Changes of Tumor Necrosis Factor-α and the Effects of Ulinastatin Injection during Cardiopulmonary Cerebral Resuscitation

Summary: The changes of tumor necrosis factor-α (TNF-α) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-α were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-α among different time points (P>0.05). In resuscitation group, the level of TNF-α was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-α showed in UTI group. There were no differences in TNF-α among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-α was expressed rapidly and kept increasing. It indicated that TNF-α might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-α and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.

Bone marrow-derived mesenchymal stem cell transplantation attenuates overexpression of inflammatory mediators in rat brain after cardiopulmonary resuscitation

Emerging evidence suggests that bone marrow-derived mesenchymal stem cell transplantation improves neurological function after cardiac arrest and cardiopulmonary resuscitation;however, the precise mechanisms remain unclear. This study aimed to investigate the effect of bone marrow-derived mesenchymal stem cell treatment on expression profiles of multiple cytokines in the brain after cardiac arrest and cardiopulmonary resuscitation. Cardiac arrest was induced in rats by asphyxia and cardiopulmonary resuscitation was initiated 6 minutes after cardiac arrest. One hour after successful cardiopulmonary resuscitation, rats were injected with either phosphate-buffered saline(control) or 1 × 10~6 bone marrow-derived mesenchymal stem cells via the tail vein. Serum S100 B levels were measured by enzyme-linked immunosorbent assay and neurological deficit scores were evaluated to assess brain damage at 3 days after cardiopulmonary resuscitation. Serum S100 B levels were remarkably decreased and neurological deficit scores were obviously improved in the mesenchymal stem cell group compared with the phosphate-buffered saline group. Brains were isolated from the rats and expression levels of 90 proteins were determined using a RayBio Rat Antibody Array, to investigate the cytokine profiles. Brain levels of the inflammatory mediators tumor necrosis factor-α, interferon-γ, macrophage inflammatory protein-1α, macrophage inflammatory protein-2, macrophage inflammatory protein-3α, macrophage-derived chemokine, and matrix metalloproteinase-2 were decreased ≥ 1.5-fold, while levels of the anti-inflammatory factor interleukin-10 were increased ≥ 1.5-fold in the mesenchymal stem cell group compared with the control group. Donor mesenchymal stem cells were detected by immunofluorescence to determine their distribution in the damaged brain, and were primarily observed in the cerebral cortex. These results indicate that bone marrow-derived mesenchymal stem cell transplantation attenuates brain damage induced by cardiac arrest and cardiopulmonary resuscitation, possibly via regulation of inflammatory mediators. This experimental protocol was approved by the Institutional Animal Care and Use Committee of Fujian Medical University, China in January 2016(approval No. 2016079).

Effect of hypertensive reperfusion on the changes between cerebral oxygen delivery and uptake after cardiac arrest and resuscitation in dogs

Objective: To study the changes between cerebral oxygen (O 2) delivery and uptake in dogs resuscitated under normotension or hypertension for 4 h. Methods: The model of ventricular fibrillation of 8 min in 12 dogs was made, followed by open cardiopulmonary resuscitation, reperfusion with normal or high mean arterial pressure (MAP), and controlled ventilation to 4 h. Animals were randomly assigned into Group NT (normotensive reperfusion, n=6) and Group HT (hypertensive reperfusion, n=6). Cerebral arteriovenous (sagittal sinus) O 2 content difference (Ca-ssO 2) and venous (sagittal sinus) PO 2 (PssO 2) were determined before cardiac arrest (CA) and 30, 60, 120, and 240 min after CA. Results: In Group NT, Ca-ssO 2 was lower at 30 min (P<0.05) but higher at 240 min (P<0.01) after CA than that before CA. In Group HT, Ca-ssO 2 was not significantly different from that in Group NT before CA but was lower than that in Group NT at 30 min after CA (P<0.01). Ca-ssO 2 was not significantly different in Group NT and HT thereafter. In both groups, PssO 2 was both higher at 30 min after reperfusion (P<0.01) and at 240 min after reperfusion lower (P<0.05) than those before CA .At 30 min after reperfusion, PssO 2 was higher (P<0.01) in Group HT than that in Group NT, with insignificant difference between two groups. Conclusion: Cerebral O 2 delivery and uptake are mismatched after CA and resuscitation. Hypertensive reperfusion improves oxygen delivery to the brain early after CA.

Influence of Microcirculatory Dysfunction on Myocardial Injury after Cardiopulmonary Resuscitation

Objective This study aimed to examine the effects of microcirculatory dysfunction and 654-1intervention after cardiopulmonary resuscitation on myocardial injury.Methods Landrace pigs were divided into a sham operation group(S group,n=6),ventricular fibrillation control group(VF-C group,n=8)and 654-1 intervention group(VF-I group,n=8).Hemodynamics was recorded at baseline,at recovery of spontaneous circulation(ROSC),and 1 h,2 h,4h and 6 h thereafter.Sidestream dark field(SDF)technology was used to evaluate and monitor the microcirculation flow index,total vessel density,perfusion vessel ratio,De-Backer score,and perfusion vessel density in animal viscera at various time points.Results After administration of 654-1 at 1.5 h post-ROSC,the hemodynamics in the VF-I group,as compared with the VF-C group,was significantly improved.The visceral microcirculation detected by SDF was also significantly improved in the VF-I group.As observed through electron microscopy,significantly less myocardial tissue injury was present in the VF-I group than the VF-C group.Conclusion Administration of 654-1 inhibited excessive inflammatory by improving the state of visceral microcirculation.

Effects of Hemin on neuroglobin expression after cardiopulmonary resuscitation in rats

BACKGROUND： Despite a large amount of resuscitation research, the survival rate after cardiac arrest remains low, and brain injury is the key issue. Neuroglobin （NGB） is an oxygen-binding heme protein found in the brain with a protection role against ischemic-hypoxic brain injury. Hemin is an effective activator of neuroglobin. This study was undertaken to assess the effect of hemin on expression of neuroglobin （NGB） in the cerebral cortex, neuro-defi cit score （NDS） and pathological changes after cardiopulmonary resuscitation （CPR） in rats.METHODS： A total of 120 male Sprague-Dawley （SD） rats were randomly divided into a control group （A）, a CPR group （B） and a Hemin group （C）. The animal model of cardiac arrest （CA） induced by asphyxia and CPR was established. NGB expression in the cerebral cortex with immunohistochemistry, NDS and pathological changes in the cerebral cortex were examined at 3, 6, 12, 24 hours after recovery of spontaneous circulation （ROSC） in each group. Experimental data were treated as one-factor analysis of variance and the Tukey test.RESULTS： In comparison with group A, NGB expression was increased signifi cantly at 12 and 24 hours after ROSC （P〈0.05 or P〈0.01）, NDS was decreased signifi cantly at each time point after ROSC （P〈0.01）, and pathological changes were severe at each time point after ROSC in group B. In comparison with group A, NGB expression was increased signifi cantly at 6, 12, 24 hours after ROSC （P〈0.05 or P〈0.01）, NDS was decreased signifi cantly at 3, 6, 12 hours after ROSC （P〈0.01） in group C. In comparison with group B, NGB expression was increased signifi cantly at 12 and 24 hours after ROSC, NDS was increased signifi cantly at 12 and 24 hours after ROSC, and pathological changes were milder in group C.CONCLUSION： There were increased NGB expression in the cerebral cortex, decreased NDS, and severe pathological changes after CPR in rats. Hemin treatment up-regulated expression of NGB, improved NDS, mitigated pathological changes, and alleviated cerebral injury after CPR.

Evaluation of Prognosis of Brain Function with Early Transcranial Color Doppler Ultrasound in Patients after Cardiopulmonary Resuscitation

Objective: To evaluate the clinical value of transcranial color Doppler ultrasound (TCCD) in assessing cerebral function after cardiopulmonary resuscitation (CPR). Methods: A prospective study was conducted in 52 patients with cardiac arrest treated by CPR from January 2018 to January 2020, and its clinical data were analyzed. According to classification of cerebral performance category (CPC), 31 cases (CPC grade 1 - 2) were selected in the good prognosis group and 21 cases (CPC grade 3 - 5) in the poor prognosis group. The cerebral blood flow was measured by transcranial Doppler ultrasound (TCCD) 24 h after CPR, and the differences were compared between the two groups in stroke index, diastolic blood flow velocity (Vd), systolic peak blood flow velocity (Vs) and mean peak blood flow velocity (Vm). The ROC curve of cerebral blood flow after CPR was drawn to predict the prognosis of brain function. Results: The data showed that the pulsatility index of middle cerebral artery of the poor prognosis group decreased within 24 h;the difference between the two groups was statistically significant (p < 0.05);the Vd, Vs, Vm increased in the good prognosis group;the difference between the two groups was statistically significant (p < 0.05). The ROC curve of cerebral blood flow after CPR was drawn to predict the prognosis of brain function, and the results showed that the area under the curve and the optimal critical value of cerebral blood flow were 0.731 and 5.69. The sensitivity and specificity were 67.3% and 79.1% respectively. Conclusion: The cerebral blood flow increase in the early stage of successful CPR is positively correlated with the prognosis of cerebral functional resuscitation. Monitoring intracranial blood flow after CPR by TCCD has clinical value to evaluate prognosis of brain function.

Functional changes in the hypothalamic-pituitary-adrenal axis after successful cardiopulmonary resuscitation

Background:Cardiac arrest(CA)is a terminal event that results in a range of pathophysiological changes in the body,most notably,systemic ischemia-reperfusion injury.The hypothalamic-pituitary-adrenal(HPA)axis is an important neuroendocrine system that modulates adrenocortical hormone release.This study was designed to investigate the changes in HPA-related hormone levels after successful cardiopulmonary resuscitation(CPR)and to explore possible etiologies to provide a basis for relevant clinical research.Methods:We collected the clinical data of 96 patients with CA admitted to the Emergency Department of Beijing Chaoyang Hospital,Capital Medical University,between January 2016 and May 2017.Serum samples were collected 6,24,and 72 hours after restoring spontaneous circulation(ROSC).The data were compared with those of the healthy control group(n=50).An enzyme-linked immunosorbent assay(ELISA)was performed to measure copeptin,adrenocorticotropic hormone(ACTH),corticotropin-releasing hormone(CRH),and total cortisol.Demographic data were collected for both groups.For the CPR group,clinical data and the end-of-study cerebral performance category(CPC)were analyzed.Patients were followed up through day 28.Death or survival after day 28 was used as the study endpoint.Simple values were expressed as medians and quartiles or ratios(%)for statistical analysis.Continuous variables are expressed as mean±standard deviation.Categorical variables were expressed as frequencies and percentages.The mean values of normally distributed measurement data were analyzed using 1-way analysis of variance(ANOVA)for among-group comparisons and the least significant difference(LSD)test for between-group comparisons.SPSS v17(SPSS,Chicago,IL,USA)was used for statistical analysis,and P<0.05 was considered statistically significant.Results:No significant between-group differences were observed in terms of age or sex.The 28-day mortality rate in the CPR group was 71%.ACTH and CRH levels were significantly lower in the CPR group than in the healthy control group(P<0.001).Copeptin and cortisol levels 6 hours after ROSC were significantly higher in the CPR group than in the healthy control group(P<0.001).No significant changes in any indicator were observed over time(6,24,and 72 hours after ROSC)(P>0.05).The CPC score was 1–2(good cerebral performance group)in 13 patients,3–4(poor cerebral performance group)in 17 patients,and 5(brain death or clinical death)in 66 patients.Patients with significantly declining ACTH and CRH levels had higher CPC scores(P<0.05);however,no significant differences were found in other indicators(P>0.05).Conclusion:After post-CA ROSC,ischemia-reperfusion injury may cause brain damage and HPA axis damage and dysfunction,the severity of which is associated with CPC score.

川芎嗪对心肺复苏后脑缺血-再灌注损伤的保护作用

目的 :观察川芎嗪对心肺复苏后对脑损伤的保护作用及其机制。方法 :将 4 2例需行心肺复苏患者按随机数表法分为治疗组 (A组 )与对照组 (B组 )。 A组 2 2例在心肺复苏开始同时给予川芎嗪 2 4 0 mg加质量分数为 5 %的葡萄糖 2 5 0 ml中静脉滴注 ,1h滴完 ,其后按上述剂量每日 1次 ,连用 7d。B组除不用川芎嗪外 ,其他治疗同 A组。检测两种治疗方法对患者血中超氧化物歧化酶 (SOD)、丙二醛 (MDA)、血栓素 B2 (TXB2 )的影响 ;并以意识恢复为主要指标评定临床疗效。结果 :A组显效 16例 (72 .72 % ) ,有效 3例 (13.6 4 % ) ,无效 3例(13.6 4 % ) ;B组显效 8例 (40 .0 0 % ) ,有效 3例 (15 .0 0 % ) ,无效 9例 (45 .0 0 % ) ,两组之间差异显著 (P<0 .0 5 )。两组治疗后静脉血 SOD、MDA和 TXB2 均有改善 ,但 A组改善程度明显优于 B组 (P均 <0 .0 1)。结论 :川芎嗪能对抗脂质过氧化 ,提高 SOD活性 ,抑制血小板活化 ,对心肺复苏后脑缺血再灌注损伤有一定的保护作用 ,早期应用可提高脑复苏成功率。

风险管理联合急诊护理在心脏骤停患者中的应用效果及对生活质量的影响

目的探究风险管理联合急诊护理在心脏骤停患者中应用效果。方法选择2021年2月至2023年2月期间在安阳市中医院急诊进行心肺复苏的心脏骤停患者98例,应用随机数表法将其分为对照组(常规护理)及观察组(风险管理联合急诊护理)各49例,对比两组护理有效率、生理指标(平均动脉压、心率、血氧饱和度、舒张压)、脑氧代谢指标[颈动脉血氧饱和度(SjvO_(2))、颈动脉血氧含量(CajvO_(2))、脑氧摄取率(ERO_(2))]、生活质量[生活质量综合评定问卷(GQOLI-74)]、并发症发生率。结果对照组护理有效率低于观察组,差异有统计学意义(P<0.05)。观察组平均动脉压、心率、血氧饱和度、舒张压水平高于对照组,差异有统计学意义(P<0.05)。对照组SjvO_(2)、CajvO_(2)、ERO_(2)低于观察组,差异有统计学意义(P<0.05)。观察组各维度生活质量评分高于对照组,差异有统计学意义(P<0.05)。对照组并发症发生率高于观察组,差异有统计学意义(P<0.05)。结论对心脏骤停患者接受风险管理联合急诊护理,护理效果显著,促使患者生命指征平稳,改善脑代谢,保护神经功能,减少并发症发生率,提升生活质量。

经股静-动脉心肺转流对犬心脏停搏后脑氧供需关系的影响

目的：观察犬电击致心室颤动 心脏停搏（ＶＦ ＣＡ）８ 分钟后经开胸心肺复苏（ＣＰＲ）和（或）经股静动脉心肺转流（ＣＰＢ）心肺复苏对脑氧供需关系的影响。方法：采用犬经胸壁电击ＶＦ ＣＡ ８ 分钟，经ＣＰＲ恢复自主循环（ＲＳＣ）后观察４小时内脑氧利用率（Ｏ２ ＵＣ）和脑静脉血氧分压（ＰｓｓＯ２）的变化。９ 只犬分为２ 组，Ⅰ组（５ 只）采用开胸心脏按压等方法复苏，Ⅱ组（４只）于开胸心脏按压同时经一侧股静、动脉心肺转流，并维持２ 小时。结果：Ⅱ组ＲＳＣ时间（６．３±２．１）分钟较Ⅰ组（１３．６±５．９）分钟显著缩短，Ｐ＜ ０．０５；Ⅰ组ＲＳＣ后３０、６０、１２０和２４０分钟脑Ｏ２ＵＣ值（０．６４±０．１０，０．７１±０．０９，０．７４±０．０８ 和０．７７±０．０６）均较ＣＡ前（０．４３±０．０８）明显升高，Ｐ均＜ ０．０５；同时１２０ 分钟后ＰｓｓＯ２ 值不断降低（Ｐ 均＜ ０．０５），２４０ 分钟时仅（２．８４±０．２０）ｋＰａ（１ ｋＰａ＝７．５ ｍ ｍ Ｈｇ），而Ⅱ组ＲＳＣ后除１２０ 分钟外各时点脑Ｏ２ＵＣ值（０．５２±０．０４，０．５６±０．０３ 和０．５７±０．０３）与ＣＡ前值０．５１±０．０３ 比较无显著升高，Ｐ均＞ ０．

NF-κB信号通路对心肺复苏后大鼠脑AQP-4 mRNA表达的调控作用

目的观察心肺复苏后大鼠脑NF-κB活性变化对水通道蛋白-4(AQP-4)mRNA表达的影响,探讨心肺复苏后大鼠脑AQP-4 mRNA表达调控的可能机制。方法雄性Sprague-Dawley大鼠54只,随机分为假手术组(A组,6只)、复苏加生理盐水组(B组,24只)和复苏加吡咯烷二硫代氨基甲酸盐(pyrrolidine dithiocarbamate,PDTC)组(C组,24只),B组和C组又分为自主循环恢复(restoration of spontaneous circulation,ROSC)3、6、12、24h四个亚组,每个亚组各6只。各组均进行呼吸频率、心率、动脉血压等生命体征监测,应用免疫组织化学染色检测NF-κB活性改变,逆转录聚合酶链式反应(RT-PCR)测定AQP-4 mRNA的表达变化。结果B组和C组各亚组的NF-κB活性和AQP-4 mRNA表达与A组相比均明显增加(P<0.01),B、C两组NF-κB活性从ROSC后3h开始便持续升高,至ROSC24h达高峰,而AQP-4 mRNA的表达表现为先升高,于ROSC后12h达顶峰,24h出现下降。C组各时间点NF-κB活性和AQP-4 mRNA表达与B组同时间点相比明显下降(P<0.05),且ROSC后的前12h内的NF-κB活性变化与AQP-4 mRNA表达变化呈正相关(r>0.775,P<0.01)。结论心肺复苏后早期大鼠脑NF-κB活性增加,AQP-4 mRNA表达增强,NF-κB活化抑制剂PDTC能明显降低AQP-4 mRNA的表达,NF-κB信号通路的激活在心肺复苏后早期大鼠脑AQP-4 mRNA表达中可能起了重要的调控作用。

心肺脑复苏后患者脑损害与其血清S-100蛋白的相关性探讨

目的探讨心肺脑复苏患者中出现脑损害与其血清S-100蛋白的相关性。方法测定80例CPCR术后患者及64例对照者血清S-100蛋白浓度,并对其进行2h、12h、24h、48h、72h的动态监测及比较。结果80例心肺脑复苏后患者血清中的S-100蛋白浓度在早期明显升高,2h达高峰,各时间段浓度均显著高于对照组(P<0.01)。2、12、24、48hS-100水平与入院时GCS评分之间存在负相关关系(P<0.01或P<0.05)。结论S-100蛋白可作为心肺脑复苏后患者脑损伤的标志物,S-100蛋白水平高,提示预后不良,其有助于心跳骤停后早期昏迷患者的病情评估。

小脑延髓池注射纳洛酮对心肺复苏大鼠脑组织c-Fos mRNA及蛋白表达的影响

目的探讨小脑延髓池注射纳洛酮对心肺复苏大鼠脑神经保护的作用机制。方法将30只雄性SD大鼠随机分为假手术组、常规复苏组和纳洛酮复苏组。采用窒息法建立大鼠心脏骤停模型,复苏的同时给予药物治疗。恢复自主循环(ROSC)后24 h取脑组织,荧光定量PCR法检测脑组织c-Fos mRNA表达水平,免疫组化法检测脑组织c-Fos蛋白的表达。结果与常规复苏组比较,纳洛酮可显著降低大鼠脑组织c-Fos mRNA及蛋白表达量(P<0.01)。结论小脑延髓池注射纳洛酮可及时有效的作用于c-Fos基因,发挥脑神经保护作用。

HMGB1抑制剂预处理对大鼠心肺复苏后脑缺血再灌注损伤及TLR4/NF-κB信号通路的影响

目的探讨高迁移率族蛋白B1(HMGB1)抑制剂预处理对大鼠心肺复苏后脑缺血再灌注损伤及Toll样受体4(TLR4)/核转录因子-κB(NF-κB)信号通路的影响。方法建立大鼠心肺复苏模型(封闭气管3~4 min),随机分为模型组,甘草酸(HMGB1抑制剂)低、中、高剂量组(分别以1、2、3 mg/mL甘草酸溶液按体重10 mL/kg灌胃),以及乌司他丁组(按体重以50000 U/kg尾静脉注射乌司他丁),每组各12只;另设假手术组12只(仅暴露气管但不封闭气管)。观察各组神经功能缺损评分,测量计算各组大鼠脑组织含水量;采用苏木精-伊红(HE)染色检测各组大鼠神经元受损情况;采用酶联免疫吸附法(ELISA)检测血清中枢神经特异性蛋白(S100β)、神经元特异性烯醇化酶(NSE)水平,以及脑组织中白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平;Western blot法检测脑组织TLR4/NF-κB通路蛋白TLR4、髓样分化因子88(MyD88)、NF-κB p65、磷酸化核转录因子-κB(p-NF-κB p65)表达情况。结果与假手术组相比,模型组大鼠脑组织神经元核皱缩、变性,神经元损伤,脑组织含水量、神经功能缺损评分、血清中S100β及NSE水平、脑组织IL-6及TNF-α、TLR4、MyD88、NF-κB p65表达明显升高(P<0.05);与模型组相比,甘草酸低、中、高剂量组、乌司他丁组大鼠脑组织神经元恢复,神经功能缺损评分、脑组织含水量、血清中S100β、NSE水平、脑组织IL-6及TNF-α、TLR4、MyD88及NF-κB p65表达均降低(P<0.05),且甘草酸各剂量组间随剂量增高而降低。甘草酸高剂量组与乌司他丁组相比,上述指标差异无统计学意义(P>0.05)。结论HMGB1抑制剂甘草酸可能对心肺复苏后大鼠脑缺血再灌注损伤有修复作用,其作用可能是通过下调TLR4/NF-κB通路实现的。

Recovering from prolonged cardiac arrest induced by electric shock:A case report

BACKGROUND Cardiac arrest(CA)induced by electric shock is a rare occurrence,particularly in cases of prolonged CA.Currently,there is limited literature on similar incidents,and we present a relevant case report.CASE SUMMARY A 27-year-old Asian male man,experiencing respiratory CA due to electric shock,was successfully restored to sinus rhythm after 50 min of cardiopulmonary resuscitation and 8 electrical defibrillation sessions.In the subsequent stages,the patient received multiple organ function protection measures,leading to a successful recovery and eventual discharge from the hospital.CONCLUSION Prolonging resuscitation time can enhance the chances of survival for patients,this study provide valuable insights into the management of electric shock-induced CA.

心脏停搏复苏后犬脑矢状窦血浆内皮素-1及脑氧代谢变化

目的观察犬心脏停搏(CA)复苏后再灌注期间脑矢状窦血浆内皮素-1(ET-1)及脑氧代谢变化。方法健康杂种家犬6只,电击引起室颤(VF)性CA 8 min后,行开胸心肺复苏,在自主循环恢复后,控制通气4 h,取动脉血及脑矢状窦血行血气分析及ET-1测定,观察CA前及CA后再灌注30、60、120、240 min时的脑矢状窦血浆ET-1及脑矢状窦氧饱和度(SsO2)、氧利用率(O2UC)的变化。结果与CA前比较,脑矢状窦血浆ET-1在CA后再灌注120、240 min时显著升高(P<0.05);脑SsO2在CA后再灌注30 min时显著升高(P<0.05),但在CA后再灌注240 min时显著降低(P<0.01);脑O2UC在CA后再灌注30 min时显著降低(P<0.05),但在CA后再灌注240 min时显著升高(P<0.01)。结论CA复苏后脑循环ET-1水平升高,可能影响大脑灌注,导致脑氧代谢发生变化。

亚低温下超长心肺脑复苏成功救治体会

目的报告1例2次心搏骤停J波综合征患者的救治经过,探讨亚低温治疗在心肺脑复苏中的作用。方法复旦大学附属中山医院青浦分院急诊科2021年9月30日收治1例院外心搏骤停J波综合征患者,在治疗过程中采取亚低温脑保护措施,院内再次发生心搏骤停,在亚低温状态下持续进行了长达230 min的心肺复苏(CPR)后恢复窦性心律,最终患者救治成功,未遗留任何神经系统后遗症,现介绍临床诊治过程,分享救治体会。结果患者女性,17岁,因跑步后突发意识丧失30 min于2021年9月30日入院。既往曾有运动后或紧张后晕厥3次。此次晕厥后立即进行徒手CPR,10 min后救护车到达现场,给予电击除颤及气管插管机械通气。入住重症监护病房(ICU)时患者持续强直性抽搐,给予镇静、抗癫痫、维持内环境稳定等,同时给予亚低温治疗,控制体温在34~36℃,夜间强直抽搐逐渐缓解。10月1日11:40心电监护提示心室纤颤(室颤),立即给予CPR、电除颤、升压等抢救。因反复室颤,反复行电击除颤,同时采用心肺复苏机进行胸外按压,给予利多卡因抗心律失常,肾上腺素、异丙肾上腺素维持心率90次/min以上,15:30左右心律趋于稳定,血压逐渐改善。复苏成功后继续亚低温等脑保护治疗,10月4日意识转清,10月6日肌力基本恢复正常,拔除气管插管。动态心电图检查提示V1~V3 ST段抬高,结合患者反复晕厥病史,既往心电图提示早期复极,考虑J波综合征,Brugada综合征可能,安装植入型心律转复除颤器(ICD)后出院。结论本例患者2次心搏骤停均复苏成功,其中院内心搏骤停后CPR在亚低温状态下进行超长时间心肺脑复苏成功,未遗留神经系统后遗症,其救治经验为临床心肺脑复苏提供了参考。

腹部提压心肺复苏技术对心脏骤停患者血流动力学、脑功能、心肌酶的影响

目的:探究腹部提压心肺复苏对心脏骤停患者血流动力学、脑功能、心肌酶的影响。方法:选取2021年1月—2023年1月新余市人民医院收治心脏骤停患者94例,以随机数字表法将其分为对照组(常规心肺复苏)及观察组(腹部提压心肺复苏技术)各47例,对比两组血流动力学[心率(HR)、平均动脉压(MAP)、中心静脉压(CVP)]、脑功能[神经元特异性烯醇化酶(NSE)、S100蛋白(S100β)、脑源性神经营养因子(BDNF)]、心肌酶谱指标[心肌肌钙蛋白(cTnI)、乳酸脱氢酶(LDH)、肌酸激酶(CK)]、氧代谢指标[颈内静脉血氧饱和度(SjvO_(2))、动脉-颈内静脉血氧含量差(Ca-jvO_(2))、脑氧摄取率(ERO_(2))]、并发症发生率。结果:复苏20 min后,观察组HR、MAP、CVP水平均高于对照组(P<0.05)。复苏1 h后,对照组NSE、S100β水平均高于观察组,BDNF低于观察组(P<0.05)。复苏1 h后,观察组cTnI、LDH、CK水平均低于对照组(P<0.05)。复苏24 h后,对照组SjvO_(2)、Ca-jvO_(2)、ERO_(2)水平均低于观察组(P<0.05)。观察组并发症发生率低于对照组(P<0.05)。结论:对心脏骤停患者进行腹部提压心肺复苏,可改善患者血流动力学,保护患者脑功能,减轻心肌损伤,降低并发症发生率。

心肺复苏大鼠脑红蛋白缺氧诱导因子-1α的表达变化

目的研究大鼠心肺复苏后不同时间点脑红蛋白（neuroglobin，Ngb）、缺氧诱导因子-1α（HIF-1α）在mRNA水平表达中的变化规律，探讨Ngb在心脏骤停后脑缺血缺氧损伤病理变化中的作用机制及其诱导表达途径。方法SD雄性大鼠40只随机分为五组（n=8）：假手术组及复苏后1h、6h、12h、24h组。窒息法致大鼠心脏骤停后予以心肺复苏，复苏后不同时间点处死大鼠，应用RT—PCR法观察脑组织NgbmRNA、HIF-1αmRNA表达情况。结果复苏组脑组织NgbmRNA表达高于假手术组（P〈0．05），并于损伤后12h达高峰；与假手术组比较，复苏组脑组织HIF-1αmRNA表达增加（P〈0．05），且于复苏后1h、6h、12h、24h呈持续上升趋势。结论大鼠心脏骤停后早期脑组织NgbmRNA、HIF—lotmRNA表达增加，且呈时相性改变。

Improved Survival and Neurological Outcomes after Cardiopulmonary Resuscitation in Toll-like Receptor 4-mutant Mice

Background：Toll-like receptor 4 （TLR4） is a crucial receptor in the innate immune system and noninfectious immune responses.It has been reported that TLR4 participates in the pathological course of ischemia/reperfusion （I/R） injury.However,the role of TLR4 in the process of I/R injury after cardiac arrest （CA） and cardiopulmonary resuscitation （CPR） is still unknown.In this study,we investigated the effects of TLR4 mutation on survival and neurological outcome in a mouse model of CA/CPR.Methods：A model of potassium-induced CA was performed on TLR4-mutant mice （C3H/HeJ） and wild-type mice （C3H/HeN）.After 3 min of untreated CA,resuscitation was attempted with chest compression,ventilation,and intravenous epinephrine.Behavioral tests were performed on mice on day 3 after CPR.The morphological changes in hippocampal neurons were assessed by light and electron microscopy.Expressions of TLR4 and intercellular adhesion molecule-1 （ICAM-l） were detected by Western blot.Levels of tumor necrosis factor-α （TNF-α） and myeloperoxidase （MPO） were measured with enzyme-linked immunosorbent assay （ELISA）.Results：On day 3 after resuscitation the overall mortality was 33.33％ in C3H/HeJ group compared with 53.33％ in C3H/HeN group （P ＜ 0.05）.And there was much higher central tendency in C3H/HeJ group than C3H/HeN group during open field test （P ＜ 0.05）.Meanwhile,the percentage of nonviable neurons was 2 1.16％ in C3 H/HeJ group compared with 53.11％ in C3H/HeN group （P ＜ 0.05）.And there were significantly lower levels ofhippocampal TNF-α and MPO in C3H/HeJ mice （TNF-α：6.85±1.19 ng/mL,MPO：0.33±0.11 U/g） than C3 H/HeN mice （TNF-α：11.36±2.12 ng/mL,MPO：0.54±0.17 U/g） （all P ＜ 0.01）.CPR also significantly increased the expressions of TLR4 and ICAM-1 in C3H/HeN group.However,the expression ofICAM-l was much lower in C3H/HeJ group than in C3H/HeN group after CPR （P ＜ 0.01）.Conclusion：TLR4 signaling is involved in brain damage and in inflammation triggered by CA/CPR.