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T Kushikata

Publications and source records attributed to T Kushikata.

At least 37 records · Page 2Linked to original sources
PubMed2000

Interleukin-13 and transforming growth factor-beta1 inhibit spontaneous sleep in rabbits.

Proinflammatory cytokines, including interleukin-1beta and tumor necrosis factor-alpha are involved in physiological sleep regulation. Interleukin (IL)-13 and transforming growth factor (TGF)-beta1 are anti-inflammatory cytokines that inhibit proinflammatory cytokines by several mechanisms. Therefore, we hypothesized that IL-13 and TGF-beta1 could attenuate sleep in rabbits. Three doses of IL-13 (8, 40, and 200 ng) and TGF-beta1 (40, 100, and 200 ng) were injected intracerebroventricularly 3 h after the beginning of the light period. In addition, one dose of IL-13 (200 ng) and one dose of TGF-beta1 (200 ng) were injected at dark onset. The two higher doses of IL-13 and the highest dose of TGF-beta1 significantly inhibited spontanenous non-rapid eye movement sleep (NREMS) when they were given in the light period. IL-13 also inhibited NREMS after dark onset administration; however, the inhibitory effect was less potent than that observed after light period administration. The 40-ng dose of IL-13 inhibited REMS duration during the dark period. TGF-beta1 administered at dark onset had no effect on sleep. These data provide additional evidence for the hypothesis that a brain cytokine network is involved in regulation of physiological sleep.

Animals↗
PubMed1999

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.

Anesthesia↗
PubMed1999

Effects of ketamine and pentobarbital on noradrenaline release from the medial prefrontal cortex in rats.

PURPOSE: To determine the effects of ketamine and pentobarbital on noradrenaline release from the medial prefrontal cortex. METHODS: In 14 male Wistar rats, a microdialysis probe with a 2 mm long semipermeable membrane was implanted in the medial prefrontal cortex. The dialysis probe was perfused at a rate of 1 microl x min(-1) with an artificial cerebrospinal fluid solution. The rats were randomly allocated to two groups: ketamine (group K, n=7) and pentobarbital (group P, n=7). Each rat was subsequently given 0 (saline), 1, 10 and 100 mg x kg(-1) ketamine i.p. in group K, and 0 (saline), 0.5, 5 and 50 mg x kg(-1) pentobarbital i.p. in group P. Sixty minutes elapsed between administration. Noradrenaline concentration was measured by HPLC with an electrochemical detector at 20 min intervals. (detection limit: 250 fg x 20 microl(-1), coefficient variation of the assay: 4.9%). The data in the 20-40 min after each dose of ketamine or pentobarbital i.p. were used for the statistical analysis. RESULTS: Noradrenaline release after 100 mg x kg(-1) ketamine increased by 7.7 +/- 2.0 (SEM) pg x collection(-1) compared with 2.7 +/- 0.7, 3.3 +/- 1.0 and 4.2 +/- 0.8 pg x collection(-1) after saline, 1 and 10 mg x kg(-1) ketamine, respectively (P < 0.05). Noradrenaline release did not change after pentobarbital. CONCLUSION: This study suggests the ketamine and pentobarbital have different effects on noradrenergic neurons in the medial prefrontal cortex. The stimulating effect of ketamine on noradrenaline release from the cortex might contribute to unique clinical features of ketamine anesthesia.

Adjuvants, Anesthesia↗
PubMed1999

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.

Animals↗
PubMed1999

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.

Analysis of Variance↗
PubMed1999

Inhibitory effect of clonidine on ketamine-induced norepinephrine release from the medial prefrontal cortex in rats.

We have investigated the effect of clonidine on ketamine-induced norepinephrine release from the medial prefrontal cortex in rats using microdialysis. Twenty-one male Wistar rats weighing 200-300 g were allocated randomly to one of four groups: i.p. injection of ketamine 100 mg kg-1 with clonidine 0 (saline: group C0, n = 6), 3 (group C3, n = 5), 30 (group C30, n = 5) and 300 micrograms kg-1 (group C300, n = 5). As reported previously, ketamine increases norepinephrine release. In groups C0 and C3, marked increases in norepinephrine release were observed with maximum values of mean 483 (SEM 55)% and 412 (53)% compared with basal values, respectively. Although significant increases in norepinephrine release were also observed (276 (43)%) in group C30, they were significantly lower than those in groups C0 and C3 (P < 0.01 and P < 0.05, respectively). In group C300, there was a significant reduction in norepinephrine release (62 (13)%) compared with basal and the three other groups (P < 0.01). This inhibitory effect of clonidine on norepinephrine may be related to reduction in undesirable emergence reactions after ketamine anaesthesia.

Adrenergic alpha-Agonists↗
PubMed1999

Brain-derived neurotrophic factor enhances spontaneous sleep in rats and rabbits.

Various growth factors are involved in sleep regulation. Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family; it and its receptors are found in normal brain. Furthermore, cerebral cortical levels of BDNF mRNA have a diurnal variation and increase after sleep deprivation. Therefore, we investigated whether BDNF would promote sleep. Twenty-four male Sprague-Dawley rats (320-380 g) and 25 male New Zealand White rabbits (4.5-5.5 kg) were surgically implanted with electroencephalographic (EEG) electrodes, a brain thermistor, and a lateral intracerebroventricular cannula. The animals were injected intracerebroventricularly with pyrogen-free saline and, on a separate day, one of the following doses of BDNF: 25 or 250 ng in rabbits; 10, 50, or 250 ng in rats. The EEG, brain temperature, and motor activity were recorded for 23 h after the intracerebroventricular injections. BDNF increased time spent in non-rapid eye movement sleep (NREMS) in rats and rabbits and REMS in rabbits. Current results provide further evidence that various growth factors are involved in sleep regulation.

Animals↗
PubMed1999

Nuclear factor-kappaB-like activity increases in murine cerebral cortex after sleep deprivation.

Several well-defined sleep regulatory substances, e.g., interleukin-1beta, activate the heterodimeric transcription factor nuclear factor-kappaB (NF-kappaB). Several substances that inhibit sleep, e.g., interleukin-4, inhibit NF-kappaB activation. NF-kappaB activation promotes production of several additional substances thought to be involved in sleep regulation, e.g., nitric oxide. We investigated, therefore, whether there are diurnal rhythms of NF-kappaB activation in brain and changes in the activation after sleep deprivation. Mice were kept on a 12:12-h light-dark cycle. In one experiment, groups of mice were killed every 3 h across the 24-h cycle. In another experiment, mice were killed at 1500 after 6 h of sleep deprivation, and a group of control mice were killed at the same time. Nuclear proteins were extracted from each brain tissue sample, and NF-kappaB-like activity was determined with an electrophoretic mobility shift assay. In cerebral cortex, but not other areas of brain, there was a diurnal rhythm in NF-kappaB-like activation; highest levels were found during the light period. NF-kappaB-like activation was higher in cerebral cortex after sleep deprivation compared with values obtained from control mice. The results are consistent with the hypothesis that sleep regulation involves multiple gene events, some of which include enhanced production of sleep regulatory substances, the actions of which involve NF-kappaB activation.

Animals↗
PubMed1998

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.

Animals↗
PubMed1998

Epidermal growth factor enhances spontaneous sleep in rabbits.

Several growth factors are implicated in sleep regulation. Epidermal growth factor (EGF) is found in the brain, and it influences the production of several sleep-promoting substances. We determined, therefore, whether administration of exogenous EGF affected spontaneous sleep in rabbits. Twenty-five rabbits were implanted with electroencephalographic electrodes, a brain thermistor, and an intracerebroventricular guide cannula. Three doses of EGF (0.5, 5, and 25 microg) were used. The animals were injected intracerebroventricularly with saline as control and one dose of EGF on 2 separate days. Five and twenty-five micrograms of EGF enhanced non-rapid eye movement sleep and increased brain temperature. The 25-microg dose of EGF also inhibited rapid eye movement sleep across the 23-h postinjection recording period. Results are consistent with the hypothesis that EGF, like other growth factors, could be involved in sleep regulation.

Animals↗
PubMed1998

Interleukin-4 inhibits spontaneous sleep in rabbits.

Proinflammatory cytokines, including interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha, are involved in sleep regulation. IL-4 is an antiinflammatory cytokine that inhibits proinflammatory cytokine production. The hypothesis that IL-4 should attenuate sleep was studied by determining the effects of IL-4 on rabbit spontaneous sleep. Thirty-six rabbits were used. Four doses of IL-4 (0.25, 2.5, 25, and 250 ng) were injected intracerebroventricularly during the rest (light) period. One dose of IL-4 (25 ng) was injected during the active (dark) cycle. Appropriate time-matched control injections of saline were done in the same rabbits on different days. The three highest doses of IL-4 significantly inhibited spontaneous non-rapid eye movement sleep if IL-4 was given during the light cycle. The highest dose of IL-4 (250 ng) also significantly decreased rapid eye movement sleep. On the other hand, IL-4 administered at dark onset had no effect on sleep. The sleep inhibitory properties of IL-4 provide additional evidence for the hypothesis that a brain cytokine network is involved in the regulation of physiological sleep.

Alpha Rhythm↗
PubMed1998

[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.

Aged↗
PubMed1997

Measurement of bronchodilatation using a superfine fibreoptic bronchoscope.

In this study, we report the development and accuracy of a direct technique to measure airway calibre using a superfine fibreoptic bronchoscope. Ten mongrel dogs were anaesthetized with pentobarbitone and the trachea intubated with a tracheal tube; the small lumen of the tube allowed passage of a superfine fibreoptic bronchoscope (od 2.2 mm). Bronchial cross-sectional area and airway pressure were recorded continuously and dynamic pulmonary compliance and airway resistance calculated. The dogs were allocated to one of two groups. In the first group (six dogs), bronchoconstriction was induced with histamine 10 micrograms kg-1 i.v. and 500 micrograms kg-1 h-1 c.i.v. Thirty minutes later, adrenaline 0-0.4 mg kg-1 was given i.v. Bronchial cross-sectional area, dynamic pulmonary compliance and airway resistance were assessed simultaneously. In the second group, 0.9% saline was given 30 min after placement of the superfine fibreoptic bronchoscope and 10 min later atropine 0.1 microgram kg-1 was administered. In the first group, histamine decreased mean percentage bronchial cross-sectional area by 49.2 (SD 11.5) %, reduced dynamic pulmonary compliance from 32.1 (12.6) to 22.3 (5.2) ml cm H2O-1 and increased airway resistance from 39.1 (11.6) to 57.2 (10.2) cm H2O litre-1 s-1. Adrenaline produced a dose-dependent increase in percentage bronchial cross-sectional area and dynamic pulmonary compliance to 119.4 (31.3)% and 27.4 (5.5) ml cm H2O-1, respectively, and a decrease in airway resistance to 43.9 (7.2) cm H2O litre-1 s-1. There were significant correlations between percentage bronchial cross-sectional area and dynamic pulmonary compliance (r = 0.720, P < 0.0001) and airway resistance (r = 0.727, P < 0.0001). Atropine 0.1 mg kg-1 increased basal bronchial cross-sectional area to 137.5 (16.9) %. These data indicate that adrenaline reversed histamine- and pentobarbitone-induced bronchoconstriction.

Airway Resistance↗
PubMed1997

A rapid increase in foot tissue temperature predicts cardiovascular collapse during anaphylactic and anaphylactoid reactions.

BACKGROUND: Cardiovascular collapse during anaphylactic and anaphylactoid reactions results from release of histamine and other vasoactive substances. Intense arteriolar vasodilation associated with severe allergic reactions is likely to increase convective transfer of heat and peripheral tissue temperature, and finally to provoke cardiovascular collapse. Therefore the authors tested the hypothesis that during anaphylactic and anaphylactoid reactions, an acute increase in peripheral tissue temperature precedes cardiovascular collapse and that the magnitude of the increase correlates with the severity of the reaction. METHODS: During a 13-yr period, approximately 120,000 patients were screened for clinical evidence of intraoperative anaphylactic and anaphylactoid reactions. Core temperature was measured in the distal esophagus, and "deep" foot tissue temperature was measured on the sole of one foot in all these patients. Otherwise unexplained cardiovascular collapse accompanied by bronchospasm and/or cutaneous signs such as urticaria, flushing, or angioedema occurred in 32 patients who were entered into a prospective diagnostic protocol. Among these, 15 met laboratory criteria for anaphylactic or anaphylactoid reactions. Anaphylaxis was confirmed in nine of them by a positive skin test to the suspected agent, the in vitro leukocyte histamine-release test, or the Praunitz-Küstner test. Reactions were considered anaphylactoid in six others when laboratory evidence did not support anaphylaxis, but plasma histamine or tryptase concentrations were much greater during episodes than 6 weeks later. RESULTS: Development of anaphylactic and anaphylactoid reactions followed a characteristic pattern: (1) Foot temperature, which was initially 3.3 +/- 1.7 degrees C less than core temperature, increased to within 0.3 degrees C of core temperature 3.2 +/- 1.4 min after drug administration; (2) onset of cardiovascular collapse ensued 1.8 +/- 0.8 min later; and (3) core temperature increased from 34.7 +/- 1.0 degrees C to peak values 37.1 +/- 0.6 degrees C 13 +/- 5 min after drug administration. The most severe reactions were associated with shorter times to comparable core and foot temperatures, faster onset of cardiovascular collapse, and higher maximum core temperatures. CONCLUSIONS: The normal core-to-peripheral tissue temperature gradient was obliterated several minutes before hemodynamic consequences associated with anaphylactic and anaphylactoid reactions. Further, a rapid increase in deep foot temperature and maximum core temperature correlated with clinical severity.

Adolescent↗
PubMed1996

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.

Analysis of Variance↗
PubMed1996

[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.

Anesthesia↗
PubMed1995

Decreased hypothalamic prostaglandin D2 and prostaglandin E2 contents during isoflurane anaesthesia in rats.

This study was undertaken to evaluate the effect of isoflurane anaesthesia on the hypothalamic contents of both prostaglandin D2 and E2 which affect the sleep-wakefulness cycle. Sixty-three Wistar rats were divided into three equal groups, control, isoflurane and recovery groups. Twenty-one rats of the control did not receive isoflurane. In the other groups 21 rats received isoflurane 2% for 30 min and 21 received isoflurane 2% for 30 min and were allowed to recover their usual behaviours, including righting reflex, spontaneously. The hypothalamus was removed and the contents of PGD2 and PGE2 were measured by enzyme immunoassay. The PGD2 content in the hypothalamus was 397.9 +/- 226.0 pg.g-1 for the control group, 134.2 +/- 41.2 pg.g-1 for the isoflurane group and 269.1 +/- 124.6 pg.g-1 for the recovery group, respectively. The hypothalamic PGE2 contents were 381.4 +/- 139.0 pg.g-1 for the control group, 183.3 +/- 26.4 pg.g-1 for the isoflurane group and 312.2 +/- 96.0 pg.g-1 for the recovery group, respectively. The hypothalamic PGD2 and PGE2 contents in the isoflurane group were lower (P < 0.05) than those in the control and recovery groups, while both the PGD2 and PGE2 contents of the control and the recovery groups were similar. We conclude that decreased hypothalamic PGD2 and PGE2 contents may be related to some manifestations of general anaesthesia with isoflurane.

Anesthesia Recovery Period↗