Objective To explore the relationship between obstructive sleep apnea hypopnea syndrome ( OSAHS) and airway hyperresponsiveness ( AHR) . Methods 197 subjects suspected for OSAHS were enrolled in the study. They were all performed overnight polysomnogram ( PSG) monitoring and lung function test. Acoording to the results of FEV1% pred, they were performed bronchial provocation test( BPT)or brochial dilation test( BDT) . The relation between apnea hypopnea index ( AHI) and the degree of airway hyperresponsiveness ( AHR, expressed as PD20 -FEV1 ) was evaluated by linear correlation analysis. Results 117 patients were diagnosed as OSAHS, in which 28 cases were complicated with AHR( 3 cases with positive BDT result, 25 cases with AHR) . In 80 non-OSAHS patients, 7 cases were complicated with AHR. Theincidence of AHR was higher in the OSAHS patients compared with the non-OSAHS patients( 23. 9% vs 8. 8% , P lt; 0. 01 ) . AHI of OSAHS patients with AHR was higher than OSAHS patients without AHR[ ( 30. 3 ±5. 1) /h vs ( 23. 7 ±2. 4) /h, P lt;0. 01] . There was a positive correlation between AHI and degree of AHR in OSAHS patients with AHR( r=0. 62, P lt;0. 05, n=25) . Conclusion OSAHS is associated with an increased risk of AHR.
ObjectiveTo explore the influence of norepinephrine on the prediction of fluid responsiveness by passive leg raising (PLR) during septic shock. MethodsForty-six septic shock patients in intensive care unit of Nanjing Drum Tower Hospital were prospectively observed from September to November 2012. Among which 36 septic shock patients were enrolled with a positive PLR test (defined by an increase in stroke volume index ≥10%). A PLR test was performed at baseline (PLR1). A second PLR test (PLR2) was performed at returning to supine position for 10 min and the dose of norepinephrine was increased to maintain MAP ≥65 mmHg for 20 min. The changes of heart rate(HR),mean arterial pressure(MAP),central venous pressure(CVP),cardiac index(CI),stroke volume index(SVI),index of systemic vascular resistance(SVRI),global end-diastolic volume index(GEDVI),and cardiac function index(CFI) were monitored by transpulmonary thermodilution technique (PiCCO). ResultsPLR1 significantly increased SVI by (20.54±9.63)%,CI by (20.57±9.89)%,MAP by (7.64±5.77)%,and CVP by (25.83±23.39)%. As the dose of norepinephrine increased,SVI was increased by (16.97±9.06)%,CI by (16.78±8.39)%,GEDVI by (9.08±4.47)%,MAP by (28.07±12.48)%,and CVP by (7.86±8.52)%. PLR2 increased SVI by (13.74±8.79)%,CI by (13.79±9.08)%,MAP by (2.93±5.06)%,and CVP by (13.36±14.74)%. The PLR2 and the dose increase of norepinephrine augmented SVI to a significantly lesser extent than the PLR1 performed at baseline (both P<0.05). However,SVI increased by <10% in 6 patients while the baseline PLR was positive in these patients. ConclusionIn septic patients with a positive PLR at baseline,norepinephrine increases cardiac preload and cardiac output and influences the fluid responsiveness.
ObjectiveTo analyze responsiveness of Chinese version of Neck Outcome Score (NOOS-C) and provide a reliable measure to assess intervention effect for patients with neck pain.MethodsCross-cultural adaptation of NOOS was performed according to the Beaton’s guidelines for cross-cultural adaptation of self-report measures. Eighty patients with neck pain were recruited between September 2016 and May 2017. Those patients were assessed using NOOS-C and Chinese version of Neck Disability Index (NDI) before and after intervention. And 71 patients completed those questionnaires. The statistic differences of the score of each subscale and the total scale before and after intervention were evaluated by paired-samples t test. Internal responsiveness was determined by effect size (ES) and standardized response mean (SRM) based on the calculated difference before and after intervention. External responsiveness was analyzed by Spearman correlation coefficient.ResultsThe differences in symptom subscale, sleep disturbance subscale, participating in everyday life subscale, every day activity and pain subscale, and the scale between before and after intervention were significant (P<0.05) except for mobility subscale (P>0.05). The difference of NDI-C before and after intervention was –12.11%±17.45%, ES was 0.77, and SRM was 0.69. The difference of NOOS-C before and after intervention was 13.74±17.22, ES was 0.83, and SRM was 0.80. Spearman correlation analysis revealed that the relativity about NOOS-C and NDI-C before and after intervention were both negative (r=–0.914, P=0.000; r=–0.872, P=0.000).ConclusionNOOS-C’s responsiveness is good.
ObjectiveTo evaluate the value of stroke volume variation (SVV) and intrathoracic blood volume index (ITBVI) to predict fluid responsiveness in mechanically ventilated septic shock patients with spontaneous breathing. MethodsA prospective observational study was conducted in the Department of Critical Care Medicine of the First Affiliated Hospital of Guangzhou Medical University. Fluid resuscitation data was collected in septic shock patients who received PiCCO monitoring from June 2013 to June 2014. Transpulmonary thermodilution data were collected before and after fluid resuscitation, including cardiac index (CI), SVV, ITBVI, and central venous pressure (CVP). Seventeen patients were defined as responders by an observed increase of≥15% in the cardiac index (CI) after fluid resuscitation, 12 patients were defined as non-responders. Pearson correlation between changes of CI (ΔCI) and SVV, ITBVI, CVP was established. Area under the receiver operating characteristic (ROC) curve of SVV, ITBVI and CVP was calculated for predicting fluid responsiveness. ResultsBaseline CI and ITBVI were significantly lower in the responders (P < 0.05).There was no significant difference in baseline SVV between the responders and the non-responders (P > 0.05). A significant correlation was found between baseline ITBVI andΔCI (r=-0.593, P < 0.001), but no significant correlation between SVV andΔCI (r=0.037, P=0.847) or CVP andΔCI (r=0.198, P=0.302). The area under ROC curve of SVV, ITBVI and SVV for predicting fluid responsiveness was 0.640 (P=0.207), 0.865 (P=0.001), and 0.463 (P=0.565), respectively. The cut-off value of ITBVI for predicting fluid responsiveness was 784 mL/m2 with a sensitivity of 100.0% and a specificity of 70.6%. ConclusionIn mechanically ventilated septic shock patients with spontaneous breathing, ITBVI may be a valuable indicator in predicting fluid responsiveness compared with SVV.
Objective To investigate the relationship of small airway function with airway sensitivity and reactivity and assess the factors influencingairway hyperresponsiveness (AHR).Methods Data of consecutive subjects with suspected asthma who had a≥20% reduction in FEV1 after ≤12.8 mmol/L cumulative doses of methacholine were analyzed from January 2005 to April 2006.Airway sensitivity was assessed by the cumulative dose of methacholine required to cause 20% reduction in FEV1 (PD20).Airway reactivity was analyzed using the slope of the dose-response curve (DRS).The DRS was defined as the reduction in FEV1 from baseline after the final dose of methacholine inhaled divided by the cumulative dose inhaled.Because of their highly skewed distribution，DRS was logarithmically transformed (log10) for all analysis.Results A total of 184 consecutive subjects aged 16 to 80 years was enrolled.There were 70 male (38.0%) and 114 female (62.0%) subjects.Subjects with higher airway sensitivity，indicated by lower PD20，also had a lower Vmax50% and Vmax25%，and vise versa.PD20 was negatively correlated wit log10DRS (r=-0.874，Plt;0.01).In a simple linear regression model，log10DNS was significantly correlated with FEV1%，Vmax50% or Vmax25% respectively (the determinant r2 were 0.062，0.097 and 0.085，respectively，all Plt;0.01).In a multiple linear regression model that included age，height，and percentage of predicted FEV1，Vmax50% and Vmax25% accounted for 3.9% and 2.6%，respectively，of variability in airway reactivity.The association between Vmax50% and log10DNS was significant in both male and female subjects.The r2 was higher in male subjects.The subjects were divided into three age groups and the association between Vmax50% or Vmax25% and log10DNS was higher in female than in male for age≤25 years，higher in male than in female for 25 -45 years.No association was found for agegt;45 years in both males and females.Conclusions Impaired small airway function is associated with higher airway sensitivity and reactivity to methacholine in subjects with suspected asthma.
ObjectiveTo explore the effect of Aspergillus fumigatus on airway eosinophilia and hyperresponsiveness in rat model of chronic asthma. MethodsWistar rats were sensitized by intraperitoneal injections with ovalbumin (OVA) followed by chronic inhalation of nebulized OVA or physiologic saline. Rats were administered via the airways with placebo or aerosolized Aspergillus fumigatus spores suspension mimicking chronic Aspergillus fumigatus exposure. The Penh after acetylcholine provocation was detected using WBP system. The concentrations of IL-5 and eotaxin in BALF were measured by ELISA. The extents of eosinophil infiltration were evaluated on hematoxylin and eosin-stained(HE) and Wright-Giemsa stained BALF cells smear. ResultsAspergillus fumigatus worsened allergic airway inflammation in OVA-challenged rats,as evidenced by enhanced bronchial responsiveness to inhaled acetylcholine and increased bronchial eosinophilia. Elevated airway eosinophilia corresponded with higher levels of IL-5 and eotaxin in the Aspergillus Fumigatus exposure group. Aspergillus fumigatus,however,did not affect bronchial responses,numbers of eosinophils,IL-5 and eotaxin levels in saline challenged mice. ConclusionThe Results show that chronic Aspergillus fumigatus exposure aggravates eosinophilic airway inflammation in asthma rats by enhancing IL-5 and eotaxin production. Aspergillus fumigatus also increases bronchial hyperresponsiveness in asthma rats.
To diminish the specific lymphocytes that responsive to the rejection of allograft. Anti-rat CD4,CD8 monoclonal antibodies and trichosnthin (TCS) was conjugated to immunotoxin by heterobifunctional reagent SPDP, 2-IT. The free TCS was removed from conjugates mixture by a column of Sephacryl S-200. The SDS-PAGE and cytotoxic assay was used to measure the biological activity of immunotoxin. SDS-PAGE showed the immunotoxin, free McAb and TCS were in the mixture of conjugation, and the free TCS can be separated by Sephacryl S-200. In Vitro, the lymphocytes of rat can be killed by antiCD4,antiCD8 immunotoxin. The kill capability was relay to the amount of immunotoxin. The authors consider that the immunology unresponsiveness can be induced by antiCD4,antiCD8 immunotoxin. That was useful in induced transplantation tolerance.
Objective To investigate the value of central venous-to-arterial carbon dioxide difference/arterial-to-venous oxygen difference ratio [P(cv-a)CO2/C(a-cv)O2] in predicting oxygen metabolism after fluid resuscitation in patients with septic shock. Methods A prospective observational study was carried out on septic shock patients admitted in the intensive care unit of Nanjng Drum Tower Hospital from November 2013 to April 2014. All patients underwent fluid challenge (300 ml saline for 20 min, rapid intravenous infusion). The patients were divided into a fluid responded group (ΔCI≥10%) and a fluid unresponded group (ΔCI＜10%), according to the change of cardiac output index (ΔCI) after fluid challenge. Then the patients were divided into two subgroups in the fluid responded group, namely a ΔVO2≥10% group and a ΔVO2＜10% group, according to the change of VO2 (ΔVO2). Cardiac output index (CI) were determined by pulse indicator continuous cardiac output (PICCO). Hemoglobin, arterial carbon dioxide (PaCO2), arterial oxygen (PaO2), arterial oxygen saturation (SaO2), arterial blood lactate, central venous carbon dioxide (PcvCO2), central venous oxygen (PcvO2) and central venous oxygen saturation (ScvO2) were measured by blood gas analysis. P(cv-a)CO2/C(a-cv)O2 and oxygen consumption (VO2) were calculated. P(cv-a)CO2/C(a-cv)O2 before and after fluid challenge was compared between two subgroups. Results Fluid challenges were performed in 23 instances in 18 patients, among which 17 instances were defined as the fluid responded group. Compared with the fluid unresponded group, P(cv-a)CO2/C(a-cv)O2, arterial lactate and ScvO2 had no significant difference [P(cv-a)CO2/C(a-cv)O2](mm Hg/ml): 2.05±0.75vs. 1.58±0.67; arterial lactate (mmol/l): 3.78±2.50vs. 3.26±2.42; ScvO2(%): 73.71±9.64vs. 70.30±12.01,P＞0.05] in the fluid responded group before resuscitation. In the fluid responded group, there were 10 instances in the ΔVO2≥10% group and 7 instances in the ΔVO2＜10% group. P(cv-a)CO2/C(a-cv)O2 (mm Hg/ml) was significantly higher in the ΔVO2≥10% group before resuscitation compared with the ΔVO2＜10% group (2.43±0.73vs. 1.51±0.37,P＜0.01). Lactate (mmol/l) was also higher in the ΔVO2≥10% group before resuscitation (4.53±2.52vs. 1.46±0.82,P＜0.01). ScvO2 (%) had no significant difference between two groups (70.79±9.15vs. 72.13±13.42,P＞0.05). The areas under ROC curve (AUCs) of P(cv-a)CO2/C(a-cv)O2, lactate and ScvO2 for predicting ΔVO2≥10% were 0.843, 0.921, and 0.529, respectively. The sensitivity and specificity of P(cv-a)CO2/C(a-cv)O2≥1.885 mm Hg/ml for predicting ΔVO2≥10% after fluid resuscitation were 70% and 86%, respectively. Conclusion For septic shock patients with fluid responsiveness, P(cv-a)CO2/C(a-cv)O2 can predict oxygen metabolism after fluid resuscitation and can be used as a reliable parameter to guide fluid resuscitation.
Objective To study the responsiveness change of neutrophils when experiencing the second insult after the initial temperature activation in cardiopulmonary bypass (CPB) by using an in vitro model. Methods The neutrophils were isolated from blood which was drawn from each of 60 health volunteers. The samples were divided into 5 groups including normothermia, tepid temperature, moderate hypothermia, deep hypothermia, and rewarming hyperthermia by random digital table with 12 in each group according to the change of temperature during CPB. An in vitro model for studying neutrophil responsiveness was established by using a polymerase chain reaction thermocycler. Five time points were set for each group, including T0: starting CPB, T1: starting rewarming, T2: 0.5 h after rewarming, T3: 1 h after rewarming, and T4: 1.5 h after rewarming. Platelet activating factor (PAF) was added into each group at T2, T3, and T4, and then the value of membranebound elastase (MBE) activity was measured as responsiveness of neutrophils. Analysis of covariance was applied by using SPSS 13.0 for statistic analysis. If the [CM(159mm]covariance had significant difference between main effects, Bonferroni method would be applied for pairwise comparison. Results The main effect difference of neutrophil responsiveness among different groups was statistically different (F=4.372,P=0.002). MBE value had no statistical difference between the normothermia and tepid temperature groups (81.9±4.5 ng/10.6 cells vs. 76.5±3.6 ng/106 cells, P=0.134). while the MBE values in these two groups were higher than those in the other three groups (P=0.001). MBE value in the rewarming hyperthermia group was higher than that in the deep hypothermia group (61.2±2.7 ng/106 cells vs. 50.9±3.7 ng/106 cells, P=0.005). There was no statistical difference between the moderate hypothermia group (56.4±3.2 ng/106 cells) and the rewarming hyperthermia group (P=0.167), so was it between the moderate hypothermia group and the deep hypothermia group (P=0.107). The main effects of neutrophil responsiveness at different time points was statistically different (F=3.566, P=0.03) when PAF was added. MBE value at T4 was higher thanthat at T2 (70.9±2.5 ng/106 cells vs. 59.9±2.3 ng/106 cells, P=0.027). There was no statistical difference among T3 (65.5±1.8 ng/106 cells), T2 (P=0.168), and T4 (P=0.292) in MBE value. Conclusion Normothermia， tepid temperature， and rewarming hyperthermia during CPB can enhance neutrophil responsiveness and MBE release when neutrophils suffer the second insult. There is a time window for neutrophils to be easily activated during rewarming period.
Objective To study the mechanism of immune hyporesponsiveness of allograft rejection induced by transfusion nonpufsed allopeptide syngeneic immature dendritic cell (imDC) generated from recipient bone marrow progenitors and to explore a possible strategy for liver allograft protection in clinic. Methods Forty experimental rats were randomly divided into 4 group: control group, cyclosporine A (CsA) group, mature DC (mDC) group and imDC group. In control group, Wistar rats only received liver transplantation. In CsA group, Wistar rats underwent liver transplantation plus CsA treatment 〔10 mg/（kg·d)〕. In mDC group, recipient-derived mDC 1×106 were infused intravenously through the penile vein to Wistar rats. In imDC group, ImDC with the dose of 1×106 were injected into Wistar rats via the dorsum vein of penile. In each group, five recipients were killed on the 10th day after transplantation, the other five recipients were left to observe survival time. The levels of ALT, AST, TBIL, IL-2, IFN-γ, IL-4 and IL-10 were detected. The acute rejection and the expression of FasL/Fas in the grafts were detected by HE and immunohistochemical staining. Western blot was used to detect Scurfin protein expression of CD4+ CD25+ T cells. Results The median survival time of the liver allografts in CsA group and imDC group were significantly longer than that in control group and mDC group ( P ＜ 0.05). The levels of ALT and TBIL in control group and mDC group were significantly higher than those in CsA group and imDC group ( P ＜ 0.05). Compared with CsA group and imDC group, the levels of IL-2 and IFN-γ were higher but the levels of IL-4 and IL-10 were lower in control group and mDC group ( P ＜ 0.01). Slightly or no rejection reaction was found in CsA group and imDC group ( P ＜ 0.05). The Scurfin protein expressions of CD4+ CD25+ T cells of imDC group were significantly higher than those of other three groups. Conclusion Application of nonpufsed allopeptide syngeneic recipient-derived imDC is an effective way to induce immune hyporesponsiveness by blocking indirect recognition in rat liver transplantation model. Survival span is significantly prolonged by its protective effect. The mechanism of immune hyporesponsiveness induced by imDC transfusion might be involved in some aspects: T cell apoptosis, immune deviation of Thl/Th2 cytokine net and inhibition of T lymphocytes responsiveness by regulatory T cells.