Biomedical subjects

V Bonhomme

Publications and source records attributed to V Bonhomme.

At least 37 records · Page 2Linked to original sources

PubMed2001

Effect of nitrous oxide on the bispectral index and the 95% spectral edge frequency of the electroencephalogram during surgery.

We studied the effect of nitrous oxide on the bispectral index and 95% spectral edge frequency of the electroencephalogram in 20 patients undergoing lumbar surgery under general anaesthesia combined with epidural administration of 5 mg morphine. Anaesthesia was induced with propofol and sufentanil, and maintained with sevoflurane in air/oxygen adjusted to keep the bispectral index between 40 and 60. One and a half hours after the start of surgery, nitrous oxide was administered in a randomised sequence of concentrations (20, 40 and 60% end-expired). Under steady-state conditions, mean (SD) bispectral index and spectral edge frequency decreased as end-tidal concentration of nitrous oxide increased, from 47.7 (4.3) and 15.6 (1.3) at 0% nitrous oxide to 39.8 (6.3) and 14.3 (1.8) at 60% nitrous oxide. A negative correlation was found between nitrous oxide concentration and bispectral index (r = -0.48; p < 0.01) and spectral edge frequency (r = -0.39; p < 0.05). We conclude that this dose-dependent decrease in bispectral index and spectral edge frequency induced by nitrous oxide may reflect the level of analgesia associated with the anaesthetic regimen.

Adult↗

PubMed2001

Neuroprotection with anaesthetic agents.

The term 'neuroprotection' is used to refer to any prophylactic measure that is initiated during the peri-ischaemic period in order to improve neuronal survival. Cell death after ischaemia has an immediate, necrotic and a delayed, apoptotic origin. The major biochemical mechanisms that are involved in this process include transmembrane ionic fluxes and intracellular calcium increase, excitotoxicity, free radical formation, peroxynitrite production, release of inflammatory mediators, mitochondrial dysfunction, cytochrome c release, and activation of caspases and transcription factors. Strategies of neuroprotection essentially impact on those biochemical pathways. The label 'neuroprotectant' requires that the therapy has basic properties that are consistent with potential mechanisms of neuroprotection, and that conclusive results are available from animal studies that can be converted into clinical benefit. The present review focuses on neuroprotective effects of anaesthetics and is based on the most recently published reports.

Journal Article↗

PubMed2001

Propofol anesthesia and cerebral blood flow changes elicited by vibrotactile stimulation: a positron emission tomography study.

We investigated the effects of the general anesthetic agent propofol on cerebral structures involved in the processing of vibrotactile information. Using positron emission tomography (PET) and the H(2)(15)O bolus technique, we measured regional distribution of cerebral blood flow (CBF) in eight healthy human volunteers. They were scanned under five different levels of propofol anesthesia. Using a computer-controlled infusion, the following plasma levels of propofol were targeted: Level W (Waking, 0 microg/ml), Level 1 (0.5 microg/ml), Level 2 (1.5 microg/ml), Level 3 (3.5 microg/ml), and Level R (Recovery). At each level of anesthesia, two 3-min scans were acquired with vibrotactile stimulation of the right forearm either on or off. The level of consciousness was evaluated before each scan by the response of the subject to a verbal command. At Level W, all volunteers were fully awake. They reported being slightly drowsy at Level 1, they had a slurred speech and slow response at Level 2, and they were not responding at all at Level 3. The following variations in regional CBF (rCBF) were observed. During the waking state (Level W), vibrotactile stimulation induced a significant rCBF increase in the left thalamus and in several cortical regions, including the left primary somatosensory cortex and the left and right secondary somatosensory cortex. During anesthesia, propofol reduced in a dose-dependent manner rCBF in the thalamus as well as in a number of visual, parietal, and prefrontal cortical regions. At Level 1 through 3, propofol also suppressed vibration-induced increases in rCBF in the primary and secondary somatosensory cortex, whereas the thalamic rCBF response was abolished only at Level 3, when volunteers lost consciousness. We conclude that propofol interferes with the processing of vibrotactile information first at the level of the cortex before attenuating its transfer through the thalamus.

Adolescent↗

PubMed2000

Tropane alkaloid production by hairy roots of Atropa belladonna obtained after transformation with Agrobacterium rhizogenes 15834 and Agrobacterium tumefaciens containing rol A, B, C genes only.

Atropa belladonna leaf disks were infected by a wild strain Agrobacterium rhizogenes 15834 harboring the Ri-TL-DNA and by a disarmed Agrobacterium tumefaciens strain harboring a construction with only rol ABC and npt II genes. Thirteen root lines were established and examined for their growth rate and alkaloid productivity to evaluate the possible role of rol genes in morphological differentiation and in tropane alkaloid formation. A great diversity has been observed in the growth rate of these 13 root lines. The root biomass increased up to 75 times. The total alkaloid contents were similar in the root lines obtained by infection with A. rhizogenes 15834 and A. tumefaciens rol ABC. The last ones accumulated between 4 (1.1 mg g(-1) DW) and 27 (8 mg g(-1) DW) times more alkaloids than the intact roots (0.3 mg g(-1) DW). This work has shown that the rol ABC genes were sufficient to increase tropane alkaloid production in A. belladonna hairy root cultures.

Agrobacterium tumefaciens↗

PubMed2000

Effects of the rol C gene on hairy root: induction development and tropane alkaloid production by Atropa belladonna.

Two series of Atropa belladonna hairy root lines were obtained, the first one transformed via Agrobacterium tumefaciens harboring rol C and npt II genes, and the other transformed with rol ABC and npt II genes. Thirteen hairy root lines were obtained and selected on hormone-free medium. The transformation was confirmed by PCR analysis, and these root lines were first examinated for their growth rate. Then hyoscyamine and scopolamine production was measured after 3 and 4 weeks of culture to evaluate the possible role of rol C gene in tropane alkaloid formation. The rol C gene alone played a significant role in the hairy root growth rate (17-fold increase). However this effect was much lower than that induced by the rol ABC genes together (75-fold increase). In contrast, the rol C gene alone was as efficient as the rol ABC genes together (mean value of total alkaloids: 0.36% dry weight, i.e., 12-fold times more than in untransformed roots) to stimulate the biosynthesis of tropane alkaloids in A. belladonna hairy root cultures.

Atropa belladonna↗

PubMed2000

Target-controlled infusion of propofol and remifentanil combined with bispectral index monitoring for awake craniotomy.

We describe the target-controlled administration of propofol and remifentanil, combined with monitoring of the bispectral index, during an awake craniotomy for removal of a left temporo-parietal tumour near the motor speech centre. Target concentrations of the two drugs were adjusted according to the patient's responses to painful stimuli and surgical events, and the need for speech testing. Allowing the effect-site concentrations of propofol and remifentanil to decrease during surgery allowed the performance of cortical speech mapping and the testing of the patient's ability to speak. Although the bispectral index was not used as a guide for the administration of the drugs, its value correlated better with the patient's responsiveness than did the predicted effect-site concentrations of propofol. Side-effects, comprising hypotension, respiratory depression and airway obstruction, were related to rapid increases in drug infusion rates and were easily managed.

Analgesia↗

PubMed2000

Auditory steady-state response and bispectral index for assessing level of consciousness during propofol sedation and hypnosis.

UNLABELLED: We assessed the effect of propofol on the auditory steady-state response (ASSR), bispectral (BIS) index, and level of consciousness in two experiments. In Experiment 1, propofol was infused in 11 subjects to obtain effect-site concentrations of 1, 2, 3, and 4 microg/mL. The ASSR and BIS index were recorded during baseline and at each concentration. The ASSR was evoked by monaural stimuli. Propofol caused a concentration-dependent decrease of the ASSR and BIS index values (r(2) = 0.76 and 0.93, respectively; P<0.0001). The prediction probability for loss of consciousness was 0.89, 0.96, and 0.94 for ASSR, BIS, and arterial blood concentration of propofol, respectively. In Experiment 2, we compared the effects of binaural versus monaural stimulus delivery on the ASSR in six subjects during awake baseline and propofol-induced unconsciousness. During baseline, the ASSR amplitude with binaural stimulation (0.47+/-0.13 microV, mean +/- SD) was significantly (P<0.002) larger than with monaural stimulation (0.35+/-0.11 microV). During unconsciousness, the amplitude was 0.09+/-0.09 microV with monaural and 0.06+/-0.04 microV with binaural stimulation (NS). The prediction probability for loss of consciousness was 0.97 (0.04 SE) for monaural and 1.00 (0.00 SE) for binaural delivery. We conclude that the ASSR and BIS index are attenuated in a concentration-dependent manner by propofol and provide a useful measure of its sedative and hypnotic effect. BIS was easier to use and slightly more sensitive. The ASSR should be recorded with binaural stimulation. The ASSR and BIS index are both useful for assessing the level of consciousness during sedation and hypnosis with propofol. However, the BIS index was simpler to use and provided a more sensitive measure of sedation. IMPLICATIONS: We have compared two methods for predicting whether the amount of propofol given to a human subject is sufficient to cause unconsciousness, defined as failure to respond to a simple verbal command. The two methods studied are the auditory steady-state response, which measures the electrical response of the brain to sound, and the bispectral index, which is a number derived from the electroencephalogram. The results showed that both methods are very good predictors of the level of consciousness; however, bispectral was easier to use.

Adolescent↗

PubMed2000

Physostigmine reverses propofol-induced unconsciousness and attenuation of the auditory steady state response and bispectral index in human volunteers.

BACKGROUND: It is postulated that alteration of central cholinergic transmission plays an important role in the mechanism by which anesthetics produce unconsciousness. The authors investigated the effect of altering central cholinergic transmission, by physostigmine and scopolamine, on unconsciousness produced by propofol. METHODS: Propofol was administered to American Society of Anesthesiologists physical status 1 (n = 17) volunteers with use of a computer-controlled infusion pump at increasing concentrations until unconsciousness resulted (inability to respond to verbal commands, abolition of spontaneous movement). Central nervous system function was assessed by use of the Auditory Steady State Response (ASSR) and Bispectral Index (BIS) analysis of electrooculogram. During continuous administration of propofol, reversal of unconsciousness produced by physostigmine (28 microgram/kg) and block of this reversal by scopolamine (8.6 microgram/kg) were evaluated. RESULTS: Propofol produced unconsciousness at a plasma concentration of 3.2 +/- 0.8 (+/- SD) microgram/ml (n = 17). Unconsciousness was associated with reductions in ASSR (0.10 +/- 0.08 microV [awake baseline 0.32 +/- 0.18 microV], P < 0.001) and BIS (55.7 +/- 8.8 [awake baseline 92.4 +/- 3.9], P < 0.001). Physostigmine restored consciousness in 9 of 11 subjects, with concomitant increases in ASSR (0.38 +/- 0.17 microV, P < 0.01) and BIS (75.3 +/- 8.3, P < 0.001). In all subjects (n = 6) scopolamine blocked the physostigmine-induced reversal of unconsciousness and the increase of the ASSR and BIS (ASSR and BIS during propofol-induced unconsciousness: 0.09 +/- 0.09 microV and 58.2 +/- 7.5, respectively; ASSR and BIS after physostigmine administration: 0.08 +/- 0.06 microV and 56.8 +/- 6.7, respectively, NS). CONCLUSIONS: These findings suggest that the unconsciousness produced by propofol is mediated at least in part via interruption of central cholinergic muscarinic transmission.

Adolescent↗

PubMed2000

Evaluation of acute normovolemic hemodilution for surgical repair of craniosynostosis.

This clinical report investigated the potential benefit of acute normovolemic hemodilution (ANH) as a blood-saving technique in the surgical repair of craniosynostosis. Over a 4-year period, 34 healthy children undergoing surgical repair of scaphocephaly or pachycephaly were randomly assigned to two groups of 17 patients each. Patients of the first group (ANH group) were submitted to ANH (target Ht: 25%) immediately before surgery and patients of the second group (Control group) were not. During surgery, estimated blood loss was compensated with a 5% albumin solution and no autologous or homologous blood was transfused. At the end of surgery, intraoperative blood loss (mean +/- SD) calculated on the basis of the Ht value and the children weight was 21.3+/-8% of the estimated blood volume (EBV) in the ANH group and 24+/-6.6% in the Control group. Children of the ANH group received their autologous blood (18.9+/-3.3% of EBV) systematically at the end of surgery. In the postoperative period, homologous blood was transfused when the Ht value was equal or less than 21%. Both groups were comparable regarding age, weight, type of craniosynostosis, duration of surgery, EBV, and preoperative Ht value. No difference was observed between ANH and Control groups in the number of patients who received homologous blood (15/17 and 14/17, respectively), in the amount of homologous blood transfused (17+/-4.7% and 19.6+/-6.3% of the EBV, respectively), and in the Ht value before hospital discharge (29.4+/-5.0% and 30.7+/-4.9%, respectively). In conclusion, this report suggests that ANH reduces neither the incidence of homologous transfusion nor the amount of homologous blood transfused in this series of children undergoing surgical repair of craniosynostosis.

Albumins↗

PubMed2000

Effects of mild hypothermic cardiopulmonary bypass on EEG bispectral index.

We studied the effect of mild hypothermic cardiopulmonary bypass (30 degrees C) on the EEG Bispectral Index in 10 patients undergoing elective CABG. BIS was recorded at 11 event-related time points during the procedure. After a significant decrease at the induction of anaesthesia, BIS was not further modified during the procedure. BIS was neither affected by surgical stimulation nor by CPB and mild hypothermia. We conclude that we did not find any reason to preclude the use of BIS to assess the hypnotic effects of anaesthetics during normothermic or mild hypothermic CPB.

Aged↗

PubMed1999

Brain mechanisms of propofol-induced loss of consciousness in humans: a positron emission tomographic study.

In the present study, we used positron emission tomography to investigate changes in regional cerebral blood flow (rCBF) during a general anesthetic infusion set to produce a gradual transition from the awake state to unconsciousness. Five right-handed human volunteers participated in the study. They were given propofol with a computer-controlled infusion pump to achieve three stable levels of plasma concentrations corresponding to mild sedation, deep sedation, and unconsciousness, the latter defined as unresponsiveness to verbal commands. During awake baseline and each of the three levels of sedation, two scans were acquired after injection of an H215O bolus. Global as well as regional CBF were determined and correlated with propofol concentrations. In addition, blood flow changes in the thalamus were correlated with those of the entire scanned volume to determine areas of coordinated changes. In addition to a generalized decrease in global CBF, large regional decreases in CBF occurred bilaterally in the medial thalamus, the cuneus and precuneus, and the posterior cingulate, orbitofrontal, and right angular gyri. Furthermore, a significant covariation between the thalamic and midbrain blood flow changes was observed, suggesting a close functional relationship between the two structures. We suggest that, at the concentrations attained, propofol preferentially decreases rCBF in brain regions previously implicated in the regulation of arousal, performance of associative functions, and autonomic control. Our data support the hypothesis that anesthetics induce behavioral changes via a preferential, concentration-dependent effect on specific neuronal networks rather than through a nonspecific, generalized effect on the brain.

Adult↗

PubMed1998

Effect of isoflurane on the auditory steady-state response and on consciousness in human volunteers.

BACKGROUND: The auditory steady state response (ASSR) is a sustained electrical response of the brain to auditory stimuli delivered at fast rates (30-50 responses/s). The aim of this study was to evaluate the effect of 0.26-0.50% isoflurane on the ASSR and on consciousness, defined as responsiveness to verbal commands. METHODS: Ten volunteers (21-31 yr) participated. Isoflurane was administered at three stable, end-tidal concentrations: 0.26%, 0.38%, and 0.50%. The ASSR in response to 18,000 stimuli (500-Hz tonebursts, 10 ms, 82-dB, the right ear, 35-45 bursts/s) was recorded from the vertex with reference to the right mastoid. Recordings were made during baseline, at each isoflurane concentration, and during recovery. RESULTS: The mean (SD) ASSR amplitudes were 0.32 (0.23) microV during baseline, 0.24 (0.17) microV during 0.26% isoflurane, 0.09 (0.05) microV during 0.38% isoflurane, 0.04 (0.03) microV during 0.50% isoflurane, and 0.29 (0.33) microV during recovery. The amplitude during baseline and recovery was larger than during 0.38% and 0.50% isoflurane (P < 0.001). The amplitude at 0.26% was larger than at the other concentrations (P < 0.025). The logarithm of the ASSR amplitude was related linearly to the concentration of isoflurane (r = 0.85; P < 0.0001). The prediction probability (Pk) for loss of consciousness was 0.95 for both ASSR and measured isoflurane concentration. An ASSR amplitude < 0.07 microV was always associated with unconsciousness. CONCLUSIONS: The ASSR is attenuated in a concentration-dependent manner by isoflurane. Suppression of consciousness and maximal attenuation of ASSR occur in the same isoflurane concentration range. Profound attenuation of ASSR appears to reflect unconsciousness, defined as unresponsiveness to verbal commands.

Acoustic Stimulation↗

PubMed1997

Ketamine increases the amplitude of the 40-Hz auditory steady-state response in humans.

The auditory middle latency response (AMLR) and the 40-Hz auditory steady-state response (40-Hz ASSR) are evoked potentials which possibly arise from the same generators in the primary auditory cortex. Both responses are attenuated by most general anaesthetics. Ketamine, however, has been reported to have no effect on the AMLR. Our aim was to evaluate the effects of ketamine on the 40-Hz ASSR. Spectral analysis of the electroencephalogram (EEG) was also conducted to independently examine the effects of ketamine. Ketamine 1.5 mg kg-1 was given to 12 patients for induction of general anaesthesia. Recordings of the 40-Hz ASSR and EEG were obtained every minute from 3 min before administration of ketamine to 5 min after injection, when the study was terminated. Similar recordings were obtained in three control subjects under identical conditions except that no medication was administered. Consciousness, defined as responsiveness to verbal commands, was assessed before each recording. Ketamine caused an increase in the amplitude of the 40-Hz ASSR (P < 0.01). Using published AMLR data, we conducted a simulation experiment that suggested that the effect of ketamine on the AMLR can explain its effects on the amplitude of the 40-Hz ASSR. There was a pronounced increase in relative theta (3.9-7.9 Hz) EEG power and a decrease in relative alpha (8.0-12.8 Hz) power (P < 0.001). These changes were not observed in the control group. Ketamine produced unconsciousness until the end of the study in five patients and transient unconsciousness in five patients. Two patients did not lose consciousness after administration of ketamine. The 40-Hz ASSR and EEG revealed no consistent differences between conscious and unconscious patients. No relationship could be demonstrated between the increase in amplitude of the 40-Hz ASSR or of relative theta power (the hallmark of ketamine effect) and loss of responsiveness to commands. We conclude that ketamine, unlike other anaesthetics, increases the amplitude of the 40-Hz ASSR.

Acoustic Stimulation↗

PubMed1995

Effect of plasma anticonvulsant level on pipecuronium-induced neuromuscular blockade: preliminary results.

Patients receiving anticonvulsants are resistant to nondepolarizing muscle relaxants (NDMR). This study examines the effect of plasma anticonvulsant levels on pipecuronium-induced neuromuscular blockade. Twenty adult patients scheduled for neurosurgery were assigned to one of two groups. Group 0 (G0) consisted of 10 patients not on anticonvulsant therapy; group 1 (G1) included 10 patients treated either with phenytoin or carbamazepine. G1 patients were further divided into G1u (n = 4) and G1w (n = 6) subgroups, according to the plasma anticonvulsant level measured the day before surgery--under (G1u) or within (G1w) the therapeutic range. Neuromuscular transmission was monitored with a Biometer International A/S Accelograph. Anesthesia was induced and maintained using propofol and sufentanil. After calibration of the accelograph, a bolus of pipecuronium 0.08 mg/kg was given IV. The time from pipecuronium injection to the peak reduction of T1 was taken as the onset time. The time in min from pipecuronium injection to recovery of T1% (first accelograph response/baseline response) x 100 and TR% (fourth accelograph response/first accelograph response) x 100 were recorded at 25, 50, and 75% of baseline. The recovery index (RI) was taken as the time from 25 to 75% of baseline. The recovery index (RI) was taken as the time from 25 to 75% recovery of the baseline response. The onset time was not different in G0 (203 +/- 60.4 s), G1 (230.5 +/- 79.3 s), and G1u (181.8 +/- 60.4 s) but prolonged in G1w (279.2 +/- 67.7 s).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Propofol protects cultured rat hippocampal neurons against N-methyl-D-aspartate receptor-mediated glutamate toxicity.

The effect of propofol on the toxicity induced by glutamate (GLU), N-methyl-D-aspartate (NMDA), kainate (KA), and amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) was investigated on cultured fetal rat hippocampal neurons. The degree of neuronal injury was quantified by measuring the release of the neuron-specific enolase (NSE) into the culture media. The toxicity induced by brief exposure to GLU (10(-4) M) or to NMDA (10(-4) M) was significantly reduced by propofol, whereas that elicited by KA, AMPA (10(-4) M), or long GLU exposure was unaffected. In conclusion, high concentrations of propofol significantly attenuate NMDA receptor-mediated glutamate neurotoxicity in vitro. Further studies are needed to confirm this beneficial effect in vivo and to evaluate propofol as a neuroprotective anesthetic agent in pathologies involving glutamate release and NMDA-mediated toxicity.

Animals↗

PubMed1994

Control of drug-resistant epilepsy after head injury with intravenous nimodipine.

The present report describes a young child who developed generalized epileptic seizures in the course of severe head injury. The start of epileptic seizures was associated with the occurrence of acute hyponatremia and hypoosmolality due to excessive Desmopressine administration. The seizures resistant to conventional therapy resolved completely with intravenous nimodipine infusion.

Brain Injuries↗

PubMed1993

Neuron-specific enolase as a marker of in vitro neuronal damage. Part I: Assessment of neuron-specific enolase as a quantitative and specific marker of neuronal damage.

Enolase in cerebrospinal fluid is a sensitive marker for many types of neurological injuries including head injury and ischemia. We assessed neuron-specific enolase (NSE) as a quantitative and specific biochemical marker of neuronal damage in an experimental model of kainate neurotoxicity. Rat hippocampal cultures were treated with various concentrations of kainate. NSE release into the culture medium was compared with neuronal death estimated either by direct cell counting or by lactate dehydrogenase (LDH) release, largely used to quantify neuronal injury. A dose-response relationship was observed between kainate concentration and the amount of NSE released (r = -0.69; p < 0.05) as well as a significant correlation between NSE release and neuronal death (r = 0.64; p < 0.05). Likewise, a significant correlation was found between LDH and NSE release (r = 0.85; p < 0.05). The specificity of NSE as an indicator of neuronal death was demonstrated using immunocyto-chemistry labeling and measurement of NSE release by pure astrocyte cultures. We concluded that NSE is a reliable, quantitative, and specific marker of neuronal injury.

Animals↗

PubMed1993

Neuron-specific enolase as a marker of in vitro neuronal damage. Part II: Investigation of the astrocyte protective effect against kainate-induced neurotoxicity.

The protective effect of astrocytes on hippocampal neurons against kainate-induced toxicity was investigated using neuron-specific enolase as an indicator of neuronal death. Astrocyte-rich and astrocyte-poor mixed rat hippocampal cultures were submitted to various concentrations of kainate. At each kainate concentration, the amount of NSE released by neurons was significantly greater in astrocyte-poor than in astrocyte-rich cultures (p < 0.05). This protective effect was not observed when neuronal survival was tested on astrocyte-poor cultures in astrocyte-conditioned culture medium with or without 10(-4) M kainate. In conclusion, astrocytes significantly attenuate kainate toxicity on hippocampal neurons, and this effect is not mediated by a diffusible factor.

Animals↗