A Remote-Controlled Airbag Device Can Improve Upper Airway Collapsibility by Producing Head Elevation With Jaw Closure in Normal Subjects Under Propofol Anesthesia.

Continuous maintenance of an appropriate position of the mandible and head purely by manual manipulation is difficult, although the maneuver can restore airway patency during sleep and anesthesia. The aim of this paper was to examine the effect of head elevation with jaw closure using a remote-controlled airbag device, such as the airbag system, on passive upper airway collapsibility during propofol anesthesia. Seven male subjects were studied. Propofol infusion was used for anesthesia induction and maintenance, with a target blood propofol concentration of 1.5-2 [Formula: see text]g/ml. Nasal mask pressure ([Formula: see text]) was intermittently reduced to evaluate upper airway collapsibility (passive [Formula: see text]) and upstream resistance ([Formula: see text]) at three different head and jaw positions, jaw opening position in the supine position, jaw opening position in the sniffing position with 6-cm head elevation, and jaw closure at a 6-cm height sniffing position. The 6-cm height sniffing position with jaw closure was achieved by an airbag device that was attached to the subject's head-like headgear. Patient demographics, [Formula: see text] and [Formula: see text] in each condition were compared using one-way ANOVA with a post hoc Tukey test. [Formula: see text] was considered significant. We also confirmed the effects of our airbag device on improvement of upper airway collapsibility in three obstructive sleep apnea patients in a clinical study. The combination of 6-cm head elevation with jaw closure using the air-inflatable robotic airbag system decreased upper airway collapsibility ([Formula: see text]-cm H[Formula: see text]O) compared with the baseline position ([Formula: see text]-cm H[Formula: see text]O, [Formula: see text]). In the clinical study, there was improvement of upper airway obstruction in sleep apnea patients, including decreased apnea and hypopnea duration and increased the lowest level of oxygen saturation. We demonstrated that establishment of head elevation with jaw closure achieved by a remote-controlled airbag device using an inflatable airbag system can produce substantial decreases in upper airway collapsibility and maintain upper airway patency during propofol anesthesia and sleep.

Effects of chewing efforts on the sensory and pain thresholds in human facial skin: a pilot study.

The aim of this study was to examine the effect of chewing efforts on sensory and pain thresholds of the orofacial skin of symptom-free subjects. Fourteen healthy volunteers were recruited. Using a stair-case method, the tactile detection threshold (TDT) and the filament-prick pain detection threshold (FPT) on the cheek skin (CS) and the skin overlying the palm side of the thenar skin (TS) were measured before and after chewing gum for 5 min (Time 1: T1) and keeping the jaw relaxed for 5 min (Time 2: T2) as a control. Both for the test and control situation, the TDT was higher in all measurement sites after 5 min. As for the FPT, the reactions between T1 and T2 were quite opposite: the FPT increased and/or remained stable in T1, while, it decreased at all sites in T2. There were significant session effects (T1-T2) on the FPT at the left CS (P<0.01), right CS (P<0.05) and TS (P<0.05). The increase of TDT after chewing/no chewing could be due to habituation, while the decrease of FPT observed in the control situation might be due to sensitization, respectively. This potential sensitization, however, was not observed after chewing efforts. Further studies are needed to clarify the modulating effect of masticatory function on the trigeminal sensory system.

The effect of nonfunctional tooth contact on sensory and pain perception in patients with myofascial pain of the jaw muscles.

PURPOSE: The aim of this study was to examine the effect of nonfunctional tooth contact on sensory threshold (tactile detection threshold: TDT) and pain thresholds (filament-prick pain detection threshold: FPT; pressure pain threshold: PPT) in the orofacial region of patients with myofascial pain of the jaw muscles. METHODS: The study was performed on 36 subjects: 20 normal subjects and 16 patients. Using a stair-case method, TDT and FPT were measured by Semmes-Weinstein monofilaments, on the cheek skin (CS) overlying the masseter muscles (MM) and on the skin overlying the palm side of the thenar skin (TS). PPT was measured at the central part of the MM using a pressure algometer. Each parameter was measured before and after keeping light tooth contact for 5 min (session 1) and keeping the jaw relaxed for 5 min (session 2) as a control. RESULTS: There were significant effects of experimental condition (before-after 5 min) on the TDT and FPT at several sites: after 5 min, TDT was higher in all measurement sites except the left CS of the patients in session 2. As for the FPT, the reactions between CS and TS were quite opposite in both sessions: after 5 min, the FPT at the CS decreased and/or remained, but the FPT at the TS increased and/or remained. Significant session effects (session 1-session 2) were only found on the FPT at the CS in patients. CONCLUSION: Sensitivity to FPT was more susceptible to tooth contact condition, especially in the patients.

The effects of hormonal status on upper airway patency in normal female subjects during propofol anesthesia.

STUDY OBJECTIVE: To determine the mechanical upper airway properties and compensatory neuromuscular responses to obstruction during propofol anesthesia in the follicular and luteal phases of the menstrual cycle. DESIGN: Prospective, randomized study. SETTING: University-affiliated hospital. SUBJECTS: 12 premenopausal female volunteers for studies of upper airway collapse throughout their menstrual cycle during the follicular phase (6 -10 days) and mid-late luteal phase (20 - 24 days). MEASUREMENTS: The level of propofol anesthesia (1.5 - 2.0 µg/mL) required to suppress arousal responses was determined by Observer's Assessment of Alertness/Sedation scoring (level 2) and confirmed by bispectral index monitoring. Pressure-flow relationships were constructed to evaluate collapsibility (P(CRIT)) and up-stream resistance (R(US)) during acute [Passive; hypotonic electromyography (EMG)] and sustained (Active; elevated EMG) changes in nasal mask pressure. The difference between passive P(CRIT) and active P(CRIT) (ΔP(CRIT A-P)) represented the magnitude of the compensatory response to obstruction. MAIN RESULTS: Passive P(CRIT) was significantly higher in the mid-late luteal phase (-4.7 cm H(2)O) than in the follicular phase (-6.2 cmH(2)O; P < 0.05). Active P(CRIT) significantly decreased compared with passive P(CRIT) in the follicular phase (-10.1 cm H(2)O) and in the mid-late luteal phase (-7.7 cm H(2)O) and (P < 0.05). No significant difference was noted in ΔP(CRIT) between the follicular (3.9 ± 2.9 cm H(2)O) and mid-late luteal phases (3.0 ± 2.6 cm H(2)O). No differences were seen in R(US) between the menstrual phases for either the passive (P = 0.8) or active (P = 0.75) states. CONCLUSIONS: Menstrual phase has an effect on anatomical alterations (mechanical properties) in the hypotonic upper airway during propofol anesthesia.

Effect of head elevation on passive upper airway collapsibility in normal subjects during propofol anesthesia.

BACKGROUND: Head elevation can restore airway patency during anesthesia, although its effect may be offset by concomitant bite opening or accidental neck flexion. The aim of this study is to examine the effect of head elevation on the passive upper airway collapsibility during propofol anesthesia. METHOD: Twenty male subjects were studied, randomized to one of two experimental groups: fixed-jaw or free-jaw. Propofol infusion was used for induction and to maintain blood at a constant target concentration between 1.5 and 2.0 µg/ml. Nasal mask pressure (PN) was intermittently reduced to evaluate the upper airway collapsibility (passive PCRIT) and upstream resistance (RUS) at each level of head elevation (0, 3, 6, and 9 cm). The authors measured the Frankfort plane (head flexion) and the mandible plane (jaw opening) angles at each level of head elevation. Analysis of variance was used to determine the effect of head elevation on PCRIT, head flexion, and jaw opening within each group. RESULTS: In both groups the Frankfort plane and mandible plane angles increased with head elevation (P < 0.05), although the mandible plane angle was smaller in the free-jaw group (i.e., increased jaw opening). In the fixed-jaw group, head elevation decreased upper airway collapsibility (PCRIT ~ -7 cm H2O at greater than 6 cm elevation) compared with the baseline position (PCRIT ~ -3 cm H2O at 0 cm elevation; P < 0.05). CONCLUSION: : Elevating the head position by 6 cm while ensuring mouth closure (centric occlusion) produces substantial decreases in upper airway collapsibility and maintains upper airway patency during anesthesia.

Effects of nitric oxide donor on hepatic arterial buffer response in anesthetized pigs.

The effects of systemic administration of exogenous nitric oxide (NO) donor on hepatic arterial buffer response (HABR) have not yet been studied in an anesthetized model. In this study, 28 anesthetized pigs received administration of sodium nitroprusside (SNP) or nitroglycerin (NTG) as exogenous NO donors. Pressure-flow (P-Q) relationships in the hepatic artery defined the pressure at zero flow (P(Qha = 0)) and flow-dependent resistance (R). The magnitude of HABR was evaluated by comparing the change in hepatic arterial blood flow (DeltaQha) divided by the change in portal venous blood flow (DeltaQpv), using the index of change in blood flow (DeltaQha/DeltaQpv). Mean arterial pressure decreased from baseline (95.6 +/- 3.8 mmHg) to SNP condition (68.3 +/- 1.9 mmHg) and decreased from baseline (92.7 +/- 4.4 mmHg) to NTG condition (66.2 +/- 1.7 mmHg). Mean index of change in blood flow (DeltaQha/DeltaQpv) was also significantly increased from baseline (0.19 +/- 0.12) to SNP condition (0.28 +/- 0.17; p = .009) and from baseline (0.18 +/- 0.17) to NTG (0.28 +/- 0.20; p < .05). In conclusion, systemic administration of SNP and NTG increases HABR with reduced hepatic arterial tone under decreased mean arterial pressure, presumably via exogenous NO enhancing another regulatory system and reducing the pressure gradient for sinusoidal washout.

Ice cube stimulation helps to improve dysgeusia.

Dysgeusia causes a decrease in appetite, and it is one of the major factors in undernutrition. Dysgeusia is elicited by numerous causes, and in many cases it is still difficult to treat the various symptoms complained of by patients. We herein report a case in which dysgeusia was improved by transient cooling of the mouth.

The effect of gender on compensatory neuromuscular response to upper airway obstruction in normal subjects under midazolam general anesthesia.

BACKGROUND: Upper airway patency may be compromised during sleep and anesthesia by either anatomical alterations (mechanical properties) or disturbances in the neural control (compensatory neuromuscular responses). The pathophysiology of upper airway obstruction during anesthesia may differ between men and women. Recently, we reported that the upper airway mechanical properties were comparable with those found during natural nonrapid eye movement sleep, as evaluated by measurements of passive critical closing pressure (P(CRIT)) and upstream resistance (R(US)) during midazolam sedation. In this study, we compared the effects of gender on compensatory neuromuscular responses to upper airway obstruction during midazolam general anesthesia. METHOD: Thirty-two subjects (14 men and 18 women) were studied. We constructed pressure-flow relationships to evaluate P(CRIT) and R(US) during midazolam anesthesia. The midazolam anesthesia was induced with an initial dose of midazolam (0.07-0.08 mg/kg bolus) and maintained by midazolam infusion (0.3-0.4 microg x kg(-1) x min(-1)), and the level of anesthesia was assessed by Ramsay score (Level 5) and Observer's Assessment of Alertness/Sedation score (Level 2). Polysomnographic and hemodynamic variables were monitored while nasal pressure (via mask), inspiratory air flow (via pneumotachograph), and genioglossal electromyograph (EMG(GG)) were recorded. P(CRIT) was obtained in both the passive condition, under conditions of decreased EMG(GG) (passive P(CRIT)), and in an active condition, whereas EMG(GG) was increased (active P(CRIT)). The difference between the active P(CRIT) and passive P(CRIT) (Delta P(CRIT) (P - A)) was calculated in each subject to determine the compensatory neuromuscular response. RESULTS: The difference between the active P(CRIT) and passive P(CRIT) (Delta P(CRIT) (A - P)) was significantly greater in women than in men (4.6 +/- 2.8 cm H(2)O and 2.2 +/- 1.7 cm H(2)O, respectively; P < 0.01), suggesting greater compensatory neuromuscular response to upper airway obstruction independent of arousal. CONCLUSION: We demonstrate that the arousal-independent compensatory neuromuscular responses to upper airway obstruction during midazolam anesthesia were partially maintained in women, and that gender may be a major determinant of the strength of compensatory responses during anesthesia.

The compensatory responses to upper airway obstruction in normal subjects under propofol anesthesia.

Upper airway obstruction during sleep can trigger compensatory neuromuscular responses and/or prolong inspiration in order to maintain adequate minute ventilation. The aim of this study was to investigate the strength of these compensatory responses during upper airway obstruction during propofol anesthesia. We assessed respiratory timing and upper airway responses to decreases in nasal pressure in nine propofol anesthetized normal subjects under condition of decreased (passive) and increased (active) neuromuscular activity. Critical closing pressure (PCRIT) and upstream resistance (RUS) were derived from pressure-flow relationships generated from each condition. The inspiratory duty cycle (IDC), maximum inspiratory flow (V1max) and respiratory rate (f) were determined at two levels of mean inspiratory airflow (VI; mild airflow limitation with VI > or = 150 ml s-1; severe airflow limitation with VI < 150 ml s-1). Compared to the passive condition, PCRIT decreased significantly (5.3 +/- 3.8 cm H2O, p < 0.05) and RUS increased (7.4 cm H2O ml-1 s, p < 0.05) in the active condition. The IDC increased progressively and comparably as decreased in both the passive and active conditions (p < 0.05). These findings imply that distinct compensatory mechanisms govern the modulation of respiratory pattern and pharyngeal patency during periods of airway obstruction under propofol anesthesia.

Effects of midazolam on acquisition and extinction of conditioned taste aversion memory in rats.

Some intravenous anesthetic agents such as midazolam are known to induce anterograde and retrograde amnesia. We analyzed the effect of midazolam by the conditioned taste aversion (CTA) acquisition and retention. After the rats were offered 0.1% sodium saccharin (Sac) as conditioned stimulus (CS), an intraperitoneal (i.p.) injection of several concentrations (5-30mg/kg) of midazolam was followed by an i.p. injection of 0.15M LiCl (2% of body weight) as unconditioned stimulus (US). The rats, which acquired CTA by every CS-US paradigm, strongly avoided Sac on the 1st test day after conditioning and maintained the avoidance for 3 days. We have already reported that Sac intake abruptly increased on the 2nd test day and the almost complete extinction occurred on the 3rd test day after conditioning by injection of subhypnotic dose of propofol before LiCl-injection. In contrast, we found that subhypnotic dose of midazolam suppressed not only CTA acquisition, but also CTA retention. On the other hand, an alpha2-adrenergic blocker, yohimbin (1mg/kg) suppressed only the CTA retention. These results suggest that the subhypnotic doses of midazolam firstly affect the acquisition mechanism of the CTA memory (CTAM), resulting the suppression of the retention of CTAM.

Management of exaggerated gag reflex using intravenous sedation in prosthodontic treatment.

The gag reflex is a somatic natural response in which the body attempts to eliminate instruments or agents from the oral cavity by muscle contraction. Some patients suffered from such severe retching that behavioral techniques did not sufficiently reduce gagging in dentistry. In these patients, pharmacological management was thought to be the last alternative to eliminate the reflex. However, the potential of intravenous (IV) sedation as a way to overcome problems in gagging management during prosthodontic (prosthetic) therapy has not been sufficiently explored. We examined the benefit of IV sedation to facilitate prosthodontic treatment for problematic gagging patients intolerable to dental therapy. The subjects were 10 severely retching patients (7 males and 3 females) who received prosthodontic or restorative therapy under propofol IV sedation. The number, location and prognosis of dentures/restorations were reviewed retrospectively. Eight dentures (3 removable and 5 fixed partial dentures) and 22 restorations (18 crowns and 4 inlays) were seated successfully in the oral cavity without serious complications related to IV sedation. The restored teeth were located predominantly in the posterior regions. Throughout the observation period of at least 6 months, no symptoms of postoperative pain or swelling were found. Five of the 10 patients showed improved tolerance to oral inspection, indicating a behavioral adjustment to dental care. In prosthodontic treatment extended to the posterior regions, propofol IV sedation proved useful in managing reflex control.

The effects of head and body positioning on upper airway collapsibility in normal subjects who received midazolam sedation.

STUDY OBJECTIVE: To test the hypothesis that the change of body and head position affects upper airway patency during midazolam sedation. DESIGN: Clinical study using 30 healthy subjects. SETTING: Research unit for sleep study. INTERVENTIONS: We used a pressure-flow relationship to evaluate critical closing pressure (Pcrit) and upper airway resistance (Rua) in different condition of body and head position. A pressure-flow relationship was obtained in 3 body postures (supine, 15 degrees elevation, and 30 degrees elevation) and was obtained in 3 head positions (supine with the head in the neutral, supine with head extension, and supine position with head rotated). MEASUREMENTS: The pressure and inspiratory flow at subjects' nose mask were recorded. Polysomnographic parameters (electroencephalograms, electrooculograms, submental electromyograms, upper esophageal pressure, and plethysmogram) were also recorded. MAIN RESULTS: In experiment 1, 30 degrees elevation of the body significantly decreased Pcrit (P < 0.05) to -13.3 +/- 1.3 cm H(2)O compared with -8.2 +/- 1.4 cm H(2)O in supine condition without changing the slope (1/Rua). In experiment 2, head extension significantly decreased Pcrit (-12.5 +/- 1.3 cm H(2)O) (P < 0.05) compared with the value (-8.2 +/- 1.0 cm H(2)O) in supine condition without changing the slope (1/Rua). CONCLUSIONS: Our findings indicate that 30 degrees body elevation and head extension significantly decreased upper airway collapsibility during midazolam sedation and established the relative potency of maneuvers that maintain upper airway patency.

The involvement of brain-derived neurotrophic factor in the pattern generator of mastication.

Brain-derived neurotrophic factor (BDNF) is a family of neurotrophins that plays crucial roles in neural development, survival, maintenance and regeneration both in central and peripheral nervous systems. To examine the effects of BDNF on mastication, jaw movement trajectories and masticatory muscle activities were electrophysiologically investigated in BDNF-deficient mice, compared with those of littermate wild-type mice. BDNF-deficient mice showed less number of chewing strokes and more irregular chewing pattern during mastication than wild-type mice. Masseter muscle activities of BDNF-deficient mice exhibited smaller values than those of wild-type mice. No significant difference in the cycle duration existed between these two types of the mice. These results indicate that the burst pattern is more susceptible to peripheral sensory inputs than the timing and suggest the involvement of BDNF in the control of jaw movement.

Characteristics of nociceptors in the periodontium--an in vitro study in rats.

Recent studies have indicated that nociceptors can be classified into various types according to their physiological properties. These studies have clarified that the frequency distribution of various nociceptor types is different among body sites and animal species. In the present study, we investigated the physiological properties of rat's periodontal nociceptors in an in vitro jaw-nerve preparation. Responses were recorded from functional single filaments in the inferior alveolar nerve. To determine the nociceptor type, calibrated von Frey filaments, heat, and bradykinin (BK) stimuli were used. We found five subtypes of nociceptors in the periodontal ligaments of the lower incisor: Adelta-high threshold mechanonociceptors (Adelta-HTM, n=28), Adelta-mechanoheat nociceptors (Adelta-MH, n=6), Adelta-polymodal nociceptors (Adelta-POLY, n=26), C-high threshold mechanonociceptors (C-HTM, n=3) and C-polymodal nociceptors (C-POLY, n=4). Most nociceptors were Adelta-innervated, while only a small number of C-innervated nociceptors were found. The present results suggest that periodontal nociceptors transmit mainly fast pain, and may thus play a role in rapid detection of injure-related stimuli during mastication.

Subhypnotic doses of propofol accelerate extinction of conditioned taste aversion.

Subhypnotic doses of propofol accelerate extinction of conditioned taste aversion. Some intravenous anesthetic agents including propofol is known to induce anterograde and retrograde amnesia. We evaluated whether propofol affect the long-term memory formed by the conditioned taste aversion (CTA) paradigm. Rats were allowed a 4h access to water through the experiments. After preconditioning water intake, the rats were offered 0.1% sodium saccharin (Sac) as conditioned stimulus (CS) for 20 min. An intraperitoneal (i.p.) injection of several concentrations (0.5-100 mg/kg) of propofol 10 min after Sac exposure was followed by an i.p. injection of 0.15M LiCl (2% of body weight) as unconditioned stimulus (US) 30 min after CS-exposure. The volumes of intake of Sac for 20 min were measured on the successive 4 days. The rats, which acquired CTA by every CS-US paradigm, strongly avoided Sac on the first test day after conditioning and maintained the avoidance for 3 days. However, when subhypnotic dose of propofol was injected before LiCl-injection, Sac intake abruptly increased on the second test day and the almost complete extinction occurred on the third test day after conditioning. The extinction process of CTA was barely affected by hypnotic dose of propofol. These results suggest that propofol affects the retention mechanism of the CTA memory in a dose-dependent manner. Subhypnotic dose of propofol may affect the sub-cellular process of the memory consolidation in CTA.

Interaction between the N-terminal and middle regions is essential for the in vivo function of HSP90 molecular chaperone.

At the primary structure level, the 90-kDa heat shock protein (HSP90) is composed of three regions: the N-terminal (Met(1)-Arg(400)), middle (Glu(401)-Lys(615)), and C-terminal (Asp(621)-Asp(732)) regions. In the present study, we investigated potential subregion structures of these three regions and their roles. Limited proteolysis revealed that the N-terminal region could be split into two fragments carrying residues Met(1) to Lys(281) (or Lys(283)) and Glu(282) (or Tyr(284)) to Arg(400). The former is known to carry the ATP-binding domain. The fragments carrying the N-terminal two-thirds (Glu(401)-Lys(546)) and C-terminal one-third of the middle region were sufficient for the interactions with the N- and C-terminal regions, respectively. Yeast HSC82 that carried point mutations in the middle region causing deficient binding to the N-terminal region could not support the growth of HSP82-depleted cells at an elevated temperature. Taken together, our data show that the N-terminal and middle regions of the HSP90 family protein are structurally divided into two respective subregions. Moreover, the interaction between the N-terminal and middle regions is essential for the in vivo function of HSP90 in yeast.