ABSTRACT
Objective To research the efficiency of short time intermittent veno-venous hemofiltration (SIVVH)on acute respiratory distress syndrome(ARDS). Methods Totally 95 patients suffered ARDS between January 2014 and October 2016 in the emergency intensive care unit(EICU)were divided to SIVVH group(n =37)and control group(n = 58). The SIVVH group received traditional therapy and SIVVH therapy,and control group traditional therapy. Vital signs,oxygenation index,APACHEⅡ scores between two groups before the treat-ment were compared. Vital signs,oxygenation index,APACHEⅡ scores,time of mechanical ventilation,length of stay of EICU and 28 day mortality between two groups after the treatment were compared. Results In two groups,vital signs,oxygenation index and APACHEⅡscores before the treatment showed no significant difference (P > 0.05). In SIVVH group ,heart rate and respiratory frequency on the 24th ,48th ,72nd and 120th hour were descended significantly when compared with those in control group(P < 0.05);body temperature on the 24th and 48th hour were descended obviously when compared with those in control group(P < 0.05);the oxygenation index on the 24th,48th,72nd and 120th hour were raised(P < 0.05);APACHEⅡ scores on the 72nd and 120th hour were lower than those in control group(P<0.05). There were shorter time of mechanical ventilation and length of stay of ICU in SIVVH group when compared with control group(P<0.05),but the 28 day mortality in SIVVH group was not lower when compared with that in control group(P>0.05). Conclusions SIVVH can improve the function of lung in ARDS,decrease the time of mechanical ventilation and the length of stay of ICU,and possible becomes an important adjunctive therapy.
ABSTRACT
Objective To research the efficiency of short time intermittent veno-venous hemofiltration (SIVVH)on acute respiratory distress syndrome(ARDS). Methods Totally 95 patients suffered ARDS between January 2014 and October 2016 in the emergency intensive care unit(EICU)were divided to SIVVH group(n =37)and control group(n = 58). The SIVVH group received traditional therapy and SIVVH therapy,and control group traditional therapy. Vital signs,oxygenation index,APACHEⅡ scores between two groups before the treat-ment were compared. Vital signs,oxygenation index,APACHEⅡ scores,time of mechanical ventilation,length of stay of EICU and 28 day mortality between two groups after the treatment were compared. Results In two groups,vital signs,oxygenation index and APACHEⅡscores before the treatment showed no significant difference (P > 0.05). In SIVVH group ,heart rate and respiratory frequency on the 24th ,48th ,72nd and 120th hour were descended significantly when compared with those in control group(P < 0.05);body temperature on the 24th and 48th hour were descended obviously when compared with those in control group(P < 0.05);the oxygenation index on the 24th,48th,72nd and 120th hour were raised(P < 0.05);APACHEⅡ scores on the 72nd and 120th hour were lower than those in control group(P<0.05). There were shorter time of mechanical ventilation and length of stay of ICU in SIVVH group when compared with control group(P<0.05),but the 28 day mortality in SIVVH group was not lower when compared with that in control group(P>0.05). Conclusions SIVVH can improve the function of lung in ARDS,decrease the time of mechanical ventilation and the length of stay of ICU,and possible becomes an important adjunctive therapy.
ABSTRACT
Objective To investigate protective effects of the hydrogen saturated saline on acute lung injury and pulmonary fibrosis in rats with paraquat (PQ) poisoning. Method Forty-eight Sprague-Dawley rats were randomly divided into 3 groups, namely control group, PQ poisoning group and intervention group (n = 16 rats in each group) . Animals in PQ poisoning group and intervention group were fed with PQ in dosage of 50 mg / kg. Rats of control group were fed equivalent amount of distilled water instead. One hour after administration of PQ, rats of intervention group were treated with 5 ml / kg hydrogen saturated saline injected intra-peritoneally twice a day until the rats were sacrificed. The rats of poisoning group and control group were treated with intra-peritoneal injection of equivalent amount of normal saline. Arterial partial pressure of oxygen ( PaO2 ), 8-hydroxy-2' -desoxyguanosine (8-OHDG) and transforming growth factor β1 (TGF-β1) of lung tissue were measured on the 3rd and 21st day after PQ administration. Quantitative data was expressed as mean ±standard deviation (x-±s) . SPSS version 12. 0 package was applied for variance analysis and SNK-q test, and statistical differences were considered significant when P ＜ 0. 05. Results ① PaO2 decreased significantly in poisoning group (9. 34 ± 0. 47 kPa) and intervention group (10. 30±0.62 kPa) compared with control group (11.87 +/- 0.42 kPa) on the 3d (P ＜0.01), and as intervention group was compared with poisoning group, there was a significant difference ( P ＜ 0. 05 ) . On the 21st day, PaO2 was still lower in poisoning group (8. 36 ±0. 51 kPa) and intervention group ( 10. 14 ±0. 27 kPa) than that in control group ( 11.87 +0. 24 kPa) (P ＜0. 01 and P ＜0. 05, respectively), and as intervention group was compared with poisoning group, there was a significant difference ( P ＜ 0. 01 ) . ②The levels of 8-OHDG in lung tissue increased significantly in poisoning group (23.58±7. 18 ng/ml ) and intervention group (9. 49± 2. 45 ng/ml) on the 3rd day after PQ administration compared with control group (7.71 + 1.96 ng/ml) (P＜0. 01 and P＜0. 05, respectively), and as intervention group was compared with poisoning group there was a significant difference ( p ＜0. 01 ) . There were no significant differences in 8-OHDG level found among the groups on the 21st day after PQ administration (P ＞ 0. 05 ) . ③ The level of TGF-β1 (measured by mean optic density, MOD) in lung tissue of rats in poisoning group ( 10. 11±2.49 MOD) and intervention group (8. 14 + 1.58 MOD) exhibited in higher levels than control group (5.93 + 1. 98 MOD) on the 3rd and (5.97 + 2. 35 MOD) on the 21st day after PQ administration (P ＜0. 01 and P ＜0. 05, respectively), and however, a lower level of TGF-β1 was observed in intervention group on 3d and 21d compared with poisoning group (P ＜0. 05 and P ＜0. 01, respectively) . Conclusions Hydrogen saturated saline can alleviate oxidative stress, mitigate oxidative damage and inhibit pulmonary fibrosis of lung induced by PQ intoxication.
ABSTRACT
Objective To elucidate cerebral cortical response to esophageal acid exposure in normal individuals by functional magnetic resonance imaging (fMRI) and the characteristics of activity. Methods Fifteen volunteers were received intraesophageal perfusion with either 0.9% of sodium chloride or acid (0.1 mmol/L HC1) solutions. The modified block-design model of fMRI scanning was performed simultaneously. All of 32 minutes were needed for resting (A, 8 minutes), 0.9% of sodium chloride perfusion (B,8 minutes), acid perfusion (C,8 minutes) and 0.9% of sodium chloride perfusion again (D,8 minutes). Each chunk was consisted of 160 scans and every scan contained 3 seconds. Six hundred and forty scans were collected in all. The clinical response to esophageal acid exposure was observed and the changes in the cerebral regions was statistically analyzed. Results After perfusion of 0.9% of sodium chloride or acid, 10 out of 15 volunteers had chemosensitive complaints, such as pain in pars laryngen pharyngis, heartburn and chest complaint. The initial active domains involved deutocerebrum, anterior part of callosal gyrus, left side of insula, two sides of amygdale and subiculum hippocampi, two outers of forehead cortex. The provoked regions of acid perfusion (C-A) and 0.9% of sodium chloride perfusion again (D-A) were as same as that of the activated domains by initial perfusion of 0.9% sodium chloride (B-A). The intensity and amplitude of most provoked regions increased gradually(D-A> B-A, P< 0.01). Conclusions The two different stimulations of saline and acid provoke similar cerebral regions that may act in the regulation of esophageal sensitivity. There are the evidences of the central mechanism of esophageal visceral hypersensitivity by acid perfusion.