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Purpose: This study was performed to examine and compare the incidence of extubation recall in surgical patients who underwent remimazolam anesthesia with flumazenil antagonism during emergence and in those who underwent propofol anesthesia., Methods: One hundred sixty-three patients who underwent surgery using general endotracheal or supraglottic airway anesthesia with propofol (n = 97) or remimazolam (n = 66) were retrospectively analyzed. Remimazolam was antagonized by flumazenil after discontinuation of remimazolam at the end of surgery. The endotracheal tube or supraglottic airway was removed after surgery was complete, and consciousness and adequate spontaneous breathing were confirmed. The incidence of extubation recall was compared between the remimazolam and propofol anesthesia groups using propensity score matching., Results: Extubation recall was observed in 28 patients (17%). After propensity score matching, the incidence of extubation recall did not significantly differ between the remimazolam and propofol anesthesia groups (15.6% vs. 18.8%; p = 1.000)., Conclusion: The incidence of extubation recall after remimazolam anesthesia with flumazenil antagonism during emergence did not significantly differ from that after propofol anesthesia., (© 2022. The Author(s) under exclusive licence to Japanese Society of Anesthesiologists.)

Purpose: Hydrogen gas (H 2 ) inhalation improved the survival rate of hemorrhagic shock. However, its mechanisms are unknown. We hypothesized that H 2 protected the endothelial glycocalyx during hemorrhagic shock and prolonged survival time., Methods: 83 Sprague-Dawley rats were anesthetized with isoflurane. The animals were randomly assigned to 5 groups: room air with no shock, 1.2% H 2 with no shock, room air with shock (Control-S), 1.2% H 2 with shock (H 2 1.2%-S), and 3.0% H 2 with shock (H 2 3.0%-S). Shock groups were bled to a mean arterial pressure of 30-35 mmHg and held for 60 min, then resuscitated with normal saline at fourfold the amount of the shed blood volume., Results: The syndecan-1 level was significantly lower in the H 2 1.2%-S [8.3 ± 6.6 ng/ml; P = 0.01; 95% confidence interval (CI), 3.2-35.8] than in the Control-S (27.9 ± 17.0 ng/ml). The endothelial glycocalyx was significantly thicker in the H 2 1.2%-S (0.15 ± 0.02 µm; P = 0.007; 95% CI, 0.02-0.2) than in the Control-S (0.06 ± 0.02 µm). The survival time was longer in the H 2 1.2%-S (327 ± 67 min, P = 0.0160) than in the Control-S (246 ± 69 min). The hemoglobin level was significantly lower in the H 2 1.2%-S (9.4 ± 0.5 g/dl; P = 0.0034; 95% CI, 0.6-2.9) than in the Control-S (11.1 ± 0.8 g/dl). However, the H 2 3.0%-S was not significant., Conclusions: Inhalation of 1.2% H 2 gas protected the endothelial glycocalyx and prolonged survival time during hemorrhagic shock. Therapeutic efficacy might vary depending on the concentration.

Purpose: Heatstroke causes systemic inflammation, followed by vascular endothelial damage. The normal vascular endothelium is coated by endothelial glycocalyx (EGCX). Dexmedetomidine (DEX) has an anti-inflammatory effect, but there has been little investigation on the influence of heatstroke on EGCX and the effect of DEX on this condition. Therefore, we examined whether EGCX was disrupted in heatstroke and if DEX improved survival and preserves EGCX., Methods: Anesthetized Wistar rats were randomly assigned to three groups: a DEX group treated with DEX (5 µg/kg/h) and 0.9% saline infused continuously at 10 ml/kg/h during heat exposure; a NSS group given 0.9% saline during heat exposure; and a SHAM group given 0.9% saline alone without heat exposure. Heatstroke was induced by exposure to an ambient temperature of 40 °C with relative humidity of 60%. The survival rate was assessed up to 2 h after the start of heat exposure. Plasma levels of syndecan-1 and the thickness of EGCX using electron microscopy were measured when the systolic blood pressure fell to less than 80 mmHg., Results: The survival rate after 2 h of heat exposure was significantly higher in the DEX group compared to the NSS group (89% vs. 22%, P = 0.004). Plasma levels of syndecan-1 were 0.6 ± 1.3, 9.7 ± 5.9, and 2.1 ± 3.4 ng/ml in the SHAM, NSS and DEX groups, respectively (P = 0.013). The thickness of EGCX was significantly higher in the DEX group compared with the NSS group (P = 0.001)., Conclusions: EGCX was disrupted in heatstroke, and DEX improved survival and preserved EGCX.

Purpose: To determine the effect of landiolol on ischemic preconditioned rat hearts., Methods: Isolated perfused rat hearts were divided into 8 groups. In the control group, there was no treatment before the 30-min global ischemia. In the landiolol infused groups, landiolol (100, 300, and 500 microM) was infused without ischemic preconditioning (IPC). In other groups, hearts were pretreated with 2 episodes of 5-min global ischemia and reperfusion before the 30-min ischemia. During the preconditioning, landiolol (0, 100, 300, and 500 microM) was infused., Results: Recoveries of coronary flow (CF) and myocardial oxygen consumption (MVO(2)) at the 120th min after global ischemia to 86 +/- 18 and 112 +/- 19% of the baseline in the IPC group was, respectively, significantly greater than that to 65 +/- 10 and 72 +/- 10% in the control group. Landiolol 300 microM also increased the CF and MVO(2) significantly (97 +/- 19 and 98 +/- 39%) compared to the control. IPC + landiolol 500 microM reduced the increase in LV end-diastolic pressure significantly compared to the control. IPC, landiolol (100, 300, and 500 microM), and IPC + landiolol (100, 300, and 500 microM) all decreased infarct sizes significantly to 23.5 +/- 15.2, 29.8 +/- 12.1, 30.2 +/- 13.3, 22.8 +/- 14.8, 21.6 +/- 7.8, 34.2 +/- 14.7 and 25.5 +/- 11.3% of the total left ventricular mass, respectively, compared to the control (53.3 +/- 12.5%), but there were no significant differences among these groups., Conclusion: IPC and landiolol have cardioprotective effects on ischemia-reperfusion injury in isolated rat hearts, but pretreatment with landiolol does not enhance the cardioprotective effect of IPC.