Establishment of a Rat Model of Capillary Leakage Syndrome Induced by Cardiopulmonary Resuscitation After Cardiac Arrest.

OBJECTIVE: Cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) is one of the main causes of capillary leakage syndrome (CLS). This study aimed to establish a stable CLS model following the CA and cardiopulmonary resuscitation (CA-CPR) model in Sprague-Dawley (SD) rats. METHODS: We conducted a prospective, randomized, animal model study. All adult male SD rats were randomly divided into a normal group (group N), a sham operation group (group S), and a cardiopulmonary resuscitation group (group T). The SD rats of the three groups were all inserted with 24-G needles through their left femoral arteries and right femoral veins. In group S and group T, the endotracheal tube was intubated. In group T, CA induced by asphyxia (AACA) was caused by vecuronium bromide with the endotracheal tube obstructed for 8 min, and the rats were resuscitated with manual chest compression and mechanical ventilation. Preresuscitation and postresuscitation measurements, including basic vital signs (BVS), blood gas analysis (BG), routine complete blood count (CBC), wet-to-dry ratio of tissues (W/D), and the HE staining results after 6 h were evaluated. RESULTS: In group T, the success rate of the CA-CPR model was 60% (18/30), and CLS occurred in 26.6% (8/30) of the rats. There were no significant differences in the baseline characteristics, including BVS, BG, and CBC, among the three groups (P>0.05). Compared with pre-asphyxia, there were significant differences in BVS, CBC, and BG, including temperature, oxygen saturation (SpO2), mean arterial pressure (MAP), central venous pressure (CVP), white blood cell count (WBC), hemoglobin, hematocrit, pH, pCO2, pO2, SO2, lactate (Lac), base excess (BE), and Na+ (P<0.05) after the return of spontaneous circulation (ROSC) in group T. At 6 h after ROSC in group T and at 6 h after surgery in groups N and S, there were significant differences in temperature, heart rate (HR), respiratory rate (RR), SpO2, MAP, CVP, WBC, pH, pCO2, Na+, and K+ among the three groups (P<0.05). Compared with the other two groups, the rats in group T showed a significantly increased W/D weight ratio (P<0.05). The HE-stained sections showed consistent severe lesions in the lung, small intestine, and brain tissues of the rats at 6 h after ROSC following AACA. CONCLUSION: The CA-CPR model in SD rats induced by asphyxia could reproduce CLS with good stability and reproducibility.

Alterations of complex IV in the tissues of a septic mouse model.

OBJECTIVES: To characterize the mitochondrial respiratory chain complex IV(complex IV) activity and protein expression during polymicrobial sepsis. MATERIAL AND METHODS: Polymicrobial peritonitis, a clinically relevant mouse model of sepsis, was generated by cecum ligation and puncture (CLP) in Sprague- Dawley rats. The rats were randomly divided into 3 groups as follows: the sepsis without resuscitation (S), sepsis and fluid resuscitated (R) group, and a control (C) group. Twelve hours after the sepsis model was established, tissue specimens were obtained from the myocardium, liver and skeletal muscle. Mitochondrial respiratory chain complex IV activity of all tissue specimens was detected by spectrophotometry. Western blot was used to measure the liver mitochondrial respiratory chain complex IV protein content. The ultrastructure changes of mitochondria were detected by transmission electron microscopy. RESULTS: In myocardial cells, complex IV activity decreased significantly in the S and R groups as compared to the C group. There were no differences in complex IV activity between groups in skeletal muscle cells while in liver cells, complex IV activity and content was significantly decreased for the S group but no differences were observed between the C and R groups. Increased matrix volume and reduced density with generalized disruption of the normal cristae pattern was most extensive in the liver, followed by cardiac muscle cells with that in skeletal muscle cells been relatively mild in the S group. Mitochondrial fusion/fission and mitochondrial autophagy was also observed in the S group by transmission electron microscopy. Mitochondrial ultrastructure was preserved in the R-group and was similar to that seen in the C-group. CONCLUSIONS: Changes in complex IV activity and mitochondrial ultrastructure, a manifestation of the mitochondrial dysfunction varied depending on cell type. These changes are partly reversed by fluid therapy. Therapies aimed at mitochondrial resuscitation should be explored.

[Investigation of nosocomial infection in the neonatal intensive care unit].

OBJECTIVE: A perspective study was conducted to describe the epidemiologic profile of nosocomial infection in the neonatal intensive care unit (NICU). METHODS: The newborn infants who were admitted in the NICU for more than 48 hrs were enrolled from February 2006 to January 2007. The clinical data were collected. The rate of nosocomial infection was calculated according to the CDC surveillance system. The risk factors of nosocomial infection were investigated by multivariate regression analysis. RESULTS: A total of 1 159 neonates were recruited. A total of 169 nosocomial infections occurred, with a cumulative rate for nosocomial infection of 14.58%. The incidence of nosocomial infection was 19.52 per 1 000 patient-days. Ninety-two cases of pneumonia, including 38 cases of ventilator-associated pneumonia (VAP), were reported, with a nosocomial infection rate of 7.94%, which was the most common nosocomial infection in the NICU. Among these infants the rate of VAP was 48.8 per 1 000 ventilator days. The major microorganisms isolated from the infected patients were Acinetobacter baumannii, Klebsiella pneumoniae, Coagulase negative staphylococcus, and aeruginosus Bacillus. Birth weight (OR 2.130, 95%CI 1.466-3.094), mechanical ventilation (OR 7.038, 95%CI 3.901-12.698), chest tube drainage (OR 7.004, 95%CI 1.841-26.653) and ibuprofen therapy (OR 2.907, 95% CI 1.303-6.487) were the risk factors for the development of nosocomial infection. CONCLUSIONS: Pulmonary infection is the most common nosocomial infection in the NICU, and the Gram-negative bacillus is the main pathogen. Low birth weight, mechanical ventilation, chest tube drainage and ibuprofen therapy are independent risk factors for nosocomial infection in the NICU.