Objective To investigate the correlation of oxygen extraction rate (ERO2) with blood lactate clearance rate and cardiac output (CO) in the early stage of post-restoration of spontaneous circulation (ROSC) in patients resuscitated from cardiogenic cardiac arrest,and to analyze the relationship between the ERO2 and prognosis.Methods Fourteen patients successfully resuscitated from in-hospital cardiogenic cardiac arrest in the emergency ICU from October 2012 to January 2014 were retrospectively analyzed.These patients were assigned to survival group (n =5) or death group (n =9) as per the outcome at 72 h after ROSC.At admission (0 h),3,6 and 12 h after ROSC,arterial blood and venous blood were drawn to detect ERO2 and lactate clearance rate.Cardiac output (CO) was measured by thoracic impedance method,APACHE Ⅱ scores were assessed,and survival time was recorded.Results The patients in the death group died during the period of 12-72 hours after ROSC.The significantly decreased ERO2 at 6 h and 12 h after ROSC,and decreased blood lactate clearance rate and decreased CO at 3 h,6 h and 12 h after ROSC were found in the death group compared with the survival group (all P ＜ 0.05).The ERO2 at 6 h and 12 h after ROSC was significantly positively related to blood lactate clearance rate (r =0.857,r =0.947,both P ＜ 0.05) and CO (r =0.968,r =0.936,both P ＜ 0.05) at 3 h,6 h and 12 h after ROSC.The ERO2 at 6 h and 12 h after ROSC was significantly negatively related to APPACHE Ⅱ score (r =-0.970,r =-0.973,both P ＜ 0.05);APPACHE Ⅱ scores were significantly negatively correlated with blood lactate clearancerates (r=-0.880,r=-0.899,r=-0.850,all P＜0.05) and CO (r=-0.876,r=-0.922,r=-0.916,all P＜0.05) at 3 h,6 h and 12 h after ROSC.Conclusions The ERO2 at 6h after ROSC may be used to assess the severity and prognosis of patients resuscitated from cardiogenic cardiac arrest.

[ ABSTRACT] AIM:To prove the purinergic signaling mechanism of the neuroprotective action of hydrogen sulfide by observing the effects of sodium hydrosulfide ( NaHS) , a donor of hydrogen sulfide, on the cell viability, intracellular Ca2+concentration ( [ Ca2+] i ) and the change of membrane permeability in the PC12 cells injured by adenosine triphos-phate ( ATP) .METHODS: PC12 cells in logarithmic growth phase were randomly divided into 4 groups.In control group, the cells were cultured without ATP treatment.In ATP group, the cells were treated with ATP after cultured for 24 h.In NaHS+ATP group, the cells were incubated with NaHS for 30 min before treated with ATP, and NaHS always exis-ted in the reaction system.In KN-62+ATP group, the cells were pretreated with KN-62 for 30 min, and the other treat-ments were as the same as those in NaHS+ATP group.The cell viability was assessed by MTT assay.The [ Ca2+] i was detected by Fura-2/AM staining.The membrane permeability was observed by staining with fluorescent dye YO-PRO-1. RESULTS:ATP at concentration of 0.3 mmol/L showed no injury effect on the cells.However, the cell viability was dropped gradually in a dose-dependent manner as the ATP at doses of 1, 3, 5 and 10 mmol/L.The decline of cell viability by ATP was obviously reversed by 200 μmol/L of NaHS in the PC12 cells (P<0.05), but exasperated by 800μmol/L of NaHS (P<0.05).At the same time, ATP evoked the increase in [Ca2+]i in a dose-dependent manner, which was inhib-ited by NaHS ( P<0.05) .Furthermore, the YO-PRO-1 uptake induced by ATP in a dose-dependent and time-dependent manner was also reduced by NaHS ( P<0.05) .CONCLUSION:Hydrogen sulfide has protective effect on the PC12 cells injured by ATP.The mechanism may be related to the reverse of the increased [ Ca2+] i and YO-PRO-1 uptake.

Objective:To investigate the risk factors for intracranial hematoma progression in patients within 24 h of traumatic brain injury.Methods:A prospective study was performed; 184 patients with traumatic brain injury admitted to our hospital from January 2018 to June 2021 were enrolled. According to the states of intracranial hematoma indicated by head CT within 24 h of injury, these patients were divided into intracranial hematoma progression group ( n=52) and intracranial hematoma stable group ( n=132). The clinical data of patients in the two groups were compared and the independent risk factors for intracranial hematoma progression were screened by multivariate Logistic regression analysis. Results:As compared with intracranial hematoma stable group, patients in the intracranial hematoma progression group had significantly advanced age, significantly higher systolic blood pressure and blood glucose levels, statistically higher proportions of patients with parenchymal hemorrhage, subarachnoid hemorrhage, and multiple hematomas, significantly longer prothrombin time, significantly higher international standardization index and D-dimer level, significantly higher proportion with patients with fibrinogen<2.0 g/L, statistically increased K value (blood coagulation time) of thromboelastic map, proportion of patients with α Angle (blood coagulation angle)<64°, level of vascular endothelial biomarker syndecan-1 (Syn-1), and von willebrand factor (vWF) activity, and significantly decreased Glasgow Coma Scale (GCS) scores at admission and platelet count ( P<0.05). Multivariate Logistic regression analysis showed that age ( OR=1.066, 95%CI: 1.018-1.117, P=0.007), systolic blood pressure ( OR=1.076, 95%CI: 1.041-1.111, P<0.001), multiple hematoma ( OR=6.559, 95%CI: 2.025-21.245, P=0.002), fibrinogen<2.0 g/L ( OR=6.164, 95%CI: 1.586-23.954, P=0.009), K value ( OR=6.500, 95%CI: 1.755-24.082, P=0.005) and Syn-1 level ( OR=1.111, 95%CI: 1.015-1.215, P=0.022) were independent risk factors for intracranial hematoma progression in patients with traumatic brain injury at early stage. Conclusion:Traumatic brain injury patients, at early stage, with advanced age, multiple intracranial hematoma, high systolic blood pressure, low fibrinogen, prolonged K value and high Syn-1 level are trend to have intracranial hematoma progression.