Role of coerulean noradrenergic neurones in general anaesthesia in rats.

BACKGROUND: Central noradrenergic neurones have a role in alertness, analgesia, and thermoregulation; these neurones are also involved in the mechanism of anaesthesia. Locus coeruleus neurones innervate various central nervous regions including the cerebral cortex and hippocampus, and are responsible for wakefulness and analgesia. We hypothesized that these neurones are also involved in both activation of the γ-aminobutyric acid type A (GABA(A)) receptor and inhibition of N-methyl-d-aspartate (NMDA) receptor-mediated anaesthesia. METHODS: Forty-seven male rats were used to compare duration of anaesthesia before and 10 days after noradrenergic neurone depletion after intraperitoneal (i.p.) administration of N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4; 0, 5, and 50 mg kg(-1)). The animals received i.p. thiopental (GABA anaesthetic, 45 mg kg(-1)) or ketamine (NMDA anaesthetic, 100 mg kg(-1)). We also tested the effects of coerulean noradrenergic neurone depletion on i.p. ketamine analgesia (15 mg kg(-1)) using the hot-plate test in a further 21 male rats. At the end of each experiment, norepinephrine contents in the cerebral cortex and hippocampus were measured. RESULTS: I.P. DSP-4 5 and 50 mg kg(-1) significantly decreased ketamine anaesthesia duration by 12.7% and 22.4%, increased thiopental anaesthesia duration by 10.8% and 24.5%, and reduced ketamine-increased hot-plate latency by 55.2% and 68.1%, respectively. In addition, i.p. DSP-4 5 and 50 mg kg(-1) significantly reduced norepinephrine contents in coerulean brain regions by ∼20% and ∼75%, respectively. There were significant correlations between norepinephrine contents in coerulean brain regions and anaesthesia durations and ketamine analgesia. CONCLUSIONS: The present data indicate that coerulean noradrenergic neurones may be responsible for both GABA- and NMDA-mediated anaesthetic actions.

Changes in plasma orexin A during propofol-fentanyl anaesthesia in patients undergoing eye surgery.

BACKGROUND: Central orexinergic and noradrenergic neurones are involved in the control of sleep and wakefulness. In addition, previous reports suggest that both neurones may have an important role to play in general anaesthesia. In the present study, we have determined whether general anaesthesia would affect plasma orexin A (OXA) and norepinephrine concentrations. METHODS: Twenty-two patients undergoing elective ophthalmic surgery under general anaesthesia with propofol, fentanyl, and vecuronium were studied. Arterial blood was collected before and 1 and 2 h after induction of anaesthesia and at emergence to measure plasma OXA, propofol, norepinephrine, and epinephrine concentrations. During anaesthesia, the propofol infusion rate was changed to maintain the bispectral index between 40 and 50. RESULTS: Plasma OXA and norepinephrine did not change during anaesthesia but significantly increased after emergence compared with pre-anaesthesia [from 19.9 (sd 3.2) to 28.3 (4.3) pM, P<0.01, and from 1351 (146) to 1798 (251) pM, P<0.05, respectively]. Plasma epinephrine did not change. There was a significant correlation between plasma OXA and norepinephrine (P<0.05) and also between plasma propofol and OXA (P<0.05) and norepinephrine (P<0.01). CONCLUSIONS: We found that plasma OXA and norepinephrine significantly increased during emergence from propofol-fentanyl anaesthesia.

Isoflurane increases norepinephrine release in the rat preoptic area and the posterior hypothalamus in vivo and in vitro: Relevance to thermoregulation during anesthesia.

General anesthetics modulate autonomic nervous system function including thermoregulatory control, which resides in the preoptic area of the anterior hypothalamus. However, the mechanism by which anesthetics modulate hypothalamic function remains unknown. We hypothesized that isoflurane increases norepinephrine release in the preoptic area and in the posterior hypothalamus causing hypothermia during anesthesia. To test this hypothesis, we performed a series of in vivo and in vitro studies in rats. In vivo studies: 1) Norepinephrine release was measured by microdialysis in the preoptic area or the posterior hypothalamus (n=9 each) before, during (30 min), and after (50 min) rats were anesthetized with 2% isoflurane. 2) In five rats, blood gases and arterial pressure were measured. 3) Body temperature changes (n=6 each) were measured after prazosin (0, 0.05, 0.5 microg), norepinephrine (0, 0.1, 1.0 microg), or 0.5 microg prazosin with 1.0 microg norepinephrine injection into the preoptic area. In vitro study: Norepinephrine release was measured from anterior or posterior hypothalamic slices (n=10 each) incubated with 0, 1, 2, or 4% isoflurane in Ca2+-containing buffer or with 4% isoflurane (n=10) in Ca2+-free buffer. Data were analyzed with repeated measures or factorial ANOVA and Student-Newman-Keuls tests. P<0.05 was significant. During anesthesia, norepinephrine release in the preoptic area was increased approximately 270%, whereas the release in the posterior hypothalamus remained unchanged. During emergence, posterior hypothalamic norepinephrine release increased by approximately 250% (P<0.05). Rectal temperature changes correlated with norepinephrine release from the preoptic area. Norepinephrine in the preoptic area enhanced isoflurane-induced hypothermia, while prazosin reversed it. Norepinephrine release from anterior hypothalamic slices increased at all isoflurane concentrations, but only at the highest concentration in posterior hypothalamic slices. Under Ca2+-free conditions, 4% isoflurane increased norepinephrine from both regions. These results suggest that augmentation of norepinephrine release in the preoptic area is responsible for hypothermia during general anesthesia.

Interleukin-10 inhibits spontaneous sleep in rabbits.

Proinflammatory cytokines, including interleukin-1beta(IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) are involved in sleep regulation. IL-10 is an anti-inflammatory cytokine that inhibits proinflammatory cytokine production. We hypothesized that IL-10 could attenuate sleep. Thirty-one male rabbits were used. Three doses of IL-10 (5 ng, 50 ng, and 250 ng) were injected intracerebroventricularly during the rest (light) period. One dose of IL-10 (250 ng) was injected during the active (dark) cycle. Appropriate time-matched control injections of saline were given to the same rabbits on different days. The two highest doses of IL-10 significantly inhibited spontaneous nonrapid eye movement sleep if IL-10 was given during the light cycle. The highest dose of IL-10 (250 ng) also significantly decreased rapid eye movement sleep. IL-10 administered at dark onset had no effect on sleep. The sleep inhibitory properties of IL-10 provide additional evidence for the hypothesis that a brain cytokine network is involved in regulation of physiologic sleep.

Orexinergic neurons and barbiturate anesthesia.

Orexins (OXs) regulate sleep with possible interactions with brain noradrenergic neurons. In addition, noradrenergic activity affects barbiturate anesthesia. As we have also recently reported that OXs selectively evoke norepinephrine release from rat cerebrocortical slices we hypothesized that barbiturate anesthesia may result from of an interaction with central orexinergic systems. To test this hypothesis, we performed a series of in vivo and in vitro studies in rats. In vivo, the effects of i.c.v. OX A, B and SB-334867-A (OX1 receptor antagonist) on pentobarbital, thiopental or phenobarbital-induced anesthesia times (loss of righting reflex) was assessed. In vitro effects of barbiturates and SB-334867-A on OX-evoked norepinephrine release from cerebrocortical slice was examined. In Chinese hamster ovary cells expressing human OX1/OX2 receptors OX A- and B-evoked increases in intracellular Ca2+ were measured with and without barbiturates. OX A and B significantly decreased pentobarbital, thiopental and phenobarbital anesthesia times by 15-40%. SB-334867-A increased thiopental-induced anesthesia time by approximately by 40%, and reversed the decrease produced by OX A. In vitro, all anesthetic barbiturates inhibited OX-evoked norepinephrine release with clinically relevant IC50 values. A GABAA antagonist, bicuculline, did not modify the inhibitory effects of thiopental and the GABAA agonist, muscimol, did not inhibit norepinephrine release. In addition there was no interaction of barbiturates with either OX1 or OX2 receptors. Collectively our data suggest that orexinergic neurons may be an important target for barbiturates, and GABAA, OX1 and OX2 receptors may not be involved in this interaction.

Orexin A and B evoke noradrenaline release from rat cerebrocortical slices.

1. Orexin A and B, recently identified in the rat hypothalamus are endogenous neuropeptide agonists for the G-protein coupled orexin-1 (OX1) and orexin-2 (OX2) receptors. 2. In the present study, we have examined the effects of orexin A, B and raised extracellular K(+) on noradrenaline release from the rat cerebrocortical slice. We have compared this with other sleep-wake-related (excitatory) neurotransmitters; dopamine, glutamate, serotonin and histamine. 3. Neurotransmitter release studies were performed in rat cerebrocortical slices incubated in modified Krebs buffer (with and without Ca(2+)+EGTA 1 mM) with various concentrations of orexin A, B and K(+) for various times. 4. Orexin A and B-evoked (10(-7) M) noradrenaline release was time-dependent reaching a maximum some 10 min after stimulation. K(+) (40 mM) evoked release was also time dependent but reached a maximum after 6 min. Orexin A, B and K(+) stimulation of release was concentration dependent with pEC(50) and E(max) (% of basal) values of 8.74+/-0.32 (1.8 nM) and 263+/-14% and 8.61+/-0.38 (2.4 nM) and 173+/-7% and 1.43+/-0.02 (37 mM) and 1430+/-70%, respectively. Orexin-evoked release was partially extracellular Ca(2+) dependent. 5. Of the other transmitters studied there was a weak orexin A and B stimulation of glutamate release. In contrast K(+) evoked dopamine, glutamate, histamine and serotonin release with pEC(50) and E(max) (% of basal) values of 1.47+/-0.05 (34 mM) and 3430+/-410%, 1.38+/-0.04 (42 mM) and 1240+/-50%, 1.47+/-0.02 (34 mM) and 480+/-10% and 1.40+/-0.05 (40 mM) and 560+/-60% respectively. 6. We conclude that the neuropeptides orexin A and B evoke noradrenaline release from rat cerebrocortical slices.

Effects of sedatives on noradrenaline release from the medial prefrontal cortex in rats.

RATIONALE: N-Methyl-d-aspartate (NMDA) receptor antagonism and GABA(A) receptor activation are believed to be critical targets for general anesthetic action. However, as NMDA antagonism of intravenous anesthetic agents causes post-anesthetic emergence reactions such as hallucination and agitation, while the GABA(A)-mimetic intravenous anesthetic agents do not, these two classes of intravenous anesthetic agents produce differential clinical profiles. OBJECTIVE: We have investigated the differential effects of the GABA(A) agonists propofol and midazolam and the NMDA antagonist ketamine on noradrenaline release from the medial prefrontal cortex of the rat using microdialysis, as noradrenergic neurons have a role to play in anesthesia and are known to be important in the control of sleep, attention and learning. METHODS: Twenty-one male Wistar rats (200-270 g) were randomly allocated into three groups: ketamine 100 mg x kg(-1) (n = 6), propofol 60 mg x kg(-1) (n = 8) and midazolam 5 mg x kg(-1) (n = 7) IP. A unilateral guide cannula was implanted stereotaxically into the medial prefrontal cortex under pentobarbital anesthesia (50 mg x kg(-1) IP). Forty-eight hours later, a dialysis probe was inserted through the guide cannula, and perfused with an artificial cerebrospinal fluid solution containing 1 mM pargyline. Following an equilibration period, samples of dialysate were collected every 10 min. Noradrenaline content was measured by high-performance liquid chromatography using an electrochemical detector. RESULTS: Anesthesia times, defined as the duration between the loss of righting reflex and recovery, were 24.7+/-5.6 (SEM), 20.5+/-1.9 and 25.2+/-1.5 min for propofol, midazolam and ketamine, respectively (no significant between-group differences). Both GABA(A )agonists, propofol and midazolam, significantly decreased noradrenaline release (75% and 71% of basal release, respectively). The NMDA antagonist ketamine markedly increased noradrenaline release (413% of basal). CONCLUSION: These data suggest that different clinical profiles observed with these two classes of sedatives may result from changes in noradrenaline release from the medial prefrontal cortex.

Physostigmine antagonizes ketamine-induced noradrenaline release from the medial prefrontal cortex in rats.

Physostigmine is known to antagonize ketamine anesthesia. In this study, effects of physostigmine (0.1 mg kg(-1) i.p.) on ketamine (100 mg kg(-1) i.p.)-induced anesthesia time and noradrenaline release from the medial prefrontal cortex in rats were examined. Ketamine produced anesthesia for 27+/-1 min and increased noradrenaline release to 405% of the basal. Physostigmine significantly reduced anesthesia time to 23+/-1 min (p<0.05), and noradrenaline to 248% (p<0.05). Therefore, noradrenaline release may play an important role in ketamine anesthesia.

Effects of two volatile anesthetics (sevoflurane and halothane) on the hypothalamic noradrenaline release in rat brain.

There are marked increases in noradrenaline (NA) release during emergence from general anesthesia induced with volatile anesthestics. These changes in NA in the posterior hypothalamus of the rat were assessed by intracranial microdialysis. Sevoflurane and halothane in equipotent concentrations were used to obtain the same depth of anesthesia. NA release increased similarly with the two agents during recovery. However, NA release remained elevated longer with halothane, from which recovery was also slower.

An interleukin-1 receptor fragment blocks ambient temperature-induced increases in brain temperature but not sleep in rabbits.

The effects of intracerebroventricular injection (i.c.v.) of an interleukin-1 (IL-1) inhibitor, a soluble IL-1 receptor fragment (IL-1RF), on sleep and brain temperature (Tbr) responses of rabbits induced by mild increases in ambient temperature (Tamb) were determined. Each rabbit was recorded under three conditions: (1) 21 degrees C Tamb plus pyrogen-free saline (PFS); (2) 27 degrees C Tamb plus PFS; (3) 27 degrees C Tamb plus the IL-1RF. The higher Tamb significantly increased Tbr during the warming period; this effect was attenuated by pretreatment with the IL-1RF. The higher Tamb alone (6 h exposure) significantly increased non-rapid eye movement sleep (NREMS) across the 23-h recording period. However, during the 6-h warming period NREMS values, obtained after IL-1 RF treatment, were not significantly different from those obtained from PFS-treated animals at 27 degrees C Tamb. The ability of the IL-1 RF to block Tamb-induced changes in Tbr and the failure of the IL-1RF to block Tamb-induced NREMS responses is different from previous results which indicated that a tumor necrosis factor receptor fragment (TNF-RF) inhibits warm Tamb-induced sleep but not Tbr responses. Thus, brain IL-1 and TNF sleep and thermo mechanisms are, in part, different.

Barbiturates inhibit K(+)-evoked noradrenaline and dopamine release from rat striatal slices--involvement of voltage sensitive Ca(2+) channels.

The cellular target site(s) for anaesthetic action remain unclear. In rat striatal slices we have previously demonstrated that K(+)-evoked noradrenaline (NA) and dopamine (DA) release is mediated predominantly via P/Q-type voltage sensitive Ca(2+) channels (VSCC). Using this model of Ca(2+) dependent transmitter release we have evaluated the effects of anaesthetic and non-anaesthetic barbiturates. Rat brain striatal slices were incubated in the absence and presence of barbiturate for 10 min at 37 degrees C. The slices were then incubated for 6 min with 40 mM KCl. All anaesthetic barbiturates produced a concentration-dependent inhibition of K(+)-evoked NA and DA release. Non-anaesthetic barbiturate, barbituric acid was ineffective. The pIC(50) for NA and DA release (thiopental: 4.90+/-0.13 and 5.00+/-0.10, pentobarbital: 4.39+/-0.07 and 4.43+/-0.14, phenobarbital: 3.85+/-0.08 and 3.59+/-0.10, respectively) correlated with lipid solubility (NA: r(2)=0.999, DA: r(2)=0.987). We therefore suggest that barbiturates inhibit catecholamine release via an interaction with P/Q VSCC further implicating this channel in anaesthetic action.

Effects of nociceptinNH2 and [Nphe1]nociceptin(1-13)NH2 on rat brain noradrenaline release in vivo and in vitro.

We have investigated the effects of nociceptin/orphanin FQ (NC) receptor agonist NCNH2 and a competitive NC receptor antagonist, [Nphe1]NC(1-13)NH2 on noradrenaline (NA) release in vivo using microdialysis in freely moving animals and in vitro from cerebrocortical slices. One nmol of NCNH2 injected into rat locus coeruleus inhibited NA release from the prefrontal cortex (E(max) 27.4+/-5.7% 30 min after injection) which was partially (33%) reversed by 100 nmol of [Nphe1]NC(1-13)NH2. In cerebrocortical slices NCNH2 inhibited NA release in a concentration-dependent manner (EC50 12 nM, E(max) 29.4%) that was reversed by [Nphe1]NC(1-13)NH2. In both preparations, [Nphe1]NC(1-13)NH2 per se was inactive. These data demonstrate an inhibition of NA release by NCNH2 in a [Nphe1]NC(1-13)NH2 sensitive manner in both in vivo brain microdialysis and in vitro cerebrocortical slices studies in rats.

Insertion of intradermal needles into painful points provides analgesia for intractable abdominal scar pain.

BACKGROUND AND OBJECTIVES: Conventional treatments are often ineffective for patients having painful abdominal scars. There are painful points in and around scar tissue. We tested the hypothesis that insertion of intradermal needles into these painful points reduces scar pain. METHODS: Patients with abdominal scar pain with painful points that is not relieved by conventional treatments were allocated to a treatment group (n = 23), a sham-treatment group (n = 23), or a control group (n = 24). In the treatment group, intradermal needles were inserted into painful points detected by a pressure threshold meter (pain < or = 2.5 kg/cm(2)). In the sham-treatment group, the same needles were inserted into nonpainful points. The needles were kept in place for 24 hours. This process was repeated 20 times over a 4-week period. Responses were evaluated before and at the end of treatment, and 4 and 26 weeks after the treatment. Continuous and lancinating pain was evaluated on a 10-cm visual analog scale. We measured the area of pain and the pressure required to initiate painful-point pain. All patients took diclofenac as needed and completed a diary of daily diclofenac consumption. RESULTS: Patients in the treatment group showed a marked reduction in all pain parameters (>70%). In contrast, analgesia was minimal in the other groups. The decreases in the pain threshold pressure correlated with the decreases in continuous and lancinating pain (r =.57 and r =.63, respectively). CONCLUSION: Our data suggest that insertion of intradermal needles into painful points is a remarkably effective treatment for intractable abdominal scar pain. Analgesia presumably results from inactivation of painful points, through a yet to be elucidated mechanism.

[Preanesthetic assessment of a patient with giant negative T waves on ECG following subarachnoid hemorrhage].

Giant negative T waves on ECG are associated with intracranial hemorrhage such as subarachnoid hemorrhage, ischemic heart disease such as subendocardial infarction, myocardial disease and others. They embarrass us in anesthetic management of urgent neurosurgical patients because of the requirement of making differential diagnosis among these diseases accompanying the ECG abnormality. An 80 year old woman undergoing radical clipping for cerebral artery aneurysm showed giant negative T waves on ECG. Although the ECG taken on admission to the hospital had been normal, huge giant negative T waves of 2 mV and QTc prolongation were detected on arrival in the operating room. Therefore, her cardiac function was evaluated by echocardiography to rule out subendocardial infarction. The echocardiogram revealed that wall motion of the left ventricle was mildly depressed, but her cardiac function was well maintained since the cardiac output was 4.1 l.min-1 and the ejection fraction was 59%. We thought that giant negative T waves were caused by subarachnoid hemorrhage and decided to perform anesthesia and surgery. Circulation during anesthesia and surgery was stable except a transient decrease in blood pressure due to massive hemorrhage during rupture of the aneurysm. We conclude that preanesthetic assessment of cardiac function by echocardiography is useful for anesthetic management of patients with giant negative T waves on ECG undergoing urgent radical operation for cerebral aneurysm.

[Possibility of rice porridge for preoperative feeding in children].

To determine the effect of rice porridge feeding before elective surgery on preoperative gastric fluid pH, volume and starvation, a prospective study was undertaken in pediatric patients. Twenty healthy children ranged in age from 5 to 12 years were allocated randomly to either a fasted or rice porridge group. The children of fasted group (control group) were allowed to take solid food until midnight before the operation. The rice porridge group (study group) patients received a small amount of rice porridge 5 hours 30 minutes before the induction of anesthesia. The patients of both groups were permitted to take clear fluid until 5 hours before the induction of anesthesia. After the induction of anesthesia, gastric fluid was aspirated through an orogastric tube. The mean gastric fluid volume was 0.43 +/- 0.32 ml.kg-1 in the control group and 0.5 +/- 0.6 ml.kg-1 in the study group. The mean gastric fluid pH was 1.43 +/- 0.27 ml.kg-1 in the control group and 1.89 +/- 0.75 ml.kg-1 in the study group. There were no significant differences between the two groups concerning the gastric fluid volume and pH. The patient of the study group complained of less hunger. Preoperative rice porridge feeding is a possible preoperative feeding for pediatric patients.

[EEG pattern during total intravenous anesthesia with droperidol, fentanyl and ketamine].

We evaluated EEG pattern during total intravenous anesthesia with droperidol, fentanyl and ketamine (DFK). Four surgical patients, ranged in age from 35 to 43, were the subjects of this study. Two male underwent oral or orthopedic surgery and the other two female patients underwent gynecological surgery. They were all free from hepato-renal dysfunction and central nervous system disorders. For the induction of anesthesia, droperidol 0.06-0.1 ml.kg-1, fentanyl 2-4 micrograms.kg-1, and ketamine 1.0-1.5 mg.kg-1 were slowly administered intravenously. A total dose of 5-15 micrograms.kg-1 of fentanyl was given intravenously with continuous infusion of ketamine 2 mg.kg-1.h-1 during the surgical procedure. The total amounts of fentanyl and ketamine administered were 4.9-22.2 micrograms.kg-1 and 240-340 mg.kg-1, respectively. We used HZI'Brain Function Monitoring system to evaluate their EEG patterns. When adequate depth of anesthesia was obtained as clinically evaluated by vital signs, theta wave pattern was dominant on the EEG tracings in any of these patients. DFK anesthesia would provide a stable anesthetic course, if those drugs are administered adequately considering vital signs including systemic blood pressure, heart rate, lacrimation and involuntary muscle movements of the face and extremities.

[Clinical study on total intravenous anesthesia with droperidol, fentanyl and ketamine--9. Control of intraoperative hypertension with diltiazem].

Intraoperative hypertension over 160 mmHg systolic and sinus tachycardia over 100 bpm are often observed during total intravenous anesthesia with droperidol, fentanyl and ketamine. Fifty-seven surgical patients who developed hypertension over 160 mmHg systolic during various operative procedures under this type of anesthesia were given diltiazem intravenously to overcome the situation. Their blood pressure and heart rate decreased soon after the administration of diltiazem. The rate pressure product was reduced significantly. Neither preoperative hypertension nor difference of doses between 5 mg and 10 mg of diltiazem had any significant relationship with hypotensive effect of intravenous diltiazem. But the higher the systolic-pressure was just before the administration of diltiazem, the more effective diltiazem was. No adverse effects with this drug was observed. We can conclude that intravenous diltiazem in a dose of 5 mg or 10 mg may be repeatedly given to overcome hypertension or sinus tachycardia during this type of anesthesia without any adverse effects.

[A case of long-term respiratory management following resection of a huge facial hemangioma].

A 49 year-old-woman was scheduled for resection of a huge hemangioma of the face and neck region. After the resection, severe edema developed on the tongue, larynx, and pharynx even leaving no space between the tracheal tube and these tissues. Prolonged respiratory management with endotracheal tube intubation was needed to maintain the upper airway for more than three weeks. Tracheostomy was performed 27 days after the operation. Two weeks later, the edema of the upper airway subsided. Thereafter her clinical course was uneventful, and she was discharged 22 days after the tracheostomy. Resection of a huge facial and neck hemangioma should be carefully managed as it can be followed by unexpected severe postoperative upper airway edema leading to suffocation.

[Clinical study on total intravenous anesthesia with droperidol, fentanyl, and ketamine--6. Effects on postoperative liver function].

We have developed a new method of total intravenous anesthesia with droperidol, fentanyl, and ketamine, and have administered it to more than 700 surgical patients. We studied whether this method of anesthesia would influence postoperative liver function or not. A total of sixty elective surgical patients were the subjects of this study. Thirty patients underwent total hysterectomy under either the total intravenous anesthesia (15 patients) or modified neurolept-anesthesia with pentazocine (15 patients). The remaining 30 patients underwent gastrectomy under either this total intravenous anesthesia (15 patients) or enflurane-N2O anesthesia (15 patients). The hepatic function was evaluated as judged by s-GOT, s-GPT, ALP, gamma-GPT and total bilirubin levels, before anesthesia and during the first to third postoperative day. The patients for gastrectomy under enflurane-N2O anesthesia had significantly increased postoperative gamma-GPT levels compared with the patients of total intravenous anesthesia. Any other variables showed no significant difference among groups. We consider that this method of total intravenous anesthesia has no adverse effects on postoperative liver function as compared with other usual anesthetic methods.

[Marked changes in the core temperature during anaphylactic shock].

Three cases of anaphylactic shock were reported in which the core temperature was measured continuously. Two core temperature thermister probes were fixed on the forehead and the sole. Temperature dissociation between the core and the periphery disappeared in a few minutes after the administration of the causative agents. The clinical signs of the anaphylactic shock such as erythema, wheal and marked hypotension also developed in a few minutes after the disappearance of temperature dissociation. Thus treatment of anaphylactic shock could be started even before the patients develop severe hypotension. This clinical study suggests that a sudden disappearance of the temperature dissociation is a incipient sign of anaphylactic shock and to monitor the core as well as the peripheral temperature is a useful method for early diagnosis and treatment of anaphylactic shock.