[The predictive value of ultrasonic measurement of the diaphragmatic thickening fraction combined with the maximal inspiratory pressure in mechanical ventilation patients].

Objective: To evaluate the value of the diaphragmatic thickening fraction (DTF) combined with the maximum inspiratory pressure (MIP) for the prediction of weaning success in mechanically ventilated patients. Methods: Patients admitted to the intensive care unit (ICU) of Yijishan Hospital of Wannan Medical College and on mechanical ventilation for 24 hours from June 2018 to April 2019 were selected as the study subjects. A low-level pressure support ventilation (PSV) method was applied to conduct a spontaneous breathing test (SBT) for 30 minutes after the patients met the screening conditions for clinical weaning; and the patients were weaned when they met the clinical weaning criteria. Before weaning, the patient's MIP was measured. The right hemidiaphragmatic excursion (DE) and the thickness of the diaphragm at the end of inspiration and at the end of exhalation were measured by ultrasound, and the DTF was calculated. The statistical relationship between the DTF, DE and MIP was analyzed. The predictive value for the success of weaning was calculated with the DTF, DE and MIP and was evaluated by the area under the receiver operating characteristic curve (AUC). Results: A total of 73 patients were included in this study, including 57 patients who were successfully weaned, and 16 patients who experienced failure. The DTF of the successful weaning group (35%, 8%) was significantly higher than that of the failed weaning group (25%±5%), and the difference was statistically significant (t=6.401, P<0.01). The MIP (34±9 cmH(2)O) in the successful weaning group was significantly higher than that in the failed weaning group (23±3 cmH(2)O), and the difference was statistically significant (t=7.186, P<0.01). The ROCs for the DTF, MIP, and diaphragmatic displacement were 0.907, 0.896, and 0.749, respectively. A DTF ≥ 27.78%, with a sensitivity of 92.98%, a specificity of 81.25%, and an AUC of 0.907 (95% CI: 0.816-0.963), was used as the standard to predict the success of weaning. An MIP>26.5 cmH(2)O, with a sensitivity of 80.7%, a specificity of 93.75%, and an AUC of 0.896 (95% CI: 0.803-0.955), was used as the standard to predict the success of weaning. The AUC of DTF ≥ 27.78% and MIP ≥ 26.5 cmH(2)O was 0.920 (95% CI:0.832-0.971), and the specificity increased to 87.7%, but the sensitivity was slightly reduced to 87.5%. Conclusions: The DTF and MIP play a crucial role in determining the appropriate time and predicting the outcome of weaning of mechanical ventilation patients. Compared with the DTF and MIP alone, the DTF combined with MIP greatly improved the accuracy of predicting successful weaning.

[Effects of calcium inhibitor on hydrogen peroxide-induced damage and calcium influx in bovine aortic endothelial cells in culture].

Hydrogen peroxide(H2O2)-induced cell damage and Ca2+ influx into bovine aortic endothelial cells (BAEC) were investigated. Our data suggested that H2O2 could dose- and time-dependently induce damage in cultured BAEC assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT) assay and increase malondialdehyde (MDA) production, which reflects the level of lipid peroxidation. Exposure of BAEC to H2O2 (100 mumol.L-1) caused significant increase in intracellular free calcium ([Ca2+]i) within 6 min, suggesting that the increase of [Ca2+]i might implicate in H2O2-induced cell damage. The calcium inhibitor nifedipine was found to dose-dependently decrease the increase of [Ca2+]i caused by H2O2 and protect BAEC against H2O2-induced damage reflected by significant decrease of MDA production and increase of MTT value. These results indicate that overload of calcium might be responsible to some extent causing oxidative damage to cells.

Protection of ebselen against anoxic damage of cultured neurons of cerebral cortex.

AIM: To study the protective effect of ebselen on anoxic damage of brain cells. METHODS: On d 10 after plating of the cortical neurons from 1-d-old rat, cultures were placed under 95% N2 + 5% CO2 for 2-6 h. Lactate dehydrogenase (LDH) in supernatant, thiobarbituric acid reactive substance (TBARS) and glutathione peroxidase (GSH-Px) activity of neurons were determined. RESULTS: Under anoxia, efflux of LDH and TBARS from cultured neurons increased while GSH-Px activity decreased. Ebselen reduced the efflux of LDH and TBARS in a dose-related manner and increased the total GSH-Px activity. CONCLUSION: Ebselen can protect neurons from anoxic damage.

[Protection of ebselen on oxygen free radical-induced lipid peroxidation damage of cultured rat cortical neuron and cortical mitochondria].

Ebselen (2-phenyl-1, 2-benzisoselenanzol-3 (2H) one, C13 H9NOSe) is a seleno-organic anti-oxidant compound. In this study, the effect of ebselen on lipid peroxidation damage induced by O2.- and .OH in vitro, of cultured rat cortical neuron and cortical mitochondria was studied. When neuron was exposed to hypoxanthine/xathine oxidase system and vitamin C/CuSO4 system, obvious damage was detected: lactic dehydrogenase(LDH) was released and TBARS content increased. Ebselen (10, 25, 50 mumol.L-1) reduced LDH efflux induced by O2.- and .OH in a dose-dependent manner. As for the TBARS content, from 5 mumol.L-1 to 50 mumol.L-1, ebselen negated its increase, also dose-dependently. Furthermore, ebselen lowered TBARS content of cortical mitochondria treated with O2.- and .OH in a dose-related manner. But ebselen showed no activity of scavenging O2.- and .OH. This suggests that ebselen has direct anti-oxidant activity on neuron and its activity is not achieved by scavenging oxygen free radical.

Effects of Ro 31-8220 on smooth muscle cell proliferation induced by fibrinogen degradation products.

AIM: To study the mitogenic activity of fibrin fibrinogen degradation products (FFDP) and the effect of a new selectively potent protein kinase C (PKC) inhibitor Ro 31-8220 (Ro). METHODS: Rat aortic smooth muscle cells (SMC) proliferation in culture was measured by crystal violet staining assay. RESULTS: FFDP stimulated the proliferation of SMC during the experimental period of 72 h, Ro 0.01-1 mumol.L-1 inhibited FFDP-induced cell proliferation in a concentration-dependent manner. CONCLUSION: Ro exerted inhibitory effect on cell proliferation induced by FFDP.

Assay of ditiocarb sodium and its methyl ester in mouse plasma by column-switching HPLC.

AIM: To establish a column-switching high pressure liquid chromatograpy (CSHPLC) with direct injection for determination of ditiocarb sodium (DTC) and its methyl ester (DTC-Me) in mouse plasma. METHODS: After automated online pretreating column enrichment and clear-up, DTC-Me was flushed and chromatographed on an ordinary reversed-phase analytical column, and monitored by UV at lambda absorption = 276 nm. DTC was methylated before determination. RESULTS: No potential interfering peaks were identified. The calibration curves of both analytes were linear within the range of 0.1-150 mg.L-1. The correlation coefficients of DTC and DTC-Me were 0.9998 and 0.9995, respectively. The detection limit was 25 micrograms.L-1 and the coefficient of variation in the assay was within 7% for both compounds. The average recoveries were in the range of 95.28 -100.06%. A typical application was presented for mouse after i.v. DTC 50 mg.kg-1. CONCLUSION: The rapid CSHPLC method with direct injection can be used for the study of pharmacokinetics of DTC and DTC-Me.

[Effects of sodium diethyldithiocarbamate on ischemia-reperfusion-induced brain injury in Mongolian gerbil].

Brain injury in Mongolian gerbil (Merisones unguiculatus) was induced by occluding bilateral common carotid arteries for 60 min followed by reperfusion for 5 or 30 min. Oxygen free radicals in brain tissue were measured by electron spin resonance (ESR) technique, malondialdehyde (MDA) was measured by fluorescence spectrometry, and superoxide dismutase (SOD) was measured by nitrite kit. Oxygen free radicals and MDA were not significantly increased, but activities of T-SOD and Mn-SOD were decreased after 60 min of cerebral ischemia. The free radicals were increased at 5-min reperfusion, and then reduced to the level of ischemia group after 30-min reperfusion. MDA was increased remarkably after reperfusion of 30 min, whereas the activity of SOD continued to decrease. Sodium diethyldithiocarbamate (DTC), i.v. 5-100 mg.kg-1 15 min before occlusion, decreased the production of MDA and increased the activities of T-SOD and Mn-SOD. The formation of oxygen free radicals was depressed by i.v. DTC 50 mg.kg-1. The result suggested that the protective effects of DTC on ischemia-reperfusion-induced brain injury might be induced by scavenging the oxygen free radicals, increasing the Mn-SOD activity and decreasing the production of MDA.