Mami Chikuda

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.