摘要
Background： Sepsis is one of the main canses of mortality in critically ill patients following progression to septic shock. To investigate the pathophysiologic changes of sepsis, we developed a novel porcine model of septic shock induced by acute respiratory distress syndrome （ARDS） due to methicillin-resistant Staphylococcus aureus （MRSA） pneumonia. Methods： Twenty-six male Landraces （Lvyuanweiye, Beijing, China） weighing 30 - 2 kg were divided into lbur groups： sham gronp （SH： n = 5）; cotton smoke inhalation group （SM; n = 6）; MRSA pneumonia group （MR; n = 6）; and septic shock group with cotton smoke inhalation ＋ MRSA pneumonia （SS; n = 9）. Extensive hemodynamics, oxygen dynamics, and lung function were monitored for 24 11 following the injury or until death. Tissues were collected, and histopathology evaluations were carried out. Results： Blood cultures from 6 of 9 animals in the SS group were positive for MRSA. Two hours following the injury, decreased mean arterial blood pressure （60 70 mmHg） and cardiac index （〈2 L-rain -＇m --） were observed in the animals in the SS group, while systemic vascular resistance index was increased. The hemodynamic characteristics of septic shock were only observed in the SS group but not significant in the other groups, The PO_JFiO2 in the SM and SS groups decreased to 300 and 100, respectively. In the SS group, extravascular lung water index increased to 20 ml/kg, whereas thoracopulmonary compliance decreased to 10 ml/H2O after injury. Deterioration of pulmonary function in the SS group was more serious than the SM and MR groups. Severe lung injury in the SS group was confinaaed by the histopathology evaluations. The lung injury confirmed by high-resolution thin-section computed tomography and histopathology in the SS group was more serious than those of other groups. Conclusions： In the present study, we developed a novel porcine model of septic shock induced by ARDS due to severe MRSA pneumonia with characteristic hyperdynamic and hypodynamic phases in 24 h, which mimicked the hemodynamic changing of septic shock in human.
Background： Sepsis is one of the main canses of mortality in critically ill patients following progression to septic shock. To investigate the pathophysiologic changes of sepsis, we developed a novel porcine model of septic shock induced by acute respiratory distress syndrome （ARDS） due to methicillin-resistant Staphylococcus aureus （MRSA） pneumonia. Methods： Twenty-six male Landraces （Lvyuanweiye, Beijing, China） weighing 30 - 2 kg were divided into lbur groups： sham gronp （SH： n = 5）; cotton smoke inhalation group （SM; n = 6）; MRSA pneumonia group （MR; n = 6）; and septic shock group with cotton smoke inhalation ＋ MRSA pneumonia （SS; n = 9）. Extensive hemodynamics, oxygen dynamics, and lung function were monitored for 24 11 following the injury or until death. Tissues were collected, and histopathology evaluations were carried out. Results： Blood cultures from 6 of 9 animals in the SS group were positive for MRSA. Two hours following the injury, decreased mean arterial blood pressure （60 70 mmHg） and cardiac index （〈2 L-rain -＇m --） were observed in the animals in the SS group, while systemic vascular resistance index was increased. The hemodynamic characteristics of septic shock were only observed in the SS group but not significant in the other groups, The PO_JFiO2 in the SM and SS groups decreased to 300 and 100, respectively. In the SS group, extravascular lung water index increased to 20 ml/kg, whereas thoracopulmonary compliance decreased to 10 ml/H2O after injury. Deterioration of pulmonary function in the SS group was more serious than the SM and MR groups. Severe lung injury in the SS group was confinaaed by the histopathology evaluations. The lung injury confirmed by high-resolution thin-section computed tomography and histopathology in the SS group was more serious than those of other groups. Conclusions： In the present study, we developed a novel porcine model of septic shock induced by ARDS due to severe MRSA pneumonia with characteristic hyperdynamic and hypodynamic phases in 24 h, which mimicked the hemodynamic changing of septic shock in human.
