Background: Hypothermia may attenuate ventilator induced-lung injury in acute respiratory distress syndrome (ARDS). However, the impact of hypothermia on extra-pulmonary organ injury in ARDS remains unclear. The purpose of this study was to investigate whether hypothermia affects extra-pulmonary organ injury in a canine ARDS model induced by oleic acid.
Objectives: Twelve anesthetized canines with oleic acid-induced ARDS were randomly divided (n=6 per group) into a hypothermia group (core temperature of 33±1°C, HT group) and a normothermia group (core temperature of 38±1°C, NT group) and treated for four hours. The liver, small intestine and kidney were assessed by evaluating biochemical parameters, plasma and tissue cytokine levels, and tissue histopathological injury scores.
Results: The HT group showed a lower plateau pressure, lung elastance and pulmonary vascular resistance. Hypothermia was associated with lower oxygen consumption (138.4±55.0mlmin(-1)vs. 72.0±11.2mlmin(-1), P<0.05) and higher oxygen saturation of mixed venous blood (62.8%±8.0% vs. 77.5%±10.1%, P<0.05). Both groups had similar levels of tumour necrosis factor-α in the plasma and extra-pulmonary organ, however, plasma interleukin-10 (97.1±25.0pgml(-1)vs. 131.4±27.0pgml(-1), P<0.05) was higher in the HT group. Further, the animals in the HT group had a lower levels of plasma creatinine (54.6±19.1UL(-1)vs. 29.1±8.0UL(-1), P<0.05), and lower renal histopathological injury scores [4.0(3.5;7.0) vs. 1.5(0.8;3.0), P<0.05]. Hypothermia did not affect the histopathological injury of the liver and small intestine.
Conclusions: Short-term mild hypothermia can reduce lung elastance and pulmonary vascular resistance, increase the systemic anti-inflammatory response and attenuate kidney histopathological injury in a canine ARDS model induced by oleic acid.
Keywords: Acute respiratory distress syndrome; Hypothermia; Kidney injury; Mechanical ventilation; Multiple organs failure; Ventilator induced-lung injury.
Copyright © 2016 Elsevier Ltd. All rights reserved.