It is well known that acute ischemic stroke (AIS) and subsequent reperfusion produce lethal levels of reactive oxygen species (ROS) in neuronal cells, which are generated in mitochondria. Mitochondrial ROS production is a self‐amplifying process, termed “ROS‐induced ROS release”. Furthermore, the mitochondrial permeability transition pore (MPTP) is deeply involved in this process, and its opening could cause cell death. Edaravone, a free radical scavenger, is the only neuroprotective agent for AIS used in Japan. It captures and reduces excessive ROS, preventing brain damage. Cyclosporine A (CsA), an immunosuppressive agent, is a potential neuroprotective agent for AIS. It has been investigated that CsA prevents cellular death by suppressing MPTP opening. In this report, we will outline the actions of edaravone and CsA as neuroprotective agents in AIS, focusing on their relationship with ROS and MPTP.

The results showed that the decrease in PWV implies a decrease in arterial elasticity, and the decrease in the arterial elasticity correlated with the decrease in intraarterial pressure. These findings demonstrated that a radial artery pressure lower than the aortic pressure after CPB may be due to the decrease in arterial elasticity.

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Summary An infusion of amino acids stimulates heat production in skeletal muscle and then attenuates the anesthesia-induced hypothermia. However, in a clinical setting, some patients have atrophic skeletal muscle caused by various factors. The present study was therefore conducted to investigate the effect of amino acids on the anesthesia-induced hypothermia in the state of muscle atrophy. As the muscle atrophy model, Sprague-Dawley rats were subjected to hindlimb immobilization for 2 wk. Normal rats and atrophy model rats were randomly assigned to one of the two treatment groups: saline or amino acids ( n ϭ 8 for each group). Test solutions were administered intravenously to the rats under sevoflurane anesthesia for 180 min, and the rectal temperature was measured. Plasma samples were collected for measurement of insulin, blood glucose, and free amino acids. The rectal temperature was significantly higher in the normal-amino acid group than in the muscle atrophy-amino acid group from 75 to 180 min. The plasma insulin level was significantly higher in the rats given amino acids than in the rats given saline in both normal and model groups. In the rats given amino acids, plasma total free amino acid concentration was higher in the model group than in the normal group. These results indicate that skeletal muscle plays an important role in changes in body temperature during anesthesia and the effect of amino acids on anesthesia-induced hypothermia decreases in the muscle atrophy state. In addition, intravenous amino acids administration during anesthesia induces an increase in the plasma insulin level.

As the result of a locking phenomenon that may occur in a guidewire inside a metal puncture needle when using the Seldinger technique to insert a central venous catheter, the guidewire can break and cause an embolism. To counter this possibility we devised a guidewire with a structure that made it difficult for locking to occur and compared it to conventional guidewires. Conventional guidewires are wound lengthways with a spring. The improved version has a special multi-ply structure. A series of 100 cases were divided into two groups: group A, the conventional guidewire group; and group B, the improved guidewire group. We punctured the internal jugular vein and attempted insertion of the guidewire through the side hole of a 22-gauge metal needle. We then compared the frequency of locking and the frequency of bending of the guidewire tips that have been withdrawn. In group A, locking occurred in 72% of the cases where the guidewire was unable to be inserted, but this figure was 0% in group B. The improved guidewire has the advantage of reducing the risk of locking and of guidewire breakage.

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Summary A decrease in core temperature during general anesthesia is attenuated by infusion of an intravenous amino acid mixture. The purpose of the present study was to investigate the influence of physical and endocrine changes caused by ovariectomy on the inhibitory effect of amino acid infusion on anesthesia-induced hypothermia. Sprague-Dawley female rats were divided into a sham-operated (Sham) group and an ovariectomized (OVX) group. Saline solution or an amino acid mixture solution was infused for 180 min during sevoflurane anesthesia, and the rectal temperature was measured (4 groups). Intraperitoneal white adipose tissue mass, bilateral gastrocnemius weight and plasma insulin levels were measured. In the Sham rats, no inhibitory effect of the amino acid mixture on anesthesia-induced hypothermia was found, while in the OVX rats, hypothermia was significantly decreased. The intraperitoneal fat weight/body weight ratio was significantly higher in the OVX rats than in the Sham rats, but the gastrocnemius weight/body weight ratio was not significantly different. After amino acid infusion, the plasma insulin level was significantly higher in the OVX rats than in the Sham rats. In conclusion, our findings suggest that, in rats, ovarian function or female hormone affects protein turnover mediated by increase in insulin secretion and, thus, decreases the inhibitory effect of an infusion of amino acid mixture on anesthesia-induced hypothermia. Key Words hypothermia, amino acids, general anesthesia, ovariectomy Redistribution hypothermia occurs in the body after induction of general anesthesia. Core body temperature gradually declines as heat is lost from the body surface, and heat production slows because of decreased metabolism. Selldén et al. reported that an amino acid infusion during anesthesia caused nutrient-induced thermogenesis (NIT), preventing the temperature reduction of redistribution hypothermia ( 1 ). Fujiwara et al. noted a similar effect after amino acid infusion but not after an infusion of glucose and fat emulsion ( 2 ). It is known that the metabolism of amino acids requires a large expenditure of energy ( 3 ), and protein synthesis induced by amino acids has been shown to correlate positively with energy expenditure ( 4 ). When rats were given the protein synthesis inhibitor puromycin, NIT did not occur after amino acid infusion ( 5 ). It has also been suggested that 75% of the increased oxygen uptake by amino acid infusion is produced in tissues other than the internal organs ( 6 ). Amino acid infusion during general anesthesia was found to stimulate protein synthesis in skeletal muscle via enhanced insulin secretion and to prevent hypothermia by heat accumulation through NIT ( 7 ). We have reported that skeletal muscle and plasma insulin levels play a major role in changes in body temperature during general anesthesia and the effect of amino acids on body temperature in a rat model of muscle atrophy ( 8 ).On the other hand, sex hormone is known to be involved in thermoregulation. In addition,...

Background: Spinal anesthesia with sedation is a common anesthetic technique in infraumbilical surgeries. Dexmedetomidine has been widely used as a sedative during spinal anesthesia, and is recognized as an adjuvant that prolongs the duration of spinal anesthesia. We compared the effects of a continuous intravenous infusion of dexmedetomidine to provide intraoperative sedation on the duration of sensory and motor blockade induced by spinal anesthesia, with those of midazolam. Methods: A double-blind randomized controlled trial was performed on 40 patients, aged between 20 and 75 years, who requested intraoperative sedation, and were classified as American Society of Anesthesiologists (ASA) physical status I-II, and underwent elective surgeries under spinal anesthesia. After spinal anesthesia with 13 mg (2.6 ml) of 0.5% hyperbaric bupivacaine, patients were randomized to receive intravenous dexmedetomidine 3 μg/kg/h for 10 mins followed by an infusion of 0.5 μg/kg/h (Group D), or intravenous midazolam 0.15 mg/kg/h for 10 mins followed by an infusion of 0.025 mg/kg/h (Group M). Sedation was titrated to Observer's Assessment of Alertness/Sedation (OAA/S) score of 3. Sensory and motor blockade was evaluated using the pinprick test and modified Bromage scale, respectively. Results: The time taken to achieve OAA/S score 3 was similar in the two groups. The maximal level of sensory blockade was 5.3 ± 1.3 min in group D and 4.1 ± 1.5 in group M (P = 0.03). No significant differences were observed in the time taken to achieve the maximal level or the two-segment regression time of sensory blockade between the two groups. The time to sensory regression to the L2 level was significantly longer in group D than in group M (234.6 ± 78.1 mins versus 172.4 ± 41.