An Expeditious Neutralization Assay for Porcine Reproductive and Respiratory Syndrome Virus Based on a Recombinant Virus Expressing Green Fluorescent Protein.

Due to the extensive genetic and antigenic variation in Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), as well as its rapid mutability and evolution, PRRS prevention and control can be challenging. An expeditious and sensitive neutralization assay for PRRSV is presented to monitor neutralizing antibodies (NAbs) in serum during vaccine research. Here, a PRRSV expressing eGFP was successfully rescued with reverse genetics based on the infectious clone HuN4-F112-eGFP which we constructed. The fluorescent protein expressions of the reporter viruses remained stable for at least five passages. Based on this reporter virus, the neutralization assay can be easily used to evaluate the level of NAbs by counting cells with green fluorescence. Compared with the classical CPE assay, the newly developed assay increases sensitivity by one- to four-fold at the early antibody response stage, thus saving 2 days of assay waiting time. By using this assay to unveil the dynamics of neutralizing antibodies against PRRSV, priming immunity through either a single virulent challenge or only vaccination could produce limited NAbs, but re-infection with PRRSV would induce a faster and stronger NAb response. Overall, the novel HuN4-F112-eGFP-based neutralization assay holds the potential to provide a highly efficient platform for evaluating the next generation of PRRS vaccines.

Prediction of in-hospital mortality in patients with exertional heatstroke: a 13-year retrospective study.

Hyperactivity of coagulation is common in exertional heatstroke (EHS). Disseminated intravascular coagulation (DIC) is the most severe form of coagulation dysfunction and associated with poor outcome. DIC, temperature and Glasgow coma scale score were identified as independent risk factors for in-hospital mortality by multivariate logistic regression analysis, and we developed a nomogram for predicting in-hospital mortality in a 13-year EHS patient cohort. The nomogram was assessed by calibration curves and bootstrap with 1,000 resamples. The receiver operating characteristic curve was constructed, and the area under the curve (AUC) was compared. Two hundred and ten patients were included. The in-hospital mortality was 9.0%, and the incidence of DIC was 17.6%. The AUC of the nomogram was 0.897 (95% CI 0.848-0.935, p < .0001) and was non-inferior to SOFA and APACHE II scores but superior to SIRS score, which were widely-used score systems of disease severity. The nomogram contributed to the adverse outcome prediction of EHS.

Glasgow Coma Scale as an Indicator of Patient Prognosis: A Retrospective Study of 257 Patients with Heatstroke from 3 Medical Centers in Guangdong, China.

BACKGROUND Coma has been considered as a valuable symptom of heatstroke. This study aimed to evaluate the role of the Glasgow Coma Scale (GCS) as an indicator of prognosis of patients with heatstroke. MATERIAL AND METHODS From Jan 1st, 2013 to Dec 31st, 2020, the clinical courses of 257 heatstroke patients from 3 medical centers in Guangdong, China, were observed. Diagnosis of heatstroke was made according to Expert Consensus in China. GCSs were calculated on the 1st, 3rd, and 5th days after admission to intensive care units (ICUs). GCS £8, as a coma criterion, was employed to predict the outcomes. RESULTS Seventy-five patients (29.18%) were comatose at admission. Twenty-seven (10.50%) patients, including 24 (24/75, 32.00%) coma patients and 3 (3/182,1.65%) non-coma patients died during ICU stay (P<0.0001). Patients with GCS ≤8 had a 2-fold higher risk of death as compared with those with GCS >8. The area under curves (AUCs) of GCSs on the 1st, 3rd, and 5th days to predict mortality were 0.81 (0.70-0.91), 0.91 (0.84-0.98), and 0.91 (0.82-0.99), respectively. Each additional 1 year of age, 1/min of respiratory rate (RR), and 1% of hematocrit (HCT) increased the risk of death of coma patients by 3%, 6%, and 4%, respectively (all P≤0.05). Patients with improving GCSs had lower mortality rates than non-improving patients (5.71% vs 55.00%, P<0.0001) within 5 days after admission. CONCLUSIONS GCS ≤8 at admission predicted worse outcomes in heatstroke patients, which possibly enhanced the risks of death for other factors, including age, RR, and HCT.

Construction and Validation of the Nomogram Based on von Willebrand Factor Predicting Mortality in Patients with Heatstroke.

Heatstroke (HS), a severe condition, can develop multiple organ dysfunction syndrome and death. However, at present, no early reliable index exists for risk stratification and prognosis. von Willebrand factor (vWF), a marker of vascular endothelial injury, is a key regulatory target of inflammation and coagulation, which is closely associated with the pathogenesis of HS. vWF was reported as a prognostic marker in several infectious and noninfectious severe illness such as COVID-19, sepsis, and trauma. Although early increased level of vWF is seen in HS, the relationship between vWF and mortality is to be elucidated. Clinical data of patients with HS in a tertiary hospital were recorded and analyzed. It was shown that plasma vWF concentrations at admission were significantly increased in the nonsurvivors (351% ± 105%) compared with survivors (278% ± 104%, p = 0.021). After multivariate logistic regression analysis it was shown that vWF (odds ratio [OR] = 1.010; 95% confidence interval [CI], 1.002-1.18; p = 0.017), hemoglobin (Hb) (OR = 0.954; 95% CI, 0.931-0.979; p < 0.001), and hematocrit (HCT) in blood (OR = 0.859; 95% CI, 0.790-0.934; p < 0.001) were independent factors of in-hospital mortality in HS. The nomogram based on vWF and Hb was constructed in patients with HS. The area under curve under the receiver operating characteristic of this prediction model was 0.860 (95% CI, 0.773-0.923) and cutoff was 0.15, with Youden index 0.5840, which were not significantly different to sequential organ failure assessment (p = 0.0644), Acute Physiology and Chronic Health Evaluation II (APACHE II) (p = 0.7976), and systemic inflammatory response syndrome (SIRS) scores (p = 0.3274). The prediction model that integrated vWF and Hb showed a better predicting efficiency than single variable, and a higher specificity (81.48%) than APACHE II (72.84%) and SIRS (72.84%) scores. In summary, vWF, as an independent risk factor for in-hospital mortality, combined with Hb, could effectively prognosis the mortality in HS patients at early stage.

HMGB1-activatied NLRP3 inflammasome induces thrombocytopenia in heatstroke rat.

Background: Thrombocytopenia, an early common complication in heatstroke (HS), has been widely considered as a mortality predictor of HS. The mechanism underlying thrombocytopenia in HS remains unknown. It is not known whether NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome is activated in HS platelet, which, in turn, induces platelet activation and thrombocytopenia. This study tried to clarify the activation of the NOD-like receptor signaling pathway under HS conditions and investigate its roles in mediating HS-induced thrombocytopenia. Methods: Rat HS models were established in a certain ambient temperature and humidity. Platelets, isolated from blood, were counted and CD62P, an index of platelet activation, was measured by flow cytometry in all rats. The colocalization of NLRP3 inflammasome in platelet was detected by confocal fluorescence microscopy. Mitochondrial-derived reactive oxygen species (ROS) was detected using the molecular probes. Plasma HMGB1 and IL-1ß levels were measured by ELISA. Results: Platelet activation, showed by upregulated CD62P, and thrombocytopenia were observed in HS rats. HS activated the NLRP3 inflammasome, which was induced by elevated levels of ROS, while the upregulated CD62P and thrombocytopenia triggered by NLRP3 inflammasome were attributed to the high mobility group box protein 1 (HMGB1) inplasma. Moreover, inhibition of the NOD-like receptor signaling pathway in rats with HS suppressed platelet activation and the decline of platelet count. Similar results were obtained when the receptor toll-like receptor 4 (TLR4)/advanced glycation end product (RAGE) was blocked. Conclusions: The NOD-like receptor signaling pathway induces platelet activation and thrombocytopenia in HS rats. These findings suggested that the NLRP3 inflammasome might be the potential target for HS treatment.

Association of D-dimer and acute kidney injury associated with rhabdomyolysis in patients with exertional heatstroke: an over 10-year intensive care survey.

Patients with rhabdomyolysis (RM) following exertional heatstroke (EHS) are often accompanied by dysfunction of coagulation and acute kidney injury (AKI). The purpose of this study was to investigate the relationship between D-dimer and AKI in patients with RM following EHS. A retrospective study was performed on patients with EHS admitted to the intensive care unit over 10-year. Data including baseline clinical information at admission, vital organ dysfunction, and 90-day mortality were collected. A total of 84 patients were finally included, of whom 41 (48.8%) had AKI. AKI patients had more severe organ injury and higher 90-day mortality (34.1 vs.0.0%, p < 0.001) than non-AKI patients. Multivariate logistic analysis showed that D-dimer (OR 1.3, 95% CI 1.1-1.7, p = 0.018) was an independent risk factor for AKI with RM following EHS. Curve fitting showed a curve relationship between D-dimer and AKI. Two-piecewise linear regression showed that D-dimer was associated with AKI in all populations (OR 1.3, 95% CI 1.2-1.5, p < 0.001) when D-dimer <10.0 mg/L, in RM group (OR 1.3, 95% CI 1.1-1.5, p < 0.001) when D-dimer >0.4 mg/L, in the non-RM group (OR 6.4, 95% CI 1.7-23.9, p = 0.005) when D-dimer <1.3 mg/L and D-dimer did not increase the incidence of AKI in the non-RM group when D-dimer >1.3 mg/L. AKI is a life-threatening complication of RM following EHS. D-dimer is associated with AKI in critically ill patients with EHS. The relationship between D-dimer and AKI depends on whether RM is present or not.

Isolation, Identification, and Evaluation of the Pathogenicity of a Porcine Enterovirus G Isolated From China.

Enterovirus G (EV-G) infects porcine populations worldwide and the infections are generally asymptomatic, with the insertion of the papain-like cysteine protease gene (PLCP) increasing the potential public health threats. However, the genetic and pathogenic characteristics of EV-G itself are not fully understood as yet. In the present study, one EV-G strain, named CH/17GXQZ/2017, was isolated and purified from piglets with diarrheic symptoms from the Guangxi Province, China. This strain produced stable cytopathic effects on Marc-145 cells with a titer of 5 × 106 PFU/mL. The spherical enterovirus particles with diameters of 25-30 nm were observed by using transmission electron microscopy. The whole genome sequence of the CH/17GXQZ/2017 strain consists of 7,364 nucleotides, and the phylogenetic tree based on the amino acid sequences of VP1 indicated this strain was clustered to the G1 genotype. Seven-day-old piglets were inoculated orally with the CH/17GXQZ/2017 strain in order to evaluate its pathogenicity. Although none of the infected piglets died during the experiment, clinical neurological symptoms were observed manifesting as mild hyperemia and Nissl bodies vacuolization in the cerebrum. In addition, the infection with the CH/17GXQZ/2017 strain decelerated the weight gain of suckling piglets significantly. This study demonstrates that CH/17GXQZ/2017 is pathogenic to neonatal piglets and advance knowledge on the biological characteristics, evolution and pathogenicity of EV-G.

Two mechanically ventilated cases of COVID-19 successfully managed with a sequential ventilation weaning protocol: Two case reports.

BACKGROUND: Patients with critical coronavirus disease 2019 (COVID-19), characterized by respiratory failure requiring mechanical ventilation (MV), are at high risk of mortality. An effective and practical MV weaning protocol is needed for these fragile cases. CASE SUMMARY: Here, we present two critical COVID-19 patients who presented with fever, cough and fatigue. COVID-19 diagnosis was confirmed based on blood cell counts, chest computed tomography (CT) imaging, and nuclei acid test results. To address the patients' respiratory failure, they first received noninvasive ventilation (NIV). When their condition did not improve after 2 h of NIV, each patient was advanced to MV [tidal volume (Vt), 6 mL/kg ideal body weight (IBW); 8-10 cmH2O of positive end-expiratory pressure; respiratory rate, 20 breaths/min; and 40%-80% FiO2] with prone positioning for 12 h/day for the first 5 d of MV. Extensive infection control measures were conducted to minimize morbidity, and pharmacotherapy consisting of an antiviral, immune-enhancer, and thrombosis prophylactic was administered in both cases. Upon resolution of lung changes evidenced by CT, the patients were sequentially weaned using a weaning screening test, spontaneous breathing test, and airbag leak test. After withdrawal of MV, the patients were transitioned through NIV and high-flow nasal cannula oxygen support. Both patients recovered well. CONCLUSION: A MV protocol attentive to intubation/extubation timing, prone positioning early in MV, infection control, and sequential withdrawal of respiratory support, may be an effective regimen for patients with critical COVID-19.

Successful management of seven cases of critical COVID-19 with early noninvasive-invasive sequential ventilation algorithm and bundle pharmacotherapy.

We report the clinical and laboratory findings and successful management of seven patients with critical coronavirus disease 2019 (COVID-19) requiring mechanical ventilation (MV). The patients were diagnosed based on epidemiological history, clinical manifestations, and nucleic acid testing. Upon diagnosis with COVID-19 of critical severity, the patients were admitted to the intensive care unit, where they received early noninvasive-invasive sequential ventilation, early prone positioning, and bundle pharmacotherapy regimen, which consists of antiviral, anti-inflammation, immune-enhancing, and complication-prophylaxis medicines. The patients presented fever (n = 7, 100%), dry cough (n = 3, 42.9%), weakness (n = 2, 28.6%), chest tightness (n = 1, 14.3%), and/or muscle pain (n = 1, 14.3%). All patients had normal or lower than normal white blood cell count/lymphocyte count, and chest computed tomography scans showed bilateral patchy shadows or ground glass opacity in the lungs. Nucleic acid testing confirmed COVID-19 in all seven patients. The median MV duration and intensive care unit stay were 9.9 days (interquartile range, 6.5-14.6 days; range, 5-17 days) and 12.9 days (interquartile range, 9.7-17.6 days; range, 7-19 days), respectively. All seven patients were extubated, weaned off MV, transferred to the common ward, and discharged as of the writing of this report. Thus, we concluded that good outcomes for patients with critical COVID-19 can be achieved with early noninvasive-invasive sequential ventilation and bundle pharmacotherapy.

COVID-19 managed with early non-invasive ventilation and a bundle pharmacotherapy: A case report.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has become an immense public health burden, first in China and subsequently worldwide. Developing effective control measures for COVID-19, especially measures that can halt the worsening of severe cases to a critical status is of urgent importance. CASE SUMMARY: A 52-year-old woman presented with a high fever (38.8 °C), chills, dizziness, and weakness. Epidemiologically, she had not been to Wuhan where COVID-19 emerged and did not have a family history of a disease cluster. A blood test yielded a white blood cell count of 4.41 × 109/L (60.6 ± 2.67% neutrophils and 30.4 ± 1.34% lymphocytes). Chest imaging revealed bilateral ground-glass lung changes. Based on a positive nasopharyngeal swab nucleic acid test result and clinical characteristics, the patient was diagnosed with COVID-19. Following treatment with early non-invasive ventilation and a bundle pharmacotherapy, she recovered with a good outcome. CONCLUSION: Early non-invasive ventilation with a bundle pharmacotherapy may be an effective treatment regimen for the broader population of patients with COVID-19.

MicroRNA-204 may participate in the pathogenesis of hypoxic-ischemic encephalopathy through targeting KLLN.

Hypoxic-ischemic encephalopathy (HIE) is a common neonatal disease that can lead to high neonatal mortality rates. Previous studies have indicated that microRNAs (miRs) may be involved in the pathogenesis of HIE; however, the specific mechanisms underlying their involvement require further investigation. The aim of the present study was to investigate the roles of miR-204 and its target gene killin p53 regulated DNA replication inhibitor (KLLN) in HIE using rat HIE models. Brain injury was induced by surgery and incubation of hypoxic incubator brain using 10-day-old pup rats. On day 3, rats were sacrificed, and the infarct size of the brain was determined using a tetrazolium chloride assay. Terminal deoxynucleotidyl transferase UTP nick-end labeling staining was performed to detect the cell death rate in the brain tissue. Following this, the brain tissues were collected, and reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunohistochemistry assays were performed to examine the expression levels of miR-204 and KLLN. Furthermore, neurons were cultured and transfected with miR-204 inhibitors or mimics, and the effect of miR-204 on the proliferation and apoptosis of neurons was examined using MTT and flow cytometric assays. Finally, a dual-luciferase reporter assay was performed to confirm whether KLLN is a direct target of miR-204. The expression of miR-204 was significantly downregulated and the expression of KLLN was significantly increased in the brain tissue of HIE rats (P<0.001). In addition, the transfection with miR-204 inhibitors significantly decreased the proliferation rates and significantly increased the apoptosis rate of neurons; however, transfection with miR-204 mimics prompted the opposite results. The dual-luciferase reporter assay also confirmed that KLLN is a direct target of miR-204. Taken together, the results of the present study demonstrated that miR-204 was downregulated in HIE and that miR-204 may serve important roles in the pathogenesis of HIE through targeting KLLN.

Mesenteric Lymph Duct Ligation Alleviating Lung Injury in Heatstroke.

To explore the roles of mesenteric lymph on lung injury in heatstroke (HS), HS rat model was prepared in a prewarmed incubator. Vascular endothelium injury biomarkers (circulating endothelial cell [CEC] as well as von Willebrand factor [vWF] and thrombomodulin [TM]), proinflammatory factors (tumor necrosis factor-α [TNF-α], interleukin-1ß [IL-1ß], IL-6, and high mobility group box 1), and coagulant markers (activated partial thromboplastin time, prothrombin time, D-Dimer, and platelet count) were tested in HS and HS with mesenteric lymph duct ligation (LDL) rats. In addition, lung histopathology; arterial blood gas; Evans Blue dye (EBD) and protein lung permeability; intralung inflammatory parameters including bronchoalveolar lavage fluid (BALF) TNF-α, IL-1ß, and IL-6 levels; myeloperoxidase (MPO) activity; and vWF immune staining were analyzed. LDL prolonged HS onset time but not HS survival time. LDL significantly attenuated endothelial cell injury for decreased CEC counts as well as plasma vWF and TM concentrations; downregulated systemic inflammation for decreased plasma TNF-α, IL-1ß, IL-6, and high mobility group box 1 levels; and ameliorated coagulant disorders for decreased activated partial thromboplastin time, prothrombin time, and D-Dimer levels as well as increased platelet counts. LDL also significantly reduced acute lung pathological injury; improved lung function indexes including arterial blood PaO2, pH, PaCO2, and lactic acid; decreased BALF TNF-α, IL-1ß, and IL-6 levels and lung MPO activity; improved EBD and protein lung permeability; and inhibited lung vascular endothelium vWF expression. However, all of these parameters were not recovered to the normal states. In summary, LDL developed protection roles systemically and alleviated lung injury in HS rats which indicated that modulating mesenteric lymph flow may have some potential benefits in HS.

[Effects of volume resuscitation on venous pressure gradient in hypovolemic patients undergoing mechanical ventilation].

OBJECTIVE: To investigate the value of venous pressure gradient [D(c-i)VP] between central venous pressure (CVP) and iliac vein pressure (IVP) in assessing the responsiveness to volume resuscitation in hypovolemic patient undergoing mechanical ventilation. METHODS: Thirty hypovolemic patients undergoing mechanical ventilation, with maintenance of similar ventilation conditions, graded volume loading was performed with 250 ml Ringer lactate solution (LR) for each infusion in hypovolemic patients, until mean arterial pressure (MAP) ≥65 mm Hg(1 mm Hg = 0.133 kPa), CVP≥8 mm Hg, strong pulse, perfusion improvement (recovery in the end) were reached. Before infusion, 10 minutes after infusion, and at the end of recovery, the heart rate (HR), MAP, CVP, IVP, stroke volume (SV), thoracic fluid content (TFC) and D(c-i)VP were measured and recorded, the correlations between D(c-i)VP and TFC, SV before and after infusion were analyzed. RESULTS: Before infusion, 10 minutes after infusion, and at the end of recovery, no significant difference was found in HR, MAP, CVP, and IVP,while D(c-i)VP (mm Hg) was obviously lowered (4.89 ± 1.70, 2.80 ± 1.44, 2.10 ± 1.30, respectively), and SV (ml) and TFC (ml) were significantly increased (SV was 42.0 ± 10.5, 49.0 ± 8.3, 58.0 ± 12.1, respectively; TFC was 30.0 ± 9.6, 38.0 ± 8.6, 43.0 ± 11.1, respectively), with statistical differences (P < 0.05 or P < 0.01). Negative correlations were found between D(c-i)VP and TFC, SV [r(1)=-0.580, P(1)=0.004; r(2)=-0.462, P(2) =0.017]. CONCLUSIONS: In the course of fluid resuscitation in hypovolemic patients undergoing mechanical ventilation, the D(c-i)VP was significantly reduced with fluid resuscitation. At the same time, significant correlations between D(c-i)VP, TFC and SV were demonstrated. The measurement of D(c-i)VP could help guide fluid resuscitation in hypovolemic patients undergoing mechanical ventilation.

[Effect of positive end-expiratory pressure on the pressure gradient of venous return in hypovolemic patients under mechanical ventilation].

OBJECTIVE: To assess the effects of positive end-expiratory pressure (PEEP) on central venous pressure (CVP) and common iliac venous pressure (CIVP), and the difference between CVP and CIVP [D(c-i)VP] in hypovolemic patients under mechanical ventilation. METHODS: From May 2007 to May 2009, 30 acute hypovolemic adult patients undergoing mechanical ventilation in intensive care unit (ICU) were enrolled. The patients were randomly divided into three groups, and PEEP with 0, 5, 10 cm H(2)O (1 cm H(2)O=0.098 kPa) levels were used respectively. Ten mechanically ventilated patients with similar basic clinical conditions but normal blood volume were selected randomly as the control group. CVP, CIVP and D(c-i)VP were measured and recorded at each PEEP level in both groups. The patients' heart rate, mean artery pressure and respiratory pressure data were also collected. The correlation analysis was used to analyze relationship between CVP and CIVP and between the changes in venous pressure and the changes in respiratory pressure. RESULTS: (1)CVP increased significantly when PEEP level was elevated in the study group. When PEEP was 0, 5 and 10 cm H(2)O, the CVP was (1.3+/-0.9), (3.1+/-1.3) and (4.5+/-1.3) mm Hg, respectively (1 mm Hg=0.133 kPa, all P<0.01). Whereas, in the control group, the changes in CVP was small. At 0, 5 and 10 cm H(2)O PEEP levels, CVP was (6.9+/-1.3), (7.2+/-1.2) and (8.0+/-1.5) mm Hg, respectively, but when CVP at PEEP0 and PEEP5 was compared with that of PEEP10, the difference was significant (P<0.01 and P<0.05). There was slight increase of CIVP in both groups when PEEP was elevated. D(c-i)VP was increased significantly in the study group compared with control group (all P<0.01). But the value was gradually decreased when with elevation of PEEP. When PEEP level was elevated from 0 to 10 cm H(2)O, D(c-i)VP value was lowered from (4.9+/-1.7) mm Hg to (2.8+/-1.4) mm Hg. No significant difference in D(c-i)VP was found in the control group. The D(c-i)VP values in the control group were equal or lower than 1.5 mm Hg at three PEEP levels. (2)No relationship was found between CVP and CIVP at each PEEP level in the study group (r(1)=0.236, r(2)=0.299, r(3)=0.262, all P>0.05), but there was a statistically significant correlation between CVP and CIVP in the control group (r(1)=0.485, r(2)=0.679, r(3)=0.748, all P<0.05). CONCLUSION: The findings suggest that it may not be appropriate to use CVP or CIVP to evaluate the patients' blood volume and effect of volume resuscitation in the hypovolemic patients undergoing mechanical ventilation in combination with PEEP.

[Effect of positive end-expiratory pressure on central venous pressure and common iliac venous pressure in mechanically ventilated patients].

OBJECTIVE: To evaluate the effects of positive end-expiratory pressure (PEEP) on central venous pressure (CVP) and common iliac venous pressure (CIVP), the relationship between CVP and CIVP, in order to analyze the correlation between CVP or CIVP and airway pressure in patients during mechanical ventilation. METHODS: Twenty mechanically ventilated adult patients with steady circulatory state and without cardiopulmonary ailment, abdominal distention or coagulopathy were enrolled for the study from February to August in 2007. 0, 5, 10 cm H(2)O (1 cm H(2)O=0.098 kPa) PEEP was used randomly in all cases during mechanical ventilation. CVP, CIVP, the gradient between CVP and CIVP at each PEEP level were measured. Linear correlation and linear regression analysis were used to analyze relative changes between CVP and CIVP. The data of airway pressure in the patients with mechanical ventilation were obtained for evaluating their correlation with CVP or CIVP. RESULTS: CVP and CIVP increased as PEEP was elevated (P<0.05 or P<0.01). There was a significant linear correlation between CVP and CIVP at 0, 5, 10 cm H(2)O PEEP level (r was 0.620, 0.658 and 0.777, respectively, P<0.01). The linear regression equation was Y (CVP)=0.402+0.732X (CIVP). The mean difference between CVP and CIVP at 0, 5, 10 cm H(2)O PEEP level was (1.9+/-1.7), (2.3+/-1.3), and (1.9+/-1.1) mm Hg (1 mm Hg=0.133 kPa, respectively P>0.05). There was a positive correlation between CVP or CIVP and the airway pressure, but only mean airway pressure and PEEP showed significant linear correlation with CVP (r was 0.634, 0.603, respectively, P<0.01) and CIVP (r was 0.751, 0.685, respectively, P<0.01). No obvious change was found in mean arterial pressure, heart rate, and expiratory tidal volume during the study. CONCLUSION: CVP and CIVP increased when PEEP is set