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Objective: To assess the efficacy and safety of visual rigid laryngoscopy and video laryngoscopy and to provide clinical information for developing a more suitable intubation tool for elderly patients. Methods: In 75 consecutive elderly patients undergoing elective surgery in a single institution, tracheal intubation was randomly performed by 2 experienced anaesthesiologists using visual rigid laryngoscopy (Group I, n = 38) or video laryngoscopy (Group II, n = 37). The primary outcome was intubation time. Secondary outcomes were the first-attempt success rate of tracheal intubation, haemodynamic responses at 1, 3, and 5 min after intubation and the incidence of postoperative airway complications, including immediate complications and postoperative complaints. Results: The intubation times were 35.0 (30.0–41.5) s and 42.5 (38.0–51.3) s in Groups I and II, respectively (P < 0.001). The difference in direct complications between the two groups was statistically significant (P < 0.05). In contrast, there was no significant difference between the two groups regarding the follow-up of the main complaint 30 min and 24 h after tracheal extubation (P > 0.05). There was no difference in the intubation success rate between the 2 groups (P > 0.05). The haemodynamic responses at 1, 3, and 5 min after intubation were not significantly different (P > 0.05). Conclusion: Compared with that of video laryngoscopy, the intubation time of visual rigid laryngoscopy in elderly patients was shorter. At the same time, visual rigid laryngoscopy reduced the incidence of immediate complications. However, during endotracheal intubation, there was no significant difference in haemodynamics between the two groups. Clinical trial registration number: ChiCTR2100054174. [ABSTRACT FROM AUTHOR]

Background: The study sought to investigate the effects of dexmedetomidine (DEX) on cognitive function after anesthesia and to examine its actual mechanism., Methods: A total of 48 rats were injected with d-galactose (D-gal) 1,000 mg·kg -1 ·d -1 and normal saline at the neck and back for 1 week to establish rats with mild cognitive impairment (MCI) and conduct behavioral tests. Sevoflurane was inhaled and DEX was pumped into each group respectively. Morris water maze (MWM) test was conducted 24 hours later. The inflammatory factors interleukin (IL)-1, interleukin (IL)-6, and a tumor necrosis factor (TNF)-α in brain homogenate were quantitatively measured by enzyme-linked immunosorbent assay (ELISA) on the next day. The apoptosis of hippocampal cells was observed by hematoxylin-eosin staining (HE staining)., Results: In relation to the model establishment, we found that there was no significant difference in body weight and swimming speed before and after modeling. There was no statistically significant difference in the escape latency between Groups A, B, C, and D before modeling. After modeling, there was no statistical difference in the escape latency between Groups A, B, and C, but the difference was statistically significant when compared to Group D (P<0.05). In relation to the DEX intervention, we found that compared to Group C, MWM test performance in Groups A and B was considerably worse longer escape latencies and fewer platform crossings within 90 seconds), and were more significant in Group A. Compared with Group D, the levels of inflammatory cytokines of the brain homogenates were elevated, and this elevation was highest in Group A, followed by Group B; the pathological changes were consistent with changes in behavioral tests. In Group A, there were obvious disorders of glial cell arrangement, apoptosis and deletion. There was no significant change in Group D. And the changes of vertebral cells in Group B and Group C were slight, with orderly arrangement and intact cell structure., Conclusions: DEX inhibits the apoptosis of hippocampal cells and reduces the cognitive dysfunction of rats with MCI induced by D-gal via the inhibition of the release of inflammatory cytokines., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://atm.amegroups.com/article/view/10.21037/atm-22-2043/coif). QZ received consulting fees from AMCA. The other authors have no conflicts of interest to declare., (2022 Annals of Translational Medicine. All rights reserved.)

Sepsis is the leading cause of death in the intensive care unit and continues to lack effective treatment. It is widely accepted that high-mobility group box 1 (HMGB1) is a key inflammatory mediator in the pathogenesis of sepsis. Moreover, some studies indicate that the functions of HMGB1 depend on its molecular localization and posttranslational modifications. Our previous study confirms that sirtuin 1, silent information regulator 2-related enzyme 1 (SIRT1), a type III deacetylase, can ameliorate sepsis-associated acute kidney injury (SA-AKI). We explored the effect and mechanism of SIRT1 on HMGB1 using a mouse model of cecal ligation and puncture-induced sepsis and LPS-treated human kidney (HK-2) cell line. We found that HMGB1 is elevated in the serum but is gradually reduced in kidney cells in the later stages of septic mice. The acetylation modification of HMGB1 is a key process before its nucleus-to-cytoplasm translocation and extracellular secretion in kidney cells, accelerating the development of SA-AKI. Moreover, SIRT1 can physically interact with HMGB1 at the deacetylated lysine sites K28, K29, and K30, subsequently suppressing downstream inflammatory signaling. Thus the SIRT1-HMGB1 signaling pathway is a crucial mechanism in the development of SA-AKI and presents a novel experimental perspective for future SA-AKI research.

Object: Recent studies have suggested that intrinsic apoptotic signaling cascade is involved in endothelial barrier dysfunction following hemorrhagic shock (HS), which results in vascular hyperpermeability. Our previous study demonstrated that ulinastatin (UTI) inhibits oxidant-induced endothelial hyperpermeability and apoptotic signaling. In present study, we hypothesized that UTI would improve HS-induced vascular hyperpermeability by regulating the intrinsic apoptotic signaling cascade., Methods: Hemorrhagic shock was induced in rats by withdrawing blood to reduce the mean arterial pressure to 40-45 mmHg for 60 min, followed by reperfusion. Mesenteric postcapillary venules were examined for changes in hyperpermeability by intravital microscopy. In vitro, Rat lung microvascular endothelial cells (RLMVECs) were exposed in hemorrhagic shock serum for 120 min, followed by transendothelial electrical resistance (TER) estimation. Mitochondrial release of cytochrome c and caspase-3 activation was estimated in vivo. In vitro, ratio of cell apoptosis was evaluated by Annexin-V/PI double stain assay; mitochondrial membrane potential (∆Ψm) was determined with JC-1; intracellular ATP content was assayed by a commercial kit; reactive oxygen species (ROS) was measured by DCFH-DA; adherens junction protein β-catenin was detected by immunofluorescense staining., Results: In vivo, UTI attenuated HS-induced vascular hyperpermeability versus the HS group (P < 0.05); In vitro, UTI attenuated shock serum induced RLMEC monolayer hyperpermeability (P < 0.05). In vivo, UTI inhibited HS-induced cytochrome c release and caspase-3 activation (P < 0.05). In vitro, shock serum induced cell apoptosis, low ATP level, ∆Ψm depolarization, ROS increase were improved by UTI pre-treatment (P < 0.05). UTI improved shock serum induced disruption of endothelial cell adherens junction., Conclusions: UTI inhibits vascular hyperpermeability following HS. UTI regulates oxidative stress and intrinsic apoptotic signaling following HS.

Purpose: We aimed to investigate the influence of perioperative goal-directed fluid therapy (GDFT) on the prognosis of elderly patients with gastric cancer and hypertension., Methods: Sixty elderly patients (>60 years old) with primary hypertension who received gastric cancer radical surgery and who were American Society of Anesthesiologists (ASA) class II or III were enrolled in the current study. Selected patients were divided randomly into two arms, comprising a conventional intraoperative fluid management arm (arm C, n=30) and a GDFT arm (arm G, n=30). Patients in arm C were infused with crystalloids or colloids according to the methods of Miller's Anesthesia (6th edition), while those in arm G were infused with 200 mL hydroxyethyl starch over 15 minutes under the FloTrac/Vigileo monitoring system, with stroke volume variation between 8% and 13%. Hemodynamics and tissue perfusion laboratory indicators in patients were recorded continuously from 30 minutes before the operation to 24 hours after the operation., Results: Compared with arm C, the average intraoperative intravenous infusion quantity in arm G was significantly reduced (2,732±488 mL versus 3,135±346 mL, P<0.05), whereas average colloid fluid volume was significantly increased (1,235±360 mL versus 760±280 mL, P<0.05). In addition, there were more patients exhibiting intraoperatively and postoperatively stable hemodynamics and less patients with low blood pressure in arm G. Postoperative complications were less frequent, and the time of postoperative hospital stay shorter, in arm G. No significant differences were observed in mortality between the two arms., Conclusion: Our research showed that GDFT stabilized perioperative hemodynamics and reduced the occurrence of postoperative complications in elderly patients who underwent gastric cancer surgery.

Oxidants are important signaling molecules known to increase endothelial permeability. Studies implicate reactive oxygen species (ROS) and the intrinsic apoptotic signaling cascades as mediators of vascular hyperpermeability. Here we report the protective effects of ulinastatin, a serine protease inhibitor with antiapoptotic properties, against oxidant-induced endothelial monolayer hyperpermeability. HUVECs were respectively pretreated with 10,000 and 50,000 u/l ulinastatin, followed by stimulation of 0.6 mM H₂O₂. Monolayer permeability was determined by transendothelial electrical resistance (TER); Mitochondrial release of cytochrome c was determined by enzyme-linked immunosorbent assay; Caspase-3 activity was measured by fluorometric assay; Adherens junction protein β-catenin was detected by immunofluorescense staining; Ratio of cell apoptosis was evaluated by Annexin-V/PI double stain assay; Mitochondrial membrane potential (Δψm) was determined with JC-1; Intracellular ATP content was assayed by a commercial kit; Bax and Bcl-2 expression were estimated by western blotting; Intracellular reactive oxygen species (ROS) level was measured by DCFH-DA. H₂O₂ exposure resulted in endothelial hyperpermeability and ROS formation (P < 0.05). The activation of mitochondrial intrinsic apoptotic signaling pathway was evidenced from BAX up-regulation, Bcl-2 down-regulation, mitochondrial depolarization, an increase in cytochrome c release, and activation of caspase-3 (P < 0.05). UTI (50,000 u/l) attenuated endothelial hyperpermeability, ROS formation, mitochondrial dysfunction, cytochrome c release, activation of caspase-3, and disruption of cell adherens junctions (P < 0.05). Together, these results demonstrate that UTI provides protection against vascular hyperpermeability by modulating the intrinsic apoptotic signaling.