Shigeharu Joh

Indigo carmine-induced bradycardia in a patient during general anesthesia.

Implications Indigo carmine is very often used to confirm if catheters for delivering anticancer drugs are placed in the appropriate vicinity of tumors. This report demonstrates that severe bradycardia can occur after intraarterial administration of indigo carmine.

The Anesthetic Management of a Patient with Hemoglobin Miwate

IMPLICATIONS Pulse oximetry is now considered essential for anesthetic management. We treated a patient with hemoglobin M(Iwate), a rare inheritable hemoglobinopathy rendering pulse oximetry completely useless because of its anomalous absorption spectrum.

Evaluation of Transcutaneous and End-Tidal Carbon Dioxide During Intravenous Sedation in Volunteers

Objective: During intravenous sedation, end-tidal carbon dioxide (ETCO2) is usually measured with a nasal cannula or mouth-nose cannula. We compared the measurement accuracy of ETCO2 between these two devices and TC-CO2 and assessed which device is more useful during intravenous sedation in volunteers. Methods: Eight male volunteers aged 25 to 35 years were evaluated in this single-institution blinded observational trial. After they lay quietly for 5 min without supplemental oxygen, the volunteers received supplemental oxygen by means of each device at a flow rate of 3 L/min for 15 min. Next, midazolam (0.05 mg/kg) was intravenously injected, flumazenil (20 mg) was injected 30 min later, and the ETCO2 and TC-CO2 waveform were recorded. Results: The differences between ETCO2 and TC-CO2 significantly increased after midazolam injection and decreased after flumazenil injection. The difference between ETCO2 and TC-CO2 using the nasal cannula was greater than that using the mouth-nose cannula. The mean difference between TC-CO2 and ETCO2 ranged from 3 to 9 mmHg after midazolam injection using a nasal mask, and the mean difference ranged from 3 to 6 mmHg after midazolam injection using a mouth-nose cannula. Conclusions: The difference between ETCO2 and TC-CO2 against TC-CO2 was within the clinically acceptable range. Both the nasal and mouth-nose cannula were useful for ETCO2 measurement with supplemental oxygen by means of each device at flow rate of 3 L/min during intravenous sedation in volunteers.

Changes in brain activation induced by visual stimulus during and after propofol conscious sedation: a functional MRI study.

Conscious sedation with propofol sometimes causes amnesia while keeping the patient awake. However, it remains unknown how propofol compromises the memory function. Therefore, we investigated the changes in brain activation induced by visual stimulation during and after conscious sedation with propofol using serial functional MRI. Healthy volunteers received a target-controlled infusion of propofol, and underwent functional MRI scans with a block-design paradigm of visual stimulus before, during, and after conscious sedation. Random-effect model analyses were performed using Statistical Parametric Mapping software. Among the areas showing significant activation in response to the visual stimulus, the visual cortex and fusiform gyrus were significantly suppressed in the sedation session and tended to recover in the early-recovery session of ∼20 min (P<0.001, uncorrected). In contrast, decreased activations of the hippocampus, thalamus, inferior frontal cortex (ventrolateral prefrontal cortex), and cerebellum were maintained during the sedation and early-recovery sessions (P<0.001, uncorrected) and were recovered in the late-recovery session of ∼40 min. Temporal changes in the signals from these areas varied in a manner comparable to that described by the random-effect model analysis (P<0.05, corrected). In conclusion, conscious sedation with propofol may cause prolonged suppression of the activation of memory-related structures, such as the hippocampus, during the early-recovery period, which may lead to transient amnesia.

An application of a reinforced laryngeal mask airway to anesthesia for dental treatment.

tape, and reinforced with a mouth prop in order to keep it in the proper place (Fig. 1A). Pushing the tube with a finger into the oral vestibule and the retrodental space opposite to the treatment site would make it possible to examine and transfer the patient’s occlusion (Fig. 1B). Because of the flexibility of the tube, either dislodgement of the mask part or obstruction of the tube part could occur. Therefore, vigorous monitoring with capnography throughout the treatment will be required. Packing gauze into the pharynx can prevent the dislodgement of the mask part.

IL‑1β and TNF‑α suppress TGF‑β‑promoted NGF expression in periodontal ligament‑derived fibroblasts through inactivation of TGF‑β‑induced Smad2/3‑ and p38 MAPK‑mediated signals

Mechanosensitive (MS) neurons in the periodontal ligament (PDL) pass information to the trigeminal ganglion when excited by mechanical stimulation of the tooth. During occlusal tooth trauma of PDL tissues, MS neurons are injured, resulting in atrophic neurites and eventual degeneration of MS neurons. Nerve growth factor (NGF), a neurotrophic factor, serves important roles in the regeneration of injured sensory neurons. In the present study, the effect of pro‑inflammatory cytokines, including interleukin 1β (IL‑1β) and tumor necrosis factor α (TNF‑α), on transforming growth factor β1 (TGF‑β1)‑induced NGF expression was evaluated in rat PDL‑derived SCDC2 cells. It was observed that TGF‑β1 promoted NGF expression via Smad2/3 and p38 mitogen‑activated protein kinase (MAPK) activation. IL‑1β and TNF‑α suppressed the TGF‑β1‑induced activation of Smad2/3 and p38 MAPK, resulting in the abrogation of NGF expression. NGF secreted by TGF‑β1‑treated SCDC2 cells promoted neurite extension and the expression of tyrosine hydroxylase, a rate‑limiting enzyme in dopamine synthesis in rat pheochromocytoma PC12 cells. These results suggested that pro‑inflammatory cytokines suppressed the TGF‑β‑mediated expression of NGF in PDL‑derived fibroblasts through the inactivation of TGF‑β‑induced Smad2/3 and p38 MAPK signaling, possibly resulting in the disturbance of the regeneration of injured PDL neurons.

Evaluation of Differences between PaCO2 and ETCO2 by Age as Measured during General Anesthesia with Patients in a Supine Position

Objective. The aim of this study was to evaluate the arterial to end-tidal partial pressure gradient of carbon dioxide according to age in the supine position during general anesthesia. Methods. From January 2001 to December 2013, we evaluated 596 patients aged ≥16 years who underwent general anesthesia in the supine position. The anesthetic charts of these 596 patients, all classified as American Society of Anesthesiologists physical status I or II, were retrospectively reviewed to investigate the accuracy of PaCO2 and ETCO2. Results. The a-ETCO2 was  mmHg for patients aged 16 to <65 years and  mmHg for patients ≥65 years. The a-ETCO2 was  mmHg for patients aged 16 to 25 years,  mmHg for patients aged 26 to 35 years,  mmHg for patients aged 36 to 45 years,  mmHg for patients aged 46 to 55 years,  mmHg for patients aged 56 to 64 years,  mmHg for patients aged 65 to 74 years, and  mmHg for patients aged 75 to 84 years. Conclusion. The arterial to end-tidal partial pressure gradient of carbon dioxide tended to increase with increasing age.

Changes in Intra-cerebral Oxygenation During Intravenous and Inhalational Sedation: A Original Research

Background: Although sedatives such as midazolam or nitrous oxide (N2O) are administered to dental patients, the effects of these drugs on intra-cerebral oxygenation are not well-known. Aims: We investigated the effects of intravenous midazolam or inhalational N2O on intra-cerebral oxygenation using near-infrared spectroscopy. Setting and Design: University hospital, prospective. Materials and Methods: During intravenous sedation, volunteers received supplemental oxygen through nasal cannula at 3 L/min for 10 min (control group). Midazolam (0.05 mg/kg) was then injected intravenously with flumazenil (20 mg) injected 30 min later. In the inhalational sedation study, volunteers lay quietly for 10 min receiving 100% oxygen, then received N2O via nasal mask at concentrations of 10%, 20%, and 25% for 5 min; 30% for 20 min; and supplemental oxygen at 100% for 15 min after N2O was discontinued. Statistical Analysis: Intra-group comparisons were made using one-way analysis of variance for repeated measures followed by Dunnett’s test for multiple comparisons. Differences were considered statistically significant at P < 0.05. Results: During intravenous sedation, oxyhemoglobin increased 10 min after midazolam administration, and total hemoglobin increased slightly until 20 min after flumazenil administration, followed by a decrease. During inhalational sedation, oxyhemoglobin increased until 5 min after starting N2O, and total hemoglobin increased until 5 min after starting N2O, followed by a decrease. Conclusions: Midazolam and N2O influenced intra-cerebral oxygenation during intravenous or inhalational sedation. Cerebral blood flow increased with intravenous sedation when midazolam was administered once at a dose of 0.05 mg/kg and with inhalational sedation when N2O was supplied at a concentration of 25-30%.

Changes in Intra-cerebral Environment in Patients Undergoing Tracheotomy: An Original Research

Background and Objectives: Microvascular flap reconstruction has recently proven to be very reliable for repairing defects in the oral and maxillofacial cavity defects. Such patients often require a tracheotomy to stay in the intensive care unit post-operatively. Although tracheotomy is usually performed after oral intubation, details of the intra-cerebral oxygenation environment during tracheotomy are unclear. Using near-infrared spectroscopy, we investigated the changes in intra-cerebral oxygenation during exchange from oral to tracheal intubation in patients undergoing tracheotomy. Materials and Methods: We evaluated eight patients with an American Society of Anesthesiologists physical Status of I or II who were scheduled to undergo tracheotomy. Changes in the intra-cerebral levels of oxyhemoglobin (oxy-Hb), deoxyhemoglobin (deoxy-Hb), total hemoglobin (total-Hb), and cytochrome oxidase (cyt) were monitored during tracheotomy. Results: Blood pressure increased rapidly during exchange from an oral to tracheal intubation tube. The maximum oxy-Hb level (3.5 ± 2.4 nmol/L) occurred 5 min after the exchange, the maximum deoxy-Hb level (0.8 ± 1.0 nmol/L) occurred 5 min after the exchange, the maximum total-Hb level (1.8 ± 2.2 nmol/L) occurred 5 min after the exchange, and the minimum cyt level (−0.5 ± 0.2 nmol/L) occurred 7 min after the start of the operation. Conclusions: The intra-cerebral oxy-Hb and total-Hb levels increased after exchange from an oral to tracheal intubation tube during tracheotomy, and these hemodynamic changes attenuated the cerebral blood flow.

Changes in Intracellular Ca2+Induced with Adrenaline in Swine Lingual Artery

Background and Objectives: Dental doctors routinely infiltrate adrenaline combined with lidocaine into the oral mucosa. However, they do not well know the physiological characteristics and mechanisms of contraction induced by adrenaline in the oral maxillofacial artery. We investigated the changes in the intracellular Ca2+ concentration by an adrenaline-induced contraction in the swine lingual artery. Materials and Methods: We prepared artery rings with denuded endothelium and simultaneously measured tension and intracellular Ca2+ concentration ([Ca2+]i). The effects of adrenaline in the presence or absence of intracellular Ca2+ on artery rings and verapamil on Ca2+ influx activated by adrenaline were assessed. Results: In the presence of intracellular Ca2+, the application of adrenaline caused a rapid increase in tension and [Ca2+ i, which then decreased slowly. In the absence of extracellular Ca2+, adrenaline caused a transient increase in [Ca2+]i and tension. The application of adrenaline in the presence of extracellular Ca2+ after depletion of the intracellular Ca2+ store caused a slow increase in [Ca2+]i and tension, while co-treatment with verapamil inhibited the increases in [Ca2+]intracellular and tension was induced by adrenaline. The tension relationship obtained with adrenaline was located on the left of the [Ca2+]i-tension relation curve obtained with KCl. Conclusions: The induction of contraction may involve three mechanisms: (1) Release of Ca2+ from the intracellular store, (2) influx of extracellular Ca2+ through voltage-gated Ca2+ channels, and (3) the Ca2+ sensitivity of the contractile apparatus.