World journal of emergency medicine最新文献

Background: Post-cardiac arrest syndrome (PCAS) significantly contributes to mortality after initially successful cardiopulmonary resuscitation (CPR) in cardiac arrest (CA) patients. Effective cardiocerebral protection is essential for improving post-resuscitation survival. This study investigated the mechanisms and common targets of myocardial dysfunction and brain injury after resuscitation.

Methods: The male Sprague-Dawley rats (10-12 weeks old, 400-500 g) were divided into two groups: the control group (n=6), which received sham surgery, and the CA/CPR group (n=10), which received ventricular fibrillation (VF) followed by CPR. After 24 h, brain and heart tissues were collected for analysis. The sequencing was used to identify differentially expressed genes (DEGs) between control and CA/CPR rats.

Results: At 24 h after resuscitation, CA/CPR rats presented 217 DEGs in the hippocampus and 80 DEGs in the left ventricle (LV) compared to the control group. In the hippocampus, the most notable biological process was the positive regulation of tumor necrosis factor production, with key pathways related to inflammation and the immune response. In the LV, the Gene Ontology (GO) enrichment analysis revealed that gene alterations were primarily associated with amyloid-beta clearance, a pathway that was also relevant in the brain. Eleven common targets were identified in the DEGs of both heart and brain tissues. The reverse transcription-polymerase chain reaction (RT-PCR) validation revealed significant differences in the mRNA expression of Timp1, Apln, Ccl7, and Lgals3 in both LV and hippocampus.

Conclusion: This study identified possible key genes and underlying mechanisms involved in PCAS. The differential genes Timp1, Apln, Ccl7, and Lgals3 might serve as common biomarkers for myocardial and neurological injury following resuscitation.

Background: Post-cardiac arrest brain injury remains the leading cause of mortality and long-term disability in patients following cardiac arrest (CA). However, optimizing clinical management strategies for bundled therapy after CA still faces challenges.

Methods: For this literature review, we searched PubMed, Web of Science, and SpringerLink databases for high-quality studies published between December 1982 and July 1, 2024. The search included randomized clinical trials, meta-analyses, systematic reviews, and observational studies. References in included studies were also checked to identify additional sources.

Results: Many studies have identified potential targets for interventions to mitigate brain injury and improve outcomes for post-resuscitated patients. To optimize clinical management strategies to minimize brain injury after CA, we developed the acronym "SOOTEST-ICU" bundle, which includes "SOOTEST" therapy to optimize peripheral oxygen delivery and "ICU" intervention to optimize the cerebral oxygen cascade. The order of the "SOOTEST" treatment was organized based on the severity and importance of brain oxygen affecting brain injury. It includes systolic blood pressure and mean arterial pressure management, oxygenation and ventilation management, original etiological treatment, temperature control, electrolytes and acid basic status, seizure control, and targeted substrate delivery. The acronym "ICU" intervention includes intracerebral oxygen delivery, cerebral oxygen diffusion, and oxygen utilization.

Conclusion: The "SOOTEST-ICU" therapy is developed to optimize oxygen and substrate cascades to minimize brain injury after CA.

Background: The present study aims to investigate whether mannitol facilitates central nervous system (CNS) entry of vancomycin and alleviates methicillin-resistant Staphylococcus aureus (MRSA) intracranial infection.

Methods: Blood-brain barrier (BBB) permeability was assessed by measuring the concentration of sodium fluorescein (NaF) in the brain tissues of rats and fluorescein isothiocyanate-dextran (FITC-dextran) in a single-cell layer model. Neutrophil infiltration in the brain tissue, inflammatory cytokine levels in the serum, neurological function, and 7-day survival rates were used to evaluate therapeutic effects of mannitol and vancomycin in MRSA-infected rats. Syndecan-1 and filamentous actin (F-actin) levels were measured, and the relationship between F-actin and the endothelial glycocalyx layer (EGL) was explored via the depolymerization agent cytochalasin D and the polymerization agent jasplakinolide.

Results: Following mannitol administration, the NaF and vancomycin concentrations in the brain tissue increased rapidly within 5 min and remained stable for 30 min, indicating that mannitol increased BBB permeability for 30 min. In vitro, mannitol treatment led to significantly greater FITC-dextran permeation through a single-cell layer compared to controls. In the MRSA intracranial infection model, rats treated with mannitol and vancomycin simultaneously presented less inflammation, improved neurological function, and increased 7-day survival rate compared to rats treated with vancomycin and mannitol at 10-hour intervals. Further experiments revealed that mannitol decreased the expression of syndecan-1 in brain tissues, which was confirmed by in vitro experiments showing that mannitol significantly decreased syndecan-1 via F-actin depolymerization.

Conclusion: Mannitol may enhance the therapeutic efficacy of vancomycin against intracranial MRSA infection by decreasing the endothelial glycocalyx of the BBB via F-actin depolymerization.