Hypothermia throughout intestinal ischaemia-reperfusion injury attenuates lung neutrophil infiltration

Secondary organ damage to the lungs is an important consequence of intestinal ischaemia reperfusion (IIR) injury. Moderate hypothermia ameliorates gut necrosis and liver energy failure after IIR but potential beneficial effects on lung neutrophil infiltration after reperfusion of ischaemic bowel have not been investigated.

Adult Sprague-Dawley rats underwent 60 minutes intestinal ischaemia followed by 120 minutes of reperfusion. The animals were maintained at either normothermia (36 degrees to 38 degrees C) or moderate hypothermia (30 degrees to 32 degrees C). Four groups were studied: (A) sham normothermia; (B) IIR normothermia; (C) sham hypothermia; and (D) IIR hypothermia. Lungs and terminal ileum were removed for measurement of myeloperoxidase activity (a marker of neutrophil infiltration). Results are expressed as milliunits per milligrams protein, mean +/- SEM, and one-way analysis of variance (ANOVA) with Tukey post-test was used for group comparisons.

Lungs: IIR at normothermia significantly increased lung neutrophil infiltration assessed by myeloperoxidase activity compared with sham-operated controls (normothermia sham 4.6 +/- 1.0, n = 8; normothermia IIR 37.7 +/- 13.8, n = 8; P =.011). Moderate hypothermia during IIR significantly attenuated lung neutrophil infiltration (7.2 +/- 2.1, n = 9) compared with normothermia IIR (P =.016) such that myeloperoxidase activity was similar to that found in sham normothermia (4.6 +/- 1.0, n = 8) and sham hypothermia (3.1 +/- 1.3, n = 8). Intestine: Gut myeloperoxidase activity was 0.9 +/- 0.5 in sham normothermia (n = 9) and 2.3 +/- 0.6 after normothermic IIR (n = 8). After IIR at hypothermia gut myeloperoxidase activity (0.5 +/- 0.2; n = 8) was significantly less than normothermic IIR (P =.035) and higher than sham hypothermia (0.2 +/- 0.1, n = 9; P =.01).

These results indicate that moderate hypothermia may prevent damage to another distant organ, ie the lungs, by preventing recruitment of neutrophils. This may be of benefit in decreasing distal organ damage in diseases in which intestinal ischaemia-reperfusion is implicated in the pathogenesis.