (4 mg/kg) and the noxious stimulus applied at 1,5, 10, and 15 min after each injection. SETTING: N/A. PATIENTS OR PARTICIPANTS: N/A. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: Noxious stimulation decreased total power (TP) from 96 +/- 33, microV2/Hz to 38 +/- 20microV2/Hz, (mean +/- SD) and increased spectral edge frequency (SEF) from 10 +/- 3 Hz to 19 +/- 5 Hz (p<0.01). Propofol administered to the torso prevented stimulus-evoked changes in TP (121+/- 80 microV2/Hz, 121 +/- 74 microV2/Hz, 114 +/- 74 microV2/Hz at 1,5, and 10 min respectively, p<0.01 compared to control evoked response) and SEF (11 +/- 6Hz, 9 +/- 2Hz, 10 +/- 6Hz, and 12 +/- 5Hz at 1, 5, 10 and 15 min, respectively, p<0.001 compared to control evoked response). Propofol administered to the cranial circulation significantly blunted the EEG and MRF response, while torso-administered propofol had slight effects on MRF responses. CONCLUSIONS: Propofol blunted the EEG response to noxious stimulation in part via a subcortical action.

Analgesics↗
PubMed2001

Variable effects of nitrous oxide at multiple levels of the central nervous system in goats.

The direct and indirect effects of nitrous oxide (N2O) on the nociceptive responses of lumbar dorsal horn neurons, and the indirect effects on midbrain reticular formation (MRF) neurons and thalamic neurons were determined in goats anaesthetized with isoflurane. The technique used enabled the differential delivery of N2O to either the torso or the cerebral circulation, thus allowing assessment of the direct spinal and indirect brain effects of N2O. Systemic delivery of N2O appeared to have divergent effects, facilitating (4/11) or depressing (7/11) the responses of dorsal horn neurons. Such divergent effects were also observed when N2O was differentially delivered to the circulation in the torso (i.e. the spinal cord). Likewise, MRF and thalamic responses to noxious stimulation were variably affected by administration of N2O to the torso, with some cells facilitated (7/13 MRF neurons, 3/8 thalamic neurons) and others depressed (6/13 MRF neurons, 5/8 thalamic neurons). It appears that N2O has variable effects on the caprine CNS. The facilitatory action of N2O might partially explain why it is a relatively weak anaesthetic.

Anesthetics, Inhalation↗
PubMed2001

Thiopental directly depresses lumbar dorsal horn neuronal responses to noxious mechanical stimulation in goats.

BACKGROUND: Thiopental has hypnotic actions in the brain, but it also depresses nociceptive transmission. In this study we examined whether thiopental had direct (spinal) and/or indirect (supraspinal) effects on the responses of single lumbar dorsal horn neurons to noxious mechanical stimulation, using a method to deliver thiopental differentially to either the torso or cranial circulation in goats. METHODS: Goats (n=10) were anesthetized with isoflurane and neck dissections performed to permit cranial bypass. A lumbar laminectomy was made to permit single-unit recording of lumbar dorsal horn neuronal activity (1-2 neurons/animal). Isoflurane was maintained at 0.8+/-0.1% to both head and torso throughout the study. During cranial bypass, thiopental was separately administered to the torso (low dose, 1.5+/-0.5 mg/kg; high dose, 3.7+/-0.5 mg/kg) or cranial (low dose, 0.12+/-0.03 mg/kg; high dose, 0.2 mg/kg) circulation. RESULTS: Thiopental administered to the torso significantly depressed dorsal horn neuronal responses to noxious stimulation at the high dose: 757+/-471 to 392+/-305 impulses/min at 1 min post-injection, P<0.006 (n=14); evoked responses recovered at 5 min post-injection. At the low dose, there was a similar numerical decrease, but this did not reach significance: 876+/-780 to 407+/-499 impulses/min at 1 min post-injection, P>0.05 (n=6). No significant change was observed when thiopental was administered to the cranial circulation: low dose, 1061+/-1167 to 965+/-874 impulses/min at 1 min post-injection, P>0.05 (n=10); high dose, 864+/-331 to 917+/-525 impulses/min at 1 min post-injection, P>0.05 (n=8). CONCLUSION: Thiopental has a direct (spinal) depressant effect on dorsal neuronal responses to noxious stimulus, but no significant supraspinal effect.

Anesthetics, Intravenous↗
PubMed2000

Propofol directly depresses lumbar dorsal horn neuronal responses to noxious stimulation in goats.

PURPOSE: We tested the hypothesis that propofol, acting in the brain, would either enhance, or have no effect, on lumbar dorsal horn neuronal responses to a noxious mechanical stimulus applied to the hindlimb. We recorded the response of lumbar dorsal horn neurons during differential delivery of propofol to the brain and torso of goats. METHODS: Goats were anesthetized with isoflurane and neck dissections performed which permitted cranial bypass. A laminectomy was made to allow microelectrode recording of lumbar dorsal horn neuronal activity. Isoflurane was maintained at 0.8+/-0.1% to both head and torso throughout the study. During cranial bypass propofol was separately administered to the torso (1 mg x kg(-1), n = 7; 3.75 mg x kg(-1), n = 8) or cranial (0.04 mg x kg(-1), n = 7; 0.14 mg kg(-1), n = 8) circulations. RESULTS: Propofol administered to the torso depressed dorsal horn neuronal responses to noxious stimulation: low dose: 500+/-243 to 174+/-240 impulses x min(-1) at one minute post-injection, P<0.001; high dose: 478+/-204 to 91+/-138 impulses x min(-1) at one minute post-injection, P<0.05). Propofol administered to the cranial circulation had no effect: low dose: 315+/-150 to 410+/-272 impulses x min(-1), P>0.05; high dose: 462+/-261 to 371+/-196 impulses x min(-1), P>0.05. CONCLUSIONS: These data indicate that propofol has a direct depressant effect on dorsal horn neuronal responses to noxious stimulation, with little or no indirect supraspinal effect.

Analysis of Variance↗
PubMed2000

Isoflurane anaesthetic depth in goats monitored using the bispectral index of the electroencephalogram.

The bispectral index (BIS) of the electroencephalogram has recently been used to monitor the depth of anaesthesia in humans. The BIS is a dimensionless number that varies between 0 and 100. We hypothesized that the BIS could also be used to monitor depth of isoflurane anaesthesia in goats. Needle electrodes were placed over the frontal region of the scalp of goats and 5%, isoflurane was administered via a mask. The BIS number was determined at clinically relevant end-points. The BIS number did not change when the animals became recumbent (95 +/- 5 to 94 +/- 7, n = 15), but decreased to 65 +/- 13 and 64 +/- 15 when the corneal reflex and withdrawal response to a noxious stimulus, respectively, were lost (p < 0.001, n = 12). Direct laryngoscopy and intubation increased the BIS (56 +/- 7 to 83 +/- 11; p < 0.05, n = 10), as did a noxious pinch to the dew-claw (57 +/- 9; to 76 +/- 9; p < 0.05, n = 10). The spectral edge (frequency below which 95% of the total power resided) paralleled the change in BIS. We conclude that the depth of isoflurane anaesthesia in goats can be monitored using the BIS, although further work is needed to determine its sensitivity and specificity.

Anesthesia↗
PubMed2000

Isoflurane action in the spinal cord blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats.

BACKGROUND: Isoflurane depresses the electroencephalographic (EEG) activity and exerts part of its anesthetic effect in the spinal cord. The authors hypothesized that isoflurane would indirectly depress the EEG and subcortical response to noxious stimulation in part by a spinal cord action. METHODS: Depth electrodes were inserted into the midbrain reticular formation (MRF) and thalamus of six of seven isoflurane-anesthetized goats, and needle-electrodes were placed into the skull periosteum. In five of seven goats, an MRF microelectrode recorded single-unit activity. The jugular veins and carotid arteries were isolated to permit cranial bypass and differential isoflurane delivery. A noxious mechanical stimulus (1 min) was applied to a forelimb dewclaw at each of two cranial-torso isoflurane combinations: 1.1+/-0.3%-1.2+/-0.3% and 1.1+/-0.3-0.3+/-0.1% (mean +/- SD). RESULTS: When cranial-torso isoflurane was 1.1-1.2%, the noxious stimulus did not alter the EEG. When torso isoflurane was decreased to 0.3%, the noxious stimulus activated the MRF, thalamic, and bifrontal-hemispheric regions (decreased high-amplitude, low-frequency power). For all channels combined, total (-33+/-15%), delta(-51+/-22%), theta (-33+/-19%), and alpha (-26+/-16%) power decreased after the noxious stimulus (P<0.05); beta power was unchanged. The MRF unit responses to the noxious stimulus were significantly higher when the spinal cord isoflurane concentration was 0.3% (1,286+/-1,317 impulses/min) as compared with 1.2% (489+/-437 impulses/min, P<0.05). CONCLUSIONS: Isoflurane blunted the EEG and MRF-thalamic response to noxious stimulation in part via an action in the spinal cord.

Anesthetics, Inhalation↗
PubMed2000

Isoflurane depresses electroencephalographic and medial thalamic responses to noxious stimulation via an indirect spinal action.

UNLABELLED: Anesthetics such as isoflurane act in the spinal cord to suppress movement in response to noxious stimulation. Spinal anesthesia decreases hypnotic/sedative requirements, possibly by decreasing afferent transmission of stimuli. We hypothesized that isoflurane action in the spinal cord would similarly depress the ascending transmission of noxious input to the thalamus and cerebral cortex. In six isoflurane-anesthetized goats, we measured electroencephalographic (EEG) and thalamic single-unit responses to a clamp applied to the forelimb. Cranial bypass permitted differential isoflurane delivery to the torso and cranial circulations. When the cranial-torso isoflurane combination was 1.3% +/- 0.2%-1.0% +/- 0.4% the noxious stimulus did not evoke significant changes in the EEG or thalamic activity: 389 (153-544) to 581 (172-726) impulses/min, (median, 25th-75th percentile range, P: > 0.05). When the cranial-torso isoflurane combination was 1.3% +/- 0.2%-0.3% +/- 0.2%, noxious stimulation increased thalamic activity: 804 (366-1162) to 1124 (766-1865) impulses/min (P: < 0.05), and the EEG "desynchronized": total EEG power decreased from 25 +/- 20 microV(2) to 12 +/- 8 microV(2) (P: < 0.05). When the cranial-torso isoflurane was 1.7% +/- 0.1%-0.3% +/- 0.2%, the noxious stimulus did not significantly affect thalamic: 576 (187-738) to 1031 (340-1442) impulses/min (P: > 0.05), or EEG activity. The indirect torso effect of isoflurane on evoked EEG total power (12.6 +/- 2.7 microV(2)/vol%, mean +/- SE) was quantitatively similar to the direct cranial effect (17.7 +/- 3.0 microV(2)/vol%; P: > 0.05). These data suggest that isoflurane acts in the spinal cord to blunt the transmission of noxious inputs to the thalamus and cerebral cortex, and thus might indirectly contribute to anesthetic endpoints such as amnesia and unconsciousness. IMPLICATIONS: Isoflurane action in the spinal cord diminished the transmission of noxious input to the brain. Because memory and consciousness are likely dependent on the "arousal" state of the brain, this indirect action of isoflurane could contribute to anesthetic-induced amnesia and unconsciousness.

Anesthetics, Inhalation↗
PubMed1999

Isoflurane indirectly depresses middle latency auditory evoked potentials by action in the spinal cord in the goat.

PURPOSE: The auditory evoked potential (AEP) has been proposed as a method to determine depth of anesthesia, as AEPs are generated in the thalamus and cerebral cortex. Because general anesthesia, in part, relies on anesthetic action in the spinal cord, we hypothesized that isoflurane would have indirect depressant effects on the AEP because of its action in the spinal cord. METHODS: Six goats were anesthetized with isoflurane and the jugular veins and carotid arteries isolated to permit cerebral bypass and differential delivery of isoflurane to the head and torso. The AEPs were determined by delivering binaural clicks at 9 Hz, and measuring the evoked response from electrodes placed in the skull and scalp. Isoflurane was maintained at 0.8% in the head while the torso isoflurane was alternated between 0.3% and 1.3%, and the AEP determined at each torso concentration. RESULTS: At isoflurane 0.3% delivered to the torso, the peak-to-trough amplitude of the mid-latency AEP waves designated as N14/P24 was 0.337+/-0.185 microV and the N36 wave amplitude was 0.115+/-0.054 microV. When torso isoflurane was 1.3%, these waves decreased to 0.297+/-0.186 microV and 0.066+/-0.037 microV, respectively (P<0.05). The latency of the N14 wave increased slightly (from 13.7+/-2.6 msec to 14.4+/-2.8 msec, P<0.05) but the latencies of the other waves were unchanged. CONCLUSIONS: Isoflurane action in the spinal cord indirectly alters the AEP, however, the effect is small. These data suggest that isoflurane can depress the transmission of afferent information from the spinal cord to thalamus, midbrain and cerebral cortex.

Anesthetics, Inhalation↗
PubMed1999

Caffeine- or halothane-induced contractures of masseter muscle are similar to those of vastus muscle in normal humans.

BACKGROUND: Skinned fibers from normal human masseter muscle have greater caffeine and calcium sensitivity than skinned fibers from vastus muscle. We examined sensitivity to caffeine and halothane in fresh, cut muscle bundles (non-skinned) from human masseter muscle. METHODS: Masseter bundles (caffeine, n=25, halothane, n=19) excised from 10 humans under general anesthesia had tension measured in 37 degrees C baths during the addition of caffeine (0.5, 1, 2, 4, 8, 32 mM) or 3% halothane. Results were compared to those of our previous studies (1989, 1997, 25 patients) of vastus bundles (caffeine, n=71, halothane, n=63) using the same protocol, technicians, and equipment. RESULTS: Baseline force in the caffeine test was 2.10+/-1.57 for masseter, and 2.02+/-1.68 and 1.82+/-1.29 respectively for vastus muscle. Force at 32 mM caffeine concentration was 11.2+/-9.9 g for masseter, 11.0+/-5.4 and 13.5+/-7.5 g for vastus. Concentration-response curves were virtually identical. In the halothane group, neither baseline values (masseter 1.47+/-1.30, vastus 1.91+/-1.32 and 2.15+/-1.71) nor contractures in response to 3% halothane were different. Most bundles had no contracture in response to 3% halothane; 3 masseter bundles and 2 vastus bundles (1989) developed contractures of less than 0.05 g. Three vastus bundles (1997) developed contractures >0.2 g. CONCLUSION: Contracture responses of intact cut masseter and vastus bundles (non-skinned) do not differ with respect to caffeine and halothane. Responses of skinned fibers might demonstrate greater sensitivity under certain conditions, but they do not reflect those of intact cut bundles.

Aged↗