Objective: To characterize perioperative dynamic changes in immune-cell phenotypes and inflammatory cytokines in patients undergoing CPB (cardiopulmonary bypass) cardiac surgery, and to explore their associations with postoperative outcomes. Methods: In this prospective cohort study, 120 adult patients who underwent elective cardiac surgery under CPB at West China Hospital from May 2022 to March 2023 were enrolled. Perioperative immune-cell phenotypes and concentrations of 40 inflammation-related cytokines were measured. The primary outcomes were the sequential organ failure assessment (SOFA) score at 24 h after surgery and ΔSOFA (the peak SOFA score within 48 h after surgery minus the preoperative SOFA score). Secondary outcomes included major adverse cardiovascular events (MACE), acute kidney injury (AKI), respiratory failure, severe liver injury, and infection. Results: The mean age of enrolled patients was 57±10 years. Of these, 52% (62/120) were male and 90% (108/120) underwent valve surgery. During the rewarming to the end of CPB, neutrophil counts rapidly increased (7.39×10 /L vs preoperative 3.07×10 /L, P<0.001), with significant upregulation of CD11b (7.30×10 /L vs preoperative 3.05×10 /L, P<0.001) and CD54 (7.15×10 /L vs preoperative 2.99×10 /L, P<0.001). Lymphocyte counts increased at the end of CPB (1.75×10 /L vs preoperative 1.12×10 /L, P<0.001) but decreased significantly at 24 h after surgery (0.59×10 /L vs preoperative 1.12×10 /L, P<0.001). Plasma analysis showed that multiple pro-inflammatory cytokines increased during CPB and remained elevated up to 24 h after surgery; five chemokines and the anti-inflammatory cytokine IL-10 peaked at the end of CPB. The SOFA score increased from 1 (1, 2) preoperatively to 7 (5, 10) at 24 h after surgery, with a ΔSOFA of 6 (4, 8). Within 30 days after surgery, 48 patients (40.0%) developed AKI, 17 (14.2%) developed infection, 4 (3.3%) developed severe liver injury, 3 (2.5%) developed respiratory failure, and 3 (2.5%) experienced MACE. During the 2-year follow-up, 8 patients (6.7%) experienced MACE and 5 (4.2%) died. Conclusion: Multi-organ dysfunction is common after cardiac surgery under CPB (median ΔSOFA, 6), accompanied by perioperative activation of multiple immune-cell subsets and upregulation of pro-inflammatory, anti-inflammatory, and chemotactic mediators. This study provides data-driven evidence and research clues for further investigation of the associations between CPB-related immune perturbations and postoperative organ dysfunction and clinical outcomes.

AIM：To investigate the change in myocardial mitochondrial Ca2＋ concentration (［Ca2+］m) and its mechanism in the early stage of severe burn. METHODS：An experimental model of 30%TBSA full-thickness skin scalding was reproduced in rats. ［Ca2+］m, cytosolic Ca2＋ concentration (［Ca2＋］c) and mitochondrial Ca2＋ transport velocity were determined. RESULTS: ① ［Ca2+］m increased evidently at 1st hour postburn, and continuously at 3rd hour, reached the peak at 6th hour postburn, then, it decreased at 12th and 24th hour, but remained in higher level than that of the control. ② There was no significant difference in ［Ca2＋］c between 1st hour postburn and the control, but ［Ca2＋］c increased evidently at 3rd, 6th, 12th, 24th hour postburn. ③ mitochondrial Ca2＋ uptake velocity at 1st hour postburn was higher than that of control, and Ca2＋ release velocity didn't change obviously, but both of them were decreased at 3rd, 6th, 12th, 24th hour postburn. ④ ［Ca2+］m was positive correlated with ［Ca2＋］c after burn, and negative correlated with mitochondrial Ca2＋ release velocity at 3rd, 6th, 12th, 24th hour postburn, respectively. CONCLUSION: There was obvious Ca2＋ overload in myocardial mitochondria after severe burn, the mechanism of which might include ascent of ［Ca2＋］c and disorder of Ca2＋ transport in mitochondria.

AIM: To study the role of mitochondrial nitric oxide synthase (mtNOS) in the damages of myocardial mitochondria during the early stage after severe burns.METHODS: An experimental model of 30% TBSA full-thickness skin scalding was reproduced in rats. Myocardial mitochondria were isolated from control and burned rats at 1, 3, 6, 12 and 24 h postburn. The mitochondrial respiratory function, content of mitochondrial calcium([Ca 2+ ] m) and activities of mtNOS and cytochrome c oxidase were determined. RESULTS: (1) Myocardial mitochondrial respiratory control rate(RCR) at 1 h was evidently higher than that of control, but at 3, 6, 12 and 24 h postburn, it was significantly lower than that of the control. The changes in ST 3 is parallel to those of RCR, and ST 4 was evidently increased only at 3 h postburn. (2) [Ca 2+ ] m was higher at all time points postburn and the activity of mtNOS was higher significantly only at 3, 6, 12 and 24 h than that of the control. The activity of cytochrome c oxidase at the 3, 6, 12 and 24 h was low comparing to the control. (3) After severe burns, RCR was negatively correlated with mtNOS activity( r=0.9347, P

AIM:To investigate the change in myocardial mitochondrial Ca 2+ concentration ([Ca 2+ ] m) and its mechanism in the early stage of severe burn. METHODS:An experimental model of 30%TBSA full-thickness skin scalding was reproduced in rats. [Ca 2+ ] m, cytosolic Ca 2+ concentration ([Ca 2+ ] c) and mitochondrial Ca 2+ transport velocity were determined. RESULTS: ① [Ca 2+ ] m increased evidently at 1st hour postburn, and continuously at 3rd hour, reached the peak at 6th hour postburn, then, it decreased at 12th and 24th hour, but remained in higher level than that of the control. ② There was no significant difference in [Ca 2+ ] c between 1st hour postburn and the control, but [Ca 2+ ] c increased evidently at 3rd, 6th, 12th, 24th hour postburn. ③ mitochondrial Ca 2+ uptake velocity at 1st hour postburn was higher than that of control, and Ca 2+ release velocity didn't change obviously, but both of them were decreased at 3rd, 6th, 12th, 24th hour postburn. ④ [Ca 2+ ] m was positive correlated with [Ca 2+ ] c after burn, and negative correlated with mitochondrial Ca 2+ release velocity at 3rd, 6th, 12th, 24th hour postburn, respectively. CONCLUSION: There was obvious Ca 2+ overload in myocardial mitochondria after severe burn, the mechanism of which might include ascent of [Ca 2+ ] c and disorder of Ca 2+ transport in mitochondria. [