Effects of pulmonary stretch reflex on lung injury in rabbits with acute respiratory distress syndrome

BACKGROUND： Pulmonary stretch reflex plays an important role in regulation of respiratorymovement. This study aimed to evaluate the effect of pulmonary stretch reflex on lung injury inrabbits with acute respiratory distress syndrome （ARDS）.METHODS： ARDS rabbits were given intratracheal infusion of hydrochloric acid and ventilatedwith neurally adjusted ventilatory assistance （NAVA） with a tidal volume （VT） of 6 mL/kg and theelectrical activity of diaphragm （EAdi）-determined positive end expiratory pressure. After isolation ofthe bilateral vagus nerve trunk, the rabbits were randomized into two groups： sham operation （SHAM）group （n=5） and bilateral vagotomy （VAG） group （n=5）. Gas exchange and respiratory mechanicswere detected at baseline, after lung injury and 1, 2, and 3 hours after ventilation respectively.Pulmonary permeability index, pathological changes and infl ammatory response were also measured.RESULTS： Compared with the SHAM group, PaO2/FiO2 in the VAG group decreased signifi cantly2 and 3 hours after ventilation （P〈0.05）. There was no significant difference in PaCO2 betweenthe SHAM and VAG groups （P〉0.05）, and the VAG group had a high VT, peak pressure （Ppeak）,and mean pressure （Pm） compared with the SHAM group 1, 2, 3 hours after ventilation （P〈0.05）.Compared to the SHAM group, dead space fraction （VD/VT） and respiratory system elastance （Ers）in the VAG group increased （P〈0.05） and static pulmonary compliance （Cst） decreased markedly（P〈0.05） after ventilation for 3 hours. Lung wet/dry weight ratio （W/D） （8.4±1.2 vs. 6.6±1.0）, lung injuryscore （6.3±1.8 vs. 3.8±1.3）, tumor necrosis factor-# （TNF-#） （779±372 pg/mL vs. 355±130 pg/mL）and interleukin-8 （IL-8） （169±21 pg/mL vs. 118±17 pg/mL） increased significantly in the VAG groupcompared with the SHAM group （P〈0.05）.CONCLUSION： Lung injury is aggravated after bilateral vagotomy, demonstrating thatpulmonary stretch refl ex may have protective effect on the lung.

Venovenous extra-corporeal membrane oxygenation for severe acute respiratory distress syndrome: a matched cohort study

Background:Although the use of extra-corporeal membrane oxygenation (ECMO) has been rapidly increasing,the benefit of ECMO in patients with acute respiratory distress syndrome (ARDS) remains unclear.Our objective was to investigate the effect of venovenous ECMO (VV-ECMO) on adult patients with severe ARDS.Methods:We conducted a multi-center,retrospective,cohort study in the intensive care units (ICUs) of six teaching hospitals between January 2013 and December 2018.Patients with severe ARDS who received W-ECMO support were included.The detailed demographic data and physiologic data were used to match ARDS patients without ECMO.The primary endpoint was the 28-day mortality.Results:Ninety-nine patients with severe ARDS supported by VV-ECMO and 72 patients without ECMO were included in this study.The acute physiology and chronic health evaluation Ⅱ score was 23.1 ± 6.3 in the ECMO group and 24.8 ± 8.5 in the control group (P =0.1195).The sequential organ failure assessment score was 12.8 ± 3.4 in the ECMO group and 13.7 ± 3.5 in the control group (P =0.0848).The 28-day mortality of patients with ECMO support was 39.4%,and that of the control group was 55.6%.The survival analysis curve showed that the 28-day mortality in the ECMO group was significantly lower than that in the control group (P =0.0097).Multivariate Cox regression analysis showed that the independent predictors of the 28-day mortality were the requirement of vasopressors before ECMO (hazard ratio [HR]:1.006;95% confidence interval [CI]:1.001-1.013;P =0.030) and duration of mechanical ventilation before ECMO (HR:3.299;95% CI:1.264-8.609;P =0.034).Conclusions:This study showed that ECMO improved the survival of patients with severe ARDS.The duration of mechanical ventilation and the requirement of vasopressors before ECMO might be associated with an increased risk of death.

Effects of Propofol on Respiratory Drive and Patient-ventilator Synchrony during Pressure Support Ventilation in Postoperative Patients： A Prospective Study

Background： Propofol is increasingly nsed during partial support mechanical ventilation such as pressure support ventilation （PSV） in postoperative patients. However breathing pattern, respiratory drive, and patient-ventilator synchrony are affected by the sedative used and the sedation depth. The present study aimed to evaluate the physiologic effects of varying depths ofpropofbl sedation oll respiratory drive and patient-ventilator synchrony during PSV in postoperative patients. Methods： Eight postoperative patients receiving PSV for 〈24 h were enrolled. Propofol was administered to achieve and maintain a Ramsay score of 4, and the inspiratory pressure support was titrated to obtain a tidal volume （VT） of 6-8 ml/kg. Then, tile propolbl dose was reduced to achieve and maintain a Ramsay score of 3 and then 2. At each Ramsay level, the patient underwent 30-rain trials of PSV. We measured the electrical activity of the diaphragm, flow, airway presstlre, neuro-ventilatory efficiency （NVE）, and patient-ventilator synchrony. Results： Increasing the depth of sedation reduced the peak and mean electrical activity of the diaphragm, which suggested a decrease in respiratory drive, while VT remained unchanged. The NVE increased with an increase in the depth of sedation. Minute ventilation and inspiratory duty cycle decreased with an increase in the depth of sedation, but this only achieved statistical significance between Ramsay 2 and both Ramsay 4 and 3 （P 〈 0.05）. The ineffective triggering index increased with increasing sedation depth （9.5 -4- 4.0%, 6.7 - 2.0%, and 4.2-2.1% for Ramsay 4, 3, and 2, respectively） and achieved statistical significance between each pair of depth of sedation （P 〈 0.05）. The depth of sedation did not affect gas exchange. Conclusions： Propofol inhibits respiratory drive and deteriorates patient-ventilator synchrony to tile extent that varies with tile depth of sedation. Propolbl has less effect on breathing pattern and has no effect on VT and gas exchange in postoperative patients with PSV.

Hepatic Perfusion Alterations in Septic Shock Patients： Impact of Early Goal-directed Therapy

Background： Early goal-directed therapy （EGDT） has become an important therapeutic management in early salvage stage of septic shock. However, splenic organs possibly remained hypoperfused and hypoxic despite fluid resuscitation. This study aimed to evaluate the effect of EGDT on hepatic perfusion in septic shock patients. Methods： A prospective observational study was carried out in early septic shock patients who were admitted to Intensive Care Unit within 24 h after onset and who met all four elements of the EGDT criteria after treatment with the standard EGDT procedure within 6 h between December 1, 2012 and November 30, 2013. The hemodynamic data were recorded, and oxygen metabolism and hepatic functions were monitored. An indocyanine green clearance test was applied to detect the hepatic perfusion. The patients＇ characteristics were compared before treatment （TO）, immediately after EGDT （T 1 ）, and 24 h after EGDT （T2）. This study is registered at ClinicalTrials.org, NCT02060773. Results： Twenty-one patients were included in the study; however, the hepatic perfusion data were not included in the analysis for two patients： therefore, 19 patients were eligible for the study. Hemodynamics data, as monitored by pulse-indicator continuous cardiac output, were obtained from 16 patients. There were no significant differences in indocyanine green plasma disappearance rate （ICG-PDR） and 15-min retention rate （Rl 5） at TO （ 11.9 ±5.0%/min and 20.0 ±13.2%）, T1 （ 11.4 ± 5.1%/min and 23.6 ± 14.9%）, and T2 （ 11.0 ±4.5%/rain and 23.7 ± 15.3%） （all P 〉 0.05）. Both of the alterations of ICG-PDR and R l 5 showed no differences at TO, T1, and T2 in the patients of different subgroups that achieved different resuscitation goal numbers when elected （P 〉 0.05）.

Role of immunodeficiency in Acinetobacter baumannii associated pneumonia in mice

Background:Acinetobacter baumannii(A.baumannii)has become one of the most important opportunistic pathogens inducing nosocomial pneumonia and increasing mortality in critically ill patients recently.The interaction between A.baumannii infection and immune response can influence the prognosis of A.baumannii related pneumonia.The target of the present study was to investigate the role of immunodeficiency in A.baumannii induced pneumonia.Methods:Male BALB/c mice were randomly divided into the normal immunity control(NIC)group,normal immunity infection(NIA)group,immune compromised control(CIC)group,and immune compromised infection(CIA)group(n=15 for each group).Intraperitoneal injection of cyclophosphamide and intranasal instillation of A.baumannii solution were used to induce compromised immunity and murine pneumonia,respectively.The mice were sacrificed at 6 and 24 h later and the specimens were collected for further tests.Seven-day mortality of mice was also assessed.Results:After A.baumannii stimulation,the recruitment of neutrophils in mice with normal immunity increased sharply(P=0.030 at 6 h),while there was no significant raise of neutrophil counts in mice with compromised immune condition(P=0.092 at 6 h,P=0.772 at 24 h).The Th cell polarization presented with pulmonary interleukin(IL)-4 and interferon(IFN)-γlevel in response to the A.baumannii in CIA group were significantly depressed in comparison with in NIA group(IFN-γ:P=0.003 at 6 h;P=0.001 at 24 h;IL-4:P<0.001 at 6 h;P<0.001 at 24 h).The pulmonary conventional dendritic cell accumulation was even found to be inhibited after A.baumannii infection in immunocompromised mice(P=0.033).Correspondingly,A.baumannii associated pneumonia in mice with compromised immunity caused more early stage death,more severe histopathological impairment in lung.Conclusion:A.baumannii could frustrate the immune response in immunocompromised conditions,and this reduced immune response is related to more severe lung injury and worse outcome in A.baumannii induced pneumonia.