To explore the role and mechanism of warm malate ringer’s solution (MR) in resuscitation of the lethal triad caused by severe trauma.

A rat model of severe trauma was established in SPF-grade SD rats (half male and half female, weighing 200~220 g) using combined multiple injuries and hemorrhagic shock, and the rats were randomly divided into 8 groups (n=8): Sham group, only arterial and venous catheterization; Trauma (Tra) groups with different time points (10, 30, 60, 90, 120, 180 min) and a Trauma group that were observed without any treatment for 180 min after model establishment. The changes of activated clotting time (ACT), reaction time (R), maximum amplitude (MA), and rate of blood clot formation (Angle) at different time points were detected by using thromboelastography, and tail bleeding, core body temperature and arterial blood gas parameters, were also observed and detected. The plasma von Willebrand Factor (vWF) level, mitochondrial respiratory control ratio in pulmonary venous endothelium, and expression levels of vascular endothelial cadherin (VE-Cadherin), peroxisome proliferator activating receptor gamma coactivator 1α (PGC1α), dynamin-related protein 1 (Drp1), p-Drp1, and mitofusin 2 (Mfn2) were detected to evaluate the vascular endothelial injury and mitochondrial dysfunction. Another group of SD rats were randomly divided into severe trauma group (no treatment for 180 min after injury), and MR solution at room temperature and at 37 ℃ groups. MR solution at room temperature or at 37 ℃ was given to the rats using a medical blood transfusion apparatus at 60 min post-trauma. Above indicators were observed and detected to investigate the resuscitation effect of the MR solution.

Compared with the Sham group, the severely traumatic rats at 180 min after injury had significantly prolonged ACT and R values (P<0.05), shortened MA and decreased Angle values (P<0.05), extended tail bleeding time (P<0.05), lower partial pressure of carbon dioxide (PCO₂) and HCO₃^- and base excess (BE) levels (P<0.05), and continuously increasing K⁺ (P<0.05) and decreasing Na⁺ (P<0.05) and Ca²⁺ levels (P<0.05). Additionally, plasma vWF level (P<0.05) and protein levels of VE-cadherin, PGC1α and Mfn2 in pulmonary vein endothelium were significantly reduced (P<0.05), the expression of p-Drp1 was enhanced and the mitochondrial respiration control rate was declined in the rats at 180 min after injury (P<0.05). MR solution resuscitation shortened tail bleeding time (P<0.05), increased core body temperature (P<0.05), elevated plasma vWF level (P<0.05), increased protein levels of VE-cadherin, PGC1α and Mfn2 (P<0.05), and decreased that of p-Drp1 protein expression (P<0.05) when compared with the rats at 180 min after severe traumatic injury. The above effects were more significant in the rats infused with the solution at 37 ℃ than those at room temperature.

Warm MR solution significantly improves the lethal triad in rats after severe trauma, which may be associated with its improving mitochondrial function and attenuating vascular endothelial damage.

Elderly patients with metabolic syndrome often present with concurrent subjective cognitive decline and frailty, yet the underlying mechanisms linking these conditions remain unclear. This study aims to explore the parallel mediating effects of physical activity levels and depression on the relationship between subjective cognitive decline and frailty in elderly patients with metabolic syndrome, identify potential pathways and key factors through which subjective cognitive decline influences frailty, and provide evidence to support the development of intervention strategies.

A cross-sectional study was conducted on 348 hospitalized elderly patients with metabolic syndrome admitted to 10 internal medicine departments (including Respiratory Medicine, Neurology, Hypertension and Endocrinology, and Cardiology) in Daping Hospital of Army Medical University from June to December 2024. Subjective cognitive decline was assessed using the Subjective Cognitive Decline Questionnaire (SCD-Q9), depression using the Center for Epidemiologic Studies Depression Scale 10 (CES-D 10), frailty using the Fatigue, Resistance, Ambulation, Illnesses, and Loss of Weight (FRAIL) Scale, and physical activity levels using the International Physical Activity Questionnaire Short Form (IPAQ-SF). Pearson correlation analysis was performed to assess the correlation coefficients between frailty, subjective cognitive decline, depression, and physical activity levels. The Process macro in SPSS 27. 0 was used to construct the mediation effect model.

Subjective cognitive decline was positively correlated with depression (r=0. 210, P<0. 001) and frailty (r=0. 275, P<0. 001), and negatively correlated with physical activity levels (r=-0. 199, P<0. 001). Physical activity levels were negatively correlated with frailty (r=-0. 228, P<0. 001), and frailty was positively correlated with depression (r=0. 251, P<0. 001). Physical activity levels and depression exerted parallel mediating effects between subjective cognitive decline and frailty, with effect values of 0. 009 (95%CI: 0. 003 to 0. 017) and 0. 012 (95%CI: 0. 004 to 0. 021), accounting for 12. 50% and 16. 67% of the total effect, respectively.

Physical activity levels and depression play parallel mediating roles between subjective cognitive decline and frailty in elderly patients with metabolic syndrome. Clinicians should emphasize screening for subjective cognitive decline in these patients. And interventions aimed at enhancing physical activity and targeting depressive symptoms may help delay frailty progression and improve quality of life.