[Airway management in a patient with Williams syndrome].

Williams syndrome is characterized by the triad of supravalvular aortic stenosis (SAS), mental retardation and elfin facies. Generally, difficult airway is expected in patients with Williams syndrome by characteristic face. A 26-year-old female with Williams syndrome was scheduled for abdominal myomectomy under general anesthesia. Difficult mask ventilation and tracheal intubation were anticipated because of micrognathia, mandibular retrusion, and a Mallanpati class III airway. Before induction of anesthesia the patient breathed 100% oxygen for 3 minutes. Anesthesia was induced and maintained with propofol, remifentanil and rocuronium bromide. Mask ventilation was easily performed. The direct laryngoscopic view was Cormack grade I and there was no difficulty in the tracheal intubation. After induction of anesthesia, anesthetic course was uneventful. According to the most previous clinical reports in patients with Williams syndrome in Japan, mask ventilation and tracheal intubation were performed easily contrary to preoperative airway assessment. In view of SAS, mental retardation, airway deformity and airway assessment in previous clinical reports, we should select the optimal strategy for airway management in patients with Williams syndrome.

[Case of severe hypokalemia during emergency surgery caused by long-term administration of Shakuyaku-kanzo-to].

An 82-year-old female underwent emergency surgery for right femoral incarcerated hernia under general anesthesia. Anesthesia was induced and maintained with remifentanil and propofol. Her laboratory data showed severe hypokalemia (1.83 mEq x l(-1)) and metabolic alkalosis (HCO3 36.9 mmol x l(-1)). We suspected that the causes of such abnormalities were due to an endocrinological abnormality, but we could not ascertain the actual cause. Drip infusion of sodium chloride and saline solution infusion, to avoid supplying lactate or acetate, the source of bicarbonate ions, were chosen for palliative treatment. No adverse event occurred during surgery. After surgery, endocrinological functions were examined. Primary aldosteronism was ruled out because serum aldosterone and rennin activity were within normal ranges. The patient had been taking a Kampo preparation, Shakuyaku-kanzo-to, for two years. Glycyrrhizin, the main component of Shakuyaku-kanzo-to, has been reported to be a cause of pseudoaldosteronism by inhibiting the enzyme converting cortisol to cortisone. With these findings we confirmed that severe hypokalemia was induced by pseudoaldosteronism by long-term administration of Shakuyaku-kanzo-to.

[Sleep and anesthesia--part 2, on the relationship between sleep and general anesthesia].

We reviewed historical and current trends on study regarding the relationship between sleep and general anesthesia. Historically, sleep has been recognized as a completely different physiological phenomenon from general anesthesia. Therefore, sleep study has been thought that it has no merit in anesthesia study. However, on the basis of recent evidence, sleep may share some part of its mechanism with general anesthesia; thus, studies focusing sleep mechanism may also contribute to elucidate some mechanism of general anesthesia. Moreover, research to solve anesthesia related-sleep disorder would be useful to improve patient's quality of life and save much medical resource.

[Sleep and anesthesia--Part 1, Recent findings in research].

We described how modern neuroscience has elucidated what is sleep and its implication, and also reviewed histological and current trends in search of sleep mechanism from view of neurocirculatory or hormonary basis studies. We conclude that anesthesia and sleep share some neuronal structure in their action and mechanism of anesthesia could be elucidated through sleep study. In addition, anesthesia-related sleep disturbance must be settled to serve satisfied quality of life of patients and to save economic and medical resources.

[Severe hypoxia during right lateral position induced by mediastinal shift].

An 87-year-old woman with osteoarthrosis of her left hip joint was scheduled for total hip arthroplasty. After induction of anesthesia the patient was put into the right lateral position for surgery. Oxygen saturation had decreased gradually and the respiratory sound of the right lung was not auscultated. Broncofiberscopic examination showed that the position of the tracheal tube was appropriate and no secretion was found. Immediately after the patient was retuned to supine, oxygenation improved and the respiratory sound of the right lung was ausculated clearly. Chest radiographs were taken in both supine and right lateral positions. The chest X-ray findings taken in the right lateral position revealed that the right lung volume was decreased remarkably due to the extreme downward-shift of the mediastinum. The operation was postponed. The right lateral chest X-ray taken during wakefulness showed that the degree of mediastinal shift was not as remarkable as during anesthesia. After 8 days, the operation was performed using the supine position. We concluded that a downward mediastinal shift induced severe right lung volume reduction in the right lateral position during anesthesia.

[Case of hemoglobinuria following glycerin enema].

A 57-year-old man with lung tumor was scheduled for right middle lobectomy under general anesthesia. The patient received glycerin enema 2 hours before anesthesia. Anesthesia was induced with propofol, fentanyl, ketamine and vecuronium. After the induction, urine of dark-red color was drained through the urinary catheter. Massive (3+) occult blood and few erythrocytes in the urine sediment were observed. Furthermore, blood analysis showed hemolysis with mild renal dysfunction (Cr 1.3 mg x dl(-1)). Although serum CPK and myoglobin increased, there was no apparent symptom that supported the onset of rhabdomyolysis induced by anesthetics, acute myocardial infarction or malignant hyperthermia. At this time, we noticed that blood sample taken before the induction had been hemolysed. With all the above information in mind, we suspected that the main cause of the hemoglobinuria could be the enema and the surgery was canceled. The patient made a good progress with laboratory data normalized on the 4th postanesthesia day. However, rectal ulcer developed as a possible late complication of the enema. Although it is well-known that glycerin enema could cause hemolysis, renal failure and rectal ulcer, the increase of CPK and myoglobin in serum made the diagnosis difficult from other conditions leading to rhabdomyolysis in this case.

Growth hormone-releasing hormone: cerebral cortical sleep-related EEG actions and expression.

Growth hormone-releasing hormone (GHRH), its receptor (GHRHR), and other members of the somatotropic axis are involved in non-rapid eye movement sleep (NREMS) regulation. Previously, studies established the involvement of hypothalamic GHRHergic mechanisms in NREMS regulation, but cerebral cortical GHRH mechanisms in sleep regulation remained uninvestigated. Here, we show that unilateral application of low doses of GHRH to the surface of the rat somatosensory cortex ipsilaterally decreased EEG delta wave power, while higher doses enhanced delta power. These actions of GHRH on EEG delta wave power occurred during NREMS but not during rapid eye movement sleep. Further, the cortical forms of GHRH and GHRHR were identical to those found in the hypothalamus and pituitary, respectively. Cortical GHRHR mRNA and protein levels did not vary across the day-night cycle, whereas cortical GHRH mRNA increased with sleep deprivation. These results suggest that cortical GHRH and GHRHR have a role in the regulation of localized EEG delta power that is state dependent, as well as in their more classic hypothalamic role in NREMS regulation.

TNFalpha siRNA reduces brain TNF and EEG delta wave activity in rats.

Tumor necrosis factor alpha (TNFalpha) is a pleiotropic cytokine with several CNS physiological and pathophysiological actions including sleep, memory, thermal and appetite regulation. Short interfering RNAs (siRNA) targeting TNFalpha were incubated with cortical cell cultures and microinjected into the primary somatosensory cortex (SSctx) of rats. The TNFalpha siRNA treatment specifically reduced TNFalpha mRNA by 45% in vitro without affecting interleukin-6 or gluR1-4 mRNA levels. In vivo the TNFalpha siRNAalpha reduced TNFalpha mRNA, interleukin-6 mRNA and gluR1 mRNA levels compared to treatment with a scrambled control siRNA. After in vivo microinjection, the density of TNFalpha-immunoreactive cells in layer V of the SSctx was also reduced. Electroencephalogram (EEG) delta wave power was decreased on days 2 and 3 on the side of the brain that received the TNFalpha siRNA microinjection relative to the side receiving the control siRNA. These findings support the hypothesis that TNFalpha siRNA attenuates TNFalpha mRNA and TNFalpha protein in the rat cortex and that those reductions reduce cortical EEG delta power. Results also are consistent with the notion that TNFalpha is involved in CNS physiology including sleep regulation.

Unilateral cortical application of interleukin-1beta (IL1beta) induces asymmetry in fos, IL1beta and nerve growth factor immunoreactivity: implications for sleep regulation.

Unilateral injection of interleukin-1 beta (IL1beta) into the somatosensory cortex enhances EEG slow wave activity ipsilaterally during non-rapid eye movement sleep [Yasuda, T., Yoshida, H., Garcia-Garcia, F., Kay, D., Krueger, J.M., 2005. Interleukin-1beta has a role in cerebral cortical state-dependent electroencephalographic slow-wave activity. Sleep 28, 177-184]. We show that a similar unilateral microinjection of IL1beta (10 ng) into layer VI or onto the surface of the primary somatosensory cortex induced increases in the neuronal activity marker, Fos, relative to the contralateral side that received saline or heat-inactivated IL1beta. When IL1beta was microinjected into layer VI, increases in Fos-immunoreactive nuclei were evident in layers II, III and VI of the somatosensory cortex and connected cortical regions, such as the endopiriform, secondary somatosensory, piriform and prefrontal cortex. Asymmetrical increases in Fos were also observed in subcortical regions, such as the reticular thalamus, which receives a main cortical projection, and hypothalamic regions implicated in sleep regulation, such as the ventrolateral preoptic area and dorsal median preoptic nucleus. Fos activation was not observed in many other brain regions. In the reticular thalamus and somatosensory cortex, the number of IL1beta-immunoreactive glial cells increased. Further, the number of NGF-immunoreactive cells in the primary somatosensory cortex and magnocellular preoptic nucleus increased on the IL1beta-injected side. These results are consistent with the hypothesis that sleep is initiated within the cortex after the local activation of specific cytokines and that whole organism sleep is coordinated via cortical connections with the subcortical sites.

State-dependent effects of light-dark cycle on somatosensory and visual cortex EEG in rats.

Somatosensory (SSctx) and visual cortex (Vctx) EEG were evaluated in rats under a 12:12-h light-dark (LD) cycle and under constant light (LL) or constant dark (DD) in each sleep or wake state. Under LD conditions during light period, relative Vctx EEG slow-wave activity (SWA) was higher than that of the SSctx, whereas during dark period, relative Vctx EEG SWA was lower than in the SSctx. These effects were state specific, occurring only during non-rapid eye movement sleep (NREMS). Under LL conditions, the duration of REMS and NREMS during the period that would have been dark if the LD cycle had continued (subjective dark period) was greater than under LD conditions. DD conditions had little effect on the duration of NREMS and REMS. SSctx and Vctx EEG SWA were suppressed by LL during the subjective dark period; however, the degree of Vctx SWA suppression was smaller than that of the SSctx. DD conditions during the subjective light period enhanced SSctx SWA, whereas Vctx SWA was suppressed. Under LL conditions during the subjective dark period, Vctx EEG power was higher than that of the SSctx across a broad frequency range during NREMS, REMS, and wakefulness. During DD, SSctx EEG power during NREMS was higher than that of the Vctx in the delta wave band, whereas SSctx power during REMS and wakefulness was higher than that of the Vctx in frequencies higher than 8 Hz. We concluded that the SSctx and Vctx EEGs are differentially affected by light during subsequent sleep. Results provide support for the notion that regional sleep intensity is dependent on prior regional afferent input.

Interleukin-1beta has a role in cerebral cortical state-dependent electroencephalographic slow-wave activity.

STUDY OBJECTIVES: To investigate the hypothesis that interleukin (IL)-1beta is involved in mediating localized electroencephalogram synchronization. DESIGN: We evaluated bilateral cortical electroencephalograms after unilateral local application of IL-1beta onto the somatosensory cortex of rats. Furthermore, we investigated the effects of unilateral application of an IL-1beta inhibitor, the IL-1 soluble receptor, on spontaneous sleep and sleep rebound after sleep deprivation. SETTING: University research laboratory. INTERVENTIONS: N/A. PARTICIPANTS: Rats. MEASUREMENTS AND RESULTS: Neither dose of IL-1beta or the IL-1 soluble receptor affected the duration of non-rapid eye movement sleep or rapid eye movement sleep. Unilateral application of IL-1beta induced state- and frequency-dependent electroencephalogram asymmetries. During non-rapid eye movement sleep, but not during other states, electroencephalographic slow-wave activity was greater on the side that received IL-1beta (10- and 50-ng doses). Electroencephalographic power in the higher frequencies was not affected by IL-1beta in any state. Unilateral application of the IL-1 soluble receptor (0.1, 1.0 and 5.0 microg) had no effect on the spontaneous sleep electroencephalogram. In contrast, unilateral application of the IL-1 soluble receptor (5.0 microg) attenuated sleep deprivation-enhanced electroencephalographic slow-wave power ipsilaterally during non-rapid eye movement sleep. CONCLUSIONS: Results suggest that IL-1beta can induce state-dependent localized increases of electroencephalographic delta wave power, suggesting an enhancement of sleep intensity within the cortex.

Unilateral cortical application of tumor necrosis factor alpha induces asymmetry in Fos- and interleukin-1beta-immunoreactive cells within the corticothalamic projection.

A unilateral microinjection of tumor necrosis factor alpha (TNFalpha) (150 ng) onto the primary somatosensory cortex induces state-dependent asymmetries in electroencephalographic (EEG) slow wave activity during non-rapid eye movement sleep in rats [H. Yoshida, Z. Peterfi, F. Garcia-Garcia, R. Kirkpatrick, T. Yasuda, J.M. Krueger, State-specific asymmetries in EEG slow wave activity induced by local application of TNF alpha, Brain Res. 1009 (2004) 129-136]. In the current study, analogous TNFalpha injections were performed to determine Fos- and interleukin-1beta (IL1beta) immunoreactivity (IR). A unilateral microinjection of TNFalpha increased the number of Fos- and IL1beta-IR cells in the primary somatosensory cortex relative to the contralateral side that received heat-inactivated TNFalpha. These asymmetric TNFalpha-induced increases in the number of Fos- and IL1beta-IR cells were evident along the outside surface of the cortex (mainly layers II and III) in a restricted rostral to caudal zone. Asymmetrical increases in the number of Fos-IR cells were also observed in the subcortical region that receives the main cortical projection from the somatosensory cortex, the somatic region of the reticular nucleus of the thalamus (reticular thalamus). The IL1beta-IR cells double-labeled with glial fibrillary acidic protein (GFAP), suggesting that many of the IL1beta-IR cells were astrocytes. The number of the IL1beta-IR cells in the reticular thalamus increased significantly ipsilateral to the TNFalpha injection. Current results indicated that Fos- and IL1beta-IR may be utilized to study the functional neuroanatomy involved in the TNFalpha-mediated state-dependent enhancement of EEG slow wave activity.

State-specific asymmetries in EEG slow wave activity induced by local application of TNFalpha.

Sleep is posited to be a fundamental property of groups of highly interconnected neurons and regulated in part by activity-dependent sleep regulatory substances such as tumor necrosis factor alpha (TNFalpha). We show that the unilateral local application of TNFalpha onto the somatosensory cortex of rats induced state- and frequency-dependent EEG asymmetries. In contrast, the unilateral injection of a TNFalpha inhibitor, a TNFalpha soluble receptor, attenuated sleep deprivation-enhanced EEG slow wave power ipsilaterally during non-rapid eye movement sleep (NREMS) but not during REMS or waking. Results are consistent with the notion that sleep begins with state changes occurring within small groups of highly interconnected neurons and is driven in part by the local production of sleep regulating substances.

Tumor necrosis factor-alpha reduces ketamine- and propofol-induced anesthesia time in rats.

UNLABELLED: Tumor necrosis factor-alpha (TNFalpha) is a crucial neuromodulator in the brain. TNFalpha is involved in many physiological events including pain response and sleep. However, the interactions between TNFalpha and anesthetics have not been elucidated yet. In the present study, we investigated the effects of four intracerebroventricular (ICV) doses (1, 10, and 100 pg, and 1 ng) and two intraperitoneal (IP) doses (10 and 100 ng) of TNFalpha on anesthesia time of ketamine (100 mg/kg IP) and propofol (80 mg/kg IP) in rats. All ICV doses of TNFalpha reduced anesthesia time of ketamine and propofol compared with the saline ICV group (ketamine control group, 45.4 +/- 6.5 min; propofol control group, 43.5 +/- 11.0 min). The maximum effect was obtained after the ICV injection of 10 pg of TNFalpha (76% and 54% of ketamine and propofol control groups, respectively). Anesthesia time of ketamine or propofol was also decreased by IP injection of TNFalpha in a dose-dependent manner. Injection of 100 ng of TNFalpha IP reduced anesthesia time of ketamine and propofol by 67% and 64% of each control group, respectively. These data show that TNFalpha can modulate the anesthesia time of IV anesthetics, suggesting that anesthetic requirements might be altered in the presence of cerebral or systemic inflammation. IMPLICATIONS: Tumor necrosis factor alpha (TNFalpha) regulates many physiological events in the brain. We investigated the effects of TNFalpha on anesthesia time in rats. Both central and peripheral administration of TNFalpha decreased anesthesia time induced by ketamine and propofol.

Middle-ear pressure variations during total intravenous anesthesia with propofol, fentanyl, and ketamine.

PURPOSE: As the middle-ear cavity is one of the noncompliant gas-filled cavities, an increase in middle-ear pressure (MEP) instead of volume expansion is observed with inhalation of nitrous oxide (N2O). Changes in MEP cause many complications, such as ear pain, temporary hearing impairment, and postoperative emesis. Therefore, we investigated changes in MEP during total intravenous anesthesia (TIVA) with propofol, fentanyl, and ketamine (PFK) and inhalation of N2O. METHODS: Twelve patients were anesthetized with PFK until 60 min after the induction of anesthesia, and then N2O (60%) inhalation was started. MEP was measured by impedance audiometry (ranging from -300 daPa to +200 daPa) at 10-min intervals during PFK, and at 2-min intervals after the inhalation of N2O. RESULTS: MEP gradually but significantly increased from the preanesthetic value of 16±8 to 34±12 (SEM) daPa 50 min after the induction of PFK. However, MEP did not exceed the normal limit. The values of MEP in all patients were more than 200 daPa within 36 min after the start of inhalation of N2O in oxygen. CONCLUSION: PFK had a minimal effect on MEP, whereas addition of N2O to PFK increased MEP dramatically. Therefore, TIVA, or at least PFK, would be a better choice for patients with middle-ear or upper-airway diseases.