Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue最新文献

Objective: To investigate the relationship between kidney injury molecule-1 (KIM-1) in urine and acute physiology and chronic health evaluation II (APACHEII) score, and the prognosis in the patients suffered from sepsis.

Methods: In the perspective study, 56 patients in intensive care unit (ICU) from March 2010 to September 2011 suffered from sepsis were enrolled and treated according to the early goal-directed therapy (EGDT). The patients were divided into two groups according to the perform in EGDT or not within 6 hours (groupI, group II). Monitoring included APACHEII score, KIM-1, blood urea nitrogen (BUN) and creatinine (Cr) at before resuscitation (T0), 6 hours after resuscitation (T6 h), and 1 day (T1 d), 2 days (T2 d), 3 days (T3 d), 4 days (T4 d) and 5 days (T5 d) after ICU admission. According to the 28-day prognosis, all the patients were divided into survival group or death group.

Results: The value of APACHEII score, urine KIM-1, BUN and Cr in groupI(n=30), decreased after fluid resuscitation and decreased to the lowest at T5 d. The value of APACHEII score, urine KIM-1, BUN and Cr in groupII(n=26), increased after failure of fluid resuscitation and increased to the highest at T5 d. The value of APACHEII score at T2 d and urine KIM-1 at T1 d in groupII were significantly higher than those in groupI (APACHEII score: 26.35±6.18 vs. 13.25±4.72, urine KIM-1: 4.721±1.432 μg/L vs. 0.909±0.325 μg/L, both P<0.05). The mortality in groupI was significantly lower than that in group II [10.0% (3/30) vs. 73.1% (19/26), P<0.05]. The value of APACHEII score, urine KIM-1, BUN and Cr in survival group (n=34) decreased with the clinical condition improved and decreased to the lowest at T5 d, while the value of APACHEII score, urine KIM-1, BUN and Cr in death group (n=22) increased and increased to the highest at T5 d. The value of APACHEII score at T1 d, and urine KIM-1 at T6 d in death group were significantly higher than those in survival group (APACHEII score:26.39±8.95 vs. 14.27±5.11, urine KIM-1:3.134±1.117 μg/L vs. 1.447±0.472 μg/L, both P<0.05).

Conclusions: KIM-1 in urine could be a good index for evaluation of sepsis, and it is helpful to understand the disease development by continuous surveillance. It is very important for the appraisal of prognosis, development and prognosis in sepsis, combined with APACHEII score.

Objective: To determine the activation of matrix metalloproteinase (MMP-2, MMP-9) in rats with acute lung injury (ALI) and the effects of unfractionated heparin (UFH) on the levels.

Methods: Eighteen male Wistar rats were divided into control group, ALI group and UFH group, with 6 rats in each group by means of random number table. ALI was induced by administering a bolus injection of lipopolysaccharide (LPS) via the caudal vein at a dose of 6 mg/kg. In UFH group the rats were treated intravenously with 100 U/kg of UFH 15 minutes before the injection of LPS. In control group, the rats were treated with the same volume of normal saline. Serum levels of MMP-2 and MMP-9 were measured by enzyme linked immunosorbent assay (ELISA) at 1, 3, 6 hours via femoral vein. Six hours after the injection of reagents, the rats were sacrificed and lung tissue samples were collected for mRNA analysis of the MMP-2 and MMP-9 by real-time fluorescence quantitate reverse transcription-polymerase chain reaction (qRT-PCR).

Results: Compared with control group, the content of MMP-2 and MMP-9 in serum of ALI group were increased, and reached the peak at 6 hours (MMP-2: 2.86±0.40 μg/L vs. 1.21±0.24 μg/L, MMP-9: 2.54±0.29 μg/L vs. 1.15±0.34 μg/L, both P<0.01); they were down-regulated in UFH group at 6 hours (MMP-2: 1.92±0.31 μg/L vs. 2.86±0.40 μg/L, MMP-9: 1.82±0.26 μg/L vs. 2.54±0.29 μg/L, both P<0.05). Compared with control group, the mRNA expressions of MMP-2 and MMP-9 in the lung tissue of ALI group were increased at 6 hours (MMP-2 mRNA: 1.88±0.09 vs. 1.00±0.10, MMP-9 mRNA: 3.15±0.47 vs. 1.00±0.17, both P<0.01); they were down-regulated in UFH group (MMP-2 mRNA: 1.26±0.14 vs. 1.88±0.09, P<0.01; MMP-9 mRNA: 2.06±0.68 vs. 3.15±0.47, P<0.05), but still above the control group (both P<0.05).

Conclusions: The present study demonstrated that the level of MMP-2 and MMP-9 increased in rats with ALI. UFH could exert protective effects by inhibiting expression of MMP-2 and MMP-9 in serum and lung tissue, in both mRNA and protein expression.

Objective: To investigate the effects of glutathione (GSH) precursor glutathione ethyl ester (GSEt) on smoke inhalation induced lung injury rats.

Methods: Sixty healthy male Sprague-Dawley (SD) rats were divided into groups by random digits table method, which included normal group, model group, GSEt high dose group and GSEt low dose group. Smoke inhalation induced lung injury rats model was established. GSEt treatments were given through intraperitoneal injection for 50 mg/kg or 150 mg/kg 5 minutes after the injury. Arterial blood gas analysis was monitored at 2, 12 and 24 hours after injury in each group. Rats were sacrificed for lungs, and bronchoalveolar lavage fluid (BALF) was collected for analysis of GSH activity; and the activity of GSH, catalase (CAT) and glutathione reductase (GR) were detected in pulmonary tissue homogenate.The changes of pulmonary tissue pathology was observed through light microscope.

Results: Compared to normal group, arterial partial pressure of oxygen (PaO(2)) in model group were decreased significantly in each time; the activity of GSH in BALF, and the activity of GSH, CAT, GR in lung tissue were also observed decreased significantly. Compared with model group, GSEt treatment (150 mg/kg) with the PaO(2) advanced at 12 hours (82.9±7.0 mm Hg vs. 63.9±6.5 mm Hg, P<0.05), the activity of GSH was increased at the 12 hours and 24 hours (12 hours: 2.19±0.41 mg/g vs. 0.79±0.21 mg/g, 24 hours: 1.75±0.47 mg/g vs. 0.67±0.10 mg/g, both P<0.05); the activity of CAT in GSEt low dose group (50 mg/kg) was increased at the 24 hours and the same increase was also observed in GSEt high dose group (150 mg/kg) at 12 hours and 24 hours (low dose group 24 hours: 70.1±5.5 U/g vs. 56.3±5.0 U/g; high dose group 12 hours: 90.9±8.1 U/g vs. 67.9±6.1 U/g, 24 hours: 94.7±7.7 U/g vs. 56.3±5.0 U/g, all P<0.05); the activity of GR in GSEt high dose group was increased at 24 hours (5.25±0.77 mmol/g vs. 4.37±0.64 mmol/g, P<0.05). The histological abnormality of lung tissue was alleviated after application of GSEt (150 mg/kg) 12 hours later, less inflammatory cells infiltration and no punctate hemorrhage in lung tissues.

Conclusion: GSEt can enhance antioxidant capacity in lung tissues, it have a good protection for pulmonary injury.

Objective: To investigate the effect of oxygenation index (PaO(2)/FiO(2)) on patients' prognosis through comparative analyzing the monitoring indicators of acute respiratory failure patients treated by invasive mechanical ventilation.

Methods: Data from 91 acute respiratory failure patients treated by invasive mechanical ventilation in respiration intensive care unit (ICU) of the General Hospital of PLA of Lanzhou from November 2006 to August 2011 were retrospectively analyzed. Patients were divided into survival group (n=55) and death group (n=36) by the outcome, the critical severity scores of the diseases and changes in blood gas analysis during ventilation were compared, and their correlation with prognosis were analyzed.

Results: There were no significant differences in acute physiology and chronic health evaluationIII (APACHEIII) score, multiple organ dysfunction syndrome (MODS) score, acute lung injury (ALI) score between survival and death group before ventilation (62.77±22.92 vs. 74.62±25.77, 6.46±2.45 vs. 6.62±3.03, 1.90±0.57 vs. 2.10±0.73, all P>0.05). There was no significant difference in PaO(2)/FiO(2) between survival and death group on the first day of mechanical ventilation (132.18±67.29 mm Hg vs. 139.24±78.36 mm Hg, P>0.05). PaO(2)/FiO(2) in survival group were significantly higher than that in death group on the 3 days and 7 days of mechanical ventilation (3 days: 205.47±74.71 mm Hg vs. 149.76±70.38 mm Hg, 7 days: 225.37±67.20 mm Hg vs. 120.94±85.58 mm Hg, P<0.05 and P<0.01).

Conclusions: The present study demonstrated that the level of PaO(2)/FiO(2) is related with the prognosis of acute respiratory failure patients treated by invasive mechanical ventilation. Continuously monitoring the changes in PaO(2)/FiO(2) can be used as an important reference index to evaluate the prognosis of critical patients.

Objective: To analyze the value of automated acid-base mapping on diagnose and treatment of patients with community acquired pneumonia (CAP) in emergency department.

Methods: According to medical history, pulmonary function test, diagnosing guideline of chronic obstructive pulmonary disease (COPD), 111 patients with CAP were divided into two groups: single CAP group (n=56) and COPD complicated with CAP group [acute exacerbation of chronic obstructive pulmonary disease (AECOPD) group, n=55]. After enquiring medical history, arterial blood samples were drawn for blood gas analysis and automated acid-base mapping was analyzed.

Results: Arterial blood gas analysis showed arterial carbon dioxide partial pressure (PaCO(2)), HCO(3)(-), base excess of AECOPD group were obviously higher than those in CAP group (PaCO(2): 7.714±2.414 kPa vs. 5.896±1.308 kPa, HCO(3)(-): 30.767±7.185 mmol/L vs. 25.014±3.043 mmol/L, BE: 4.345±5.371 mmol/L vs. -0.354±3.180 mmol/L, all P<0.01). Automated acid-base mapping showed acid-base disturbance of AECOPD group was 89.1% and CAP group was 66.1%. Chi-square analysis were done for patients of normal (10.9%, 33.9%), acute respiratory acidosis (12.7%, 14.3%), chronic respiratory acidosis (49.1%, 10.7%), respiratory alkalosis (7.3%, 14.3%), metabolic acidosis (12.7%, 17.9%), metabolic alkalosis (12.7%, 8.9%) between AECOPD group and CAP group, and statistical significance was found between AECOPD group and single CAP group (χ (2)=24.421, P=0.001). Advanced Chi-square analysis for patients of normal, acute respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis were done and showed no statistical difference (χ (2)=5.280, P=0.260). It is indicated chronic respiratory acidosis occurrences rate in AECOPD patients was higher than single CAP patients.

Conclusions: Our study demonstrated that automated acid-base mapping may be helpful for emergency physician to rapidly recognize multi-acid-base disturbance in patients with CAP, and to promptly identify acute or chronic phase of respiratory disease.

Objective: To observe the effects of three dosages of nebulized unfractionated heparin (UFH) on alveolar coagulation, inflammation and lung histology in endotoxin-induced acute lung injury rat model, and investigate the appropriated dose of local UFH in managing intrapulmonary coagulopathy.

Methods: Twenty-nine male Wistar rats were divided into control (n=5) and UFH group (n=24) in table of random number, which were duplicated to be endotoxin-induced ALI rat model with lipopolysaccharide (LPS) injecting by intravenous route. The UFH group was divided into three subgroups, which were administered once with 6, 12 and 18 U/g aerosolized UFH in 10 ml at 2 hours after challenge, respectively, while the control group was simply nebulized with normal saline. All rats were sacrificed at 6 hours after intravenous administration of LPS, bronchoalveolar lavage was performed, and the fluid was collected. Enzyme-linked immune sorbent assay (ELISA) was used to measure the level of thrombin-antithrombin complex (TATc), tumor necrosis factor-α (TNF-α) in bronchoalveolar lavage fluid (BALF), and lung wet/dry (W/D) weight ratio, histology score were recorded.

Results: At 6 hours after LPS-induced lung injury, the levels of TATc and TNF-α, lung W/D weight ratio and histology score in 6 U/g and 12 U/g group were all lower than those of control group significantly (TATc: 0.959±0.681 μg/L, 1.165±0.854 μg/L vs. 2.141±0.791 μg/L, TNF-α: 4.449±5.054 ng/L, 9.096±4.099 ng/L vs. 18.184±3.869 ng/L, W/D weight ratio: 7.018±1.137, 7.367±0.349 vs. 8.472±0.614, histology score: 16.0±1.0, 16.5±1.5 vs. 19.6±0.4, P<0.05 or P<0.01). There was no significant difference in the comparisons between the subgroups of UFH in TATc level in BALF and lung histology score. For the TNF-αlevel in BALF, 18 U/g group evidently exceeded that of 6 U/g group (15.503±8.753 ng/L vs. 4.449±5.054 ng/L, P<0.01), and lung W/D weight ratio in 18 U/g group was also significantly higher comparing to 6 U/g (8.850±1.157 vs. 7.018±1.137, P<0.05) and 12 U/g group (8.850±1.157 vs. 7.367±0.349, P<0.05).

Conclusion: It was appropriate for the dose of nebulized UFH to be administered no more than 12 U/g in ALI treatment, which was enough to inhibit alveolar coagulant cascade, decrease early inflammatory response and alleviate lung tissue injury.