The Journal of surgical research · 2019
Characterization of Fecal Peritonitis-Induced Sepsis in a Porcine Model.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
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Park Inwon, Lee Jae Hyuk, Jang Dong-Hyun, Kim Doyun, Chang Hyunglan, Kwon Hyuksool, Kim Seonghye, Kim Taek Soo, Jo You Hwan
Аннотация
BACKGROUND: Although there are well-established small-animal sepsis models, the longitudinal assessment of hemodynamic variables, laboratory values, and blood culture in a single living sepsis model is limited. Therefore, we aimed to comprehensively characterize fecal peritonitis-induced sepsis in a porcine model.
MATERIALS AND METHODS: Autologous feces (1 g/kg) was administered into the peritoneum of 11 male pigs (49 ± 8 kg). The pigs were monitored up to 12 h with full fluid and vasopressor support to maintain the mean arterial pressure at >65 mm Hg. Longitudinal blood culture and laboratory values were obtained at defined time intervals. The cytokine levels in plasma were analyzed. Furthermore, a clinical registry of sepsis patients at a single emergency department was used to compare the Sepsis-related Organ Failure Assessment scores with those of the porcine model.
RESULTS: The hyperdynamic phase of increasing cardiac output with decreasing systemic vascular resistance was maintained until 2 h, followed by the reverse (hypodynamic phase). With the escalating requirement for fluid and vasopressor, the lactate level progressively increased while the platelet count, urine output, and serum albumin level consistently decreased. Bacteremia developed 7 h (median) after the administration of feces, and Escherichia coli was the most common pathogen. The pattern of Sepsis-related Organ Failure Assessment scores with prominent cardiovascular failure was comparable to clinical data.
CONCLUSIONS: We implemented a porcine fecal peritonitis-induced sepsis model that demonstrates culture-proven bacteremia and multiple organ failure, particularly cardiovascular system failure. This model could facilitate the development of technologies for the early diagnosis of bacterial pathogens in blood.
MATERIALS AND METHODS: Autologous feces (1 g/kg) was administered into the peritoneum of 11 male pigs (49 ± 8 kg). The pigs were monitored up to 12 h with full fluid and vasopressor support to maintain the mean arterial pressure at >65 mm Hg. Longitudinal blood culture and laboratory values were obtained at defined time intervals. The cytokine levels in plasma were analyzed. Furthermore, a clinical registry of sepsis patients at a single emergency department was used to compare the Sepsis-related Organ Failure Assessment scores with those of the porcine model.
RESULTS: The hyperdynamic phase of increasing cardiac output with decreasing systemic vascular resistance was maintained until 2 h, followed by the reverse (hypodynamic phase). With the escalating requirement for fluid and vasopressor, the lactate level progressively increased while the platelet count, urine output, and serum albumin level consistently decreased. Bacteremia developed 7 h (median) after the administration of feces, and Escherichia coli was the most common pathogen. The pattern of Sepsis-related Organ Failure Assessment scores with prominent cardiovascular failure was comparable to clinical data.
CONCLUSIONS: We implemented a porcine fecal peritonitis-induced sepsis model that demonstrates culture-proven bacteremia and multiple organ failure, particularly cardiovascular system failure. This model could facilitate the development of technologies for the early diagnosis of bacterial pathogens in blood.