Objectives To evaluate the resuscitative effects of mechanical and manual chest compression in patients with out-of-hospital cardiac arrest (OHCA). Methods All randomized controlled and cohort studies comparing the effects of mechanical compression and manual compression on cardiopulmonary resuscitation in OHCA patients were retrieved from the Cochrane Library, PubMed, EMBASE, and Ovid databases from the date of their establishment to January 14, 2019. The included outcomes were as follows: the return of spontaneous circulation (ROSC) rate, the rate of survival to hospital admission, the rate of survival to hospital discharge, and neurological function. After evaluating the quality of the studies and summarizing the results, RevMan5.3 software was used for the meta-analysis. Results In total, 15 studies (9 randomized controlled trials and 6 cohort studies) were included. The results of the meta-analysis showed that there were no significant differences in the resuscitative effects of mechanical and manual chest compression in terms of the ROSC rate, the rate of survival to hospital admission and survival to hospital discharge, and neurological function in OHCA patients (ROSC: RCT: OR = 1.12, 95% CI (0.90, 1.39), P = 0.31; cohort study: OR = 1.08, 95% CI (0.85, 1.36), P = 0.54; survival to hospital admission: RCT: OR = 0.95, 95% CI (0.75, 1.20), P = 0.64; cohort study: OR = 0.98 95% CI (0.79, 1.20), P = 0.82; survival to hospital discharge: RCT: OR = 0.87, 95% CI (0.68, 1.10), P = 0.24; cohort study: OR = 0.78, 95% CI (0.53, 1.16), P = 0.22; Cerebral Performance Category (CPC) score: RCT: OR = 0.88, 95% CI (0.64, 1.20), P = 0.41; cohort study: OR = 0.68, 95% CI (0.34, 1.37), P = 0.28). When the mechanical compression group was divided into Lucas and Autopulse subgroups, the Lucas subgroup showed no difference from the manual compression group in ROSC, survival to admission, survival to discharge, and CPC scores; the Autopulse subgroup showed no difference from the manual compression subgroup in ROSC, survival to discharge, and CPC scores. Conclusion There were no significant differences in resuscitative effects between mechanical and manual chest compression in OHCA patients. To ensure the quality of CPR, we suggest that manual chest compression be applied in the early stage of CPR for OHCA patients, while mechanical compression can be used as part of advanced life support in the late stage.
Objective To observe whether metformin (MET) plays a protective role in acute lung injury (ALI) induced by paraquat (PQ) poisoning in rats by activating the AMPK/NF-κB signaling pathway. Methods PQ exposure was used to construct a rat model of ALI and a model of acute type II alveolar epithelial cell (RLE-6TN) injury, and MET intervention was performed. Rat lung tissue samples were collected to evaluate pathological changes in rat lung tissue, the oxidation index, and inflammatory factors; cell viability was detected by CCK-8 assays, and the protein expression levels of phospho-AMPK and phospho-NF-κBp65 in rat lung tissue and RLE-6TN cells were observed by Western blotting. Results Compared with the PQ group, the MET treatment group showed significantly (1) reduced lung wet/dry ratio (W/D: 4.67 ± 0.31 vs. 5.45 ± 0.40, P < 0.001), (2) reduced pathological changes in lung tissue, (3) decreased MDA levels (nmol/mg prot: 2.70 ± 0.19 vs. 3.08 ± 0.15, P < 0.001) and increased SOD and GSH-Px activities (U/mg prot: 76.17 ± 5.22 vs. 45.23 ± 6.58, 30.40 ± 2.84 vs. 21.00 ± 3.20; all P < 0.001) in lung tissue homogenate, (4) reduced levels of IL-1β, IL-6, and TNF-α in lung tissue homogenates (pg/mL: 47.87 ± 5.06 vs. 66.77 ± 6.55; 93.03 ± 7.41 vs. 107.39 ± 9.81; 75.73 ± 6.08 vs. 89.12 ± 8.94; all P < 0.001), (5) increased activity of RLE-6TN cells (%: 0.69 ± 0.09, 0.76 ± 0.06, and 0.58 ± 0.03 vs. 0.50 ± 0.05; all P < 0.05), (6) decreased protein levels of phospho-NF-κBp65 in lung homogenates and RLE-6TN cells (p-NF-κB/NF-κB: 0.47 ± 0.09 vs. 0.81 ± 0.13; 0.26 ± 0.07 vs. 0.79 ± 0.13; all P < 0.01), and (7) upregulated protein expression of phospho-AMPK in lung homogenates and RLE-6TN cells (p-AMPK/AMPK: 0.88 ± 0.05 vs. 0.36 ± 0.12; 0.93 ± 0.03 vs. 0.56 ± 0.15; all P < 0.01). After the addition of the AMPK inhibitor Compound C (Com C), the protein expression levels of phospho-AMPK and phospho-NF-κBp65 returned to baseline. Conclusion MET can effectively alleviate ALI induced by paraquat poisoning and increase the viability of cells exposed to paraquat. The mechanism may be related to the activation of the AMPK/NF-κB pathway, downregulation of inflammatory mediators such as IL-6 and TNF-α, and upregulation of the SOD and GSH-Px oxidation index, and these effects can be inhibited by the AMPK inhibitor Com C.
Objectives: This study conducted a meta-analysis to assess the effectiveness, stability, and safety of mild therapeutic hypothermia (TH) induced by endovascular cooling (EC) and surface cooling (SC) and its effect on ICU, survival rate, and neurological function integrity in adult CA patients. Methods: We developed inclusion criteria, intervention protocols, results, and data collection. The results included outcomes during target temperature management as well as ICU stay, survival rate, and neurological functional integrity. The characteristics of the included population and each study were analyzed. Results: Four thousand nine hundred thirteen participants met the inclusion criteria. Those receiving EC had a better cooling efficiency (cooling rates MD = 0.31[0.13, 0.50], p < 0.01; induced cooling times MD = − 90.45[− 167.57, − 13.33], p = 0.02; patients achieving the target temperature RR = 1.60[1.19, 2.15], p < 0.01) and thermal stability during the maintenance phase (maintenance time MD = 2.35[1.22, 3.48], p < 0.01; temperature fluctuation MD = − 0.68[− 1.03, − 0.33], p < 0.01; overcooling RR = 0.33[0.23, 0.49], p < 0.01). There were no differences in ICU survival rate (RR = 1.22[0.98, 1.52], p = 0.07, I 2 = 0%) and hospital survival rate (RR = 1.02 [0.96, 1.09], p = 0.46, I 2 = 0%), but EC reduced the length of stay in ICU (MD = − 1.83[− 3.45, − 0.21], p = 0.03, I 2 = 49%) and improved outcome of favorable neurological function at discharge (RR = 1.15[1.04, 1.28], p < 0.01, I 2 = 0%). EC may delay the hypothermia initiation time, and there was no significant difference between the two cooling methods in the time from the start of patients' cardiac arrest to achieve the target temperature (MD = − 46.64[− 175.86, 82.58]). EC was superior to non-ArcticSun in terms of cooling efficiency. Although there was no statistical difference in ICU survival rate, ICU length of stay, and hospitalization survival rate, in comparison to non-ArcticSun, EC improved rates of neurologically intact survival (RR = 1.16 [1.01, 1.35], p = 0.04, I 2 = 0%).
Objective. To investigate the optimal temperature of hypothermia treatment in rats with cardiac arrest caused by ventricular fibrillation (VF) after the return of spontaneous circulation (ROSC). Methods. A total of forty-eight male Sprague-Dawley rats were induced by VF through the guidewire with a maximum of 5 mA current and untreated for 8 min. Cardiopulmonary resuscitation (CPR) was performed for 8 min followed by defibrillation (DF). Resuscitated rats were then randomized into the normothermia (37°C) group, milder (35°C) group, mild (33°C) group, or moderate (28°C) group. Hypothermia was immediately induced with surface cooling. The target temperature was maintained for 4 h before rewarming to 37 ± 0.5 ° C . Moreover, at the end of the 4 h, a rat in each group was randomly selected to be sacrificed for the cerebral cortex electron microscopy observation ( n = 1 ). The other resuscitated animals were observed for up to 72 h after ROSC ( n = 7 ). Left ventricular ejection fraction (LVEF) and left ventricular end diastolic volume (LVEDV) were measured. Survival time, survival rate, and neurological deficit score (NDS) were recorded for 72 h. Results. During hypothermia, higher LVEF was observed in the hypothermia groups when compared with normothermia group (35°C vs. 37°C, p < 0.05 , 33°C and 28°C vs. 37°C, p < 0.01 ). Among the hypothermia groups, LVEF was higher in the 28°C group than that of 35°C ( p < 0.05 ). However, both the heart rate (HR) ( p < 0.01 ) and LVEDV (28°C vs. 35°C, p < 0.01 , 28°C vs. 37°C and 33°C, p < 0.05 ) were lowest in the 28°C group when compared with the other groups. There were no significant differences of LVEF and LVEDV between the group 35°C and 33°C ( p > 0.05 ). After rewarming, the LVEF of 35°C group was higher than that of group 37°C, 33°C, and 28°C (35°C vs. 37°C and 28°C, p < 0.01 , 35°C vs. 33°C, p < 0.05 ). Group 35°C and 33°C resulted in longer survival ( p < 0.01 ), higher survival rate ( p < 0.01 ), and lower NDS (35°C vs. 37°C and 28°C, p < 0.01 , 33°C vs. 37°C and 28°C, p < 0.05 ) compared with the group 37°C and 28°C. The extent of damage to cerebral cortex cells in group of 35°C and 33°C was lighter than that in group of 37°C and 28°C. The 35°C group spent less time in the process of cooling and rewarming than the group 33°C and 28°C ( p < 0.01 ). Conclusions. An almost equal protective effect of milder hypothermia (35°C) and mild hypothermia (33°C) in cardiac arrest (CA) rats was achieved with more predominant effect than moderate hypothermia (28°C) and normothermia (37°C). More importantly, shorter time spent in cooling and rewarming was required in the 35°C group, indicating its potential clinical application. These findings support the possible use of milder hypothermia (35°C) as a therapeutic agent for postresuscitation.
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