Abstract

BackgroundLimb ischemia/reperfusion causes inflammation and elicits oxidative stress that may lead to local tissue damage and remote organ such as lung injury. This study investigates pulmonary function after limb ischemia/reperfusion and the protective effect of a lipid emulsion (Intralipid).MethodsTwenty-four rats were divided into three groups: sham operation group (group S), ischemia/reperfusion group (group IR), and lipid emulsion treatment group (group LE). limb ischemia/reperfusion was induced through occlusion of the infrarenal abdominal aorta for 3 h. The microvascular clamp was removed carefully and reperfusion was provided for 3 h.ResultsThe mean arterial pressure in group LE was higher than group IR during the reperfusion period (P = 0.024). The heart rate of both group LE and IR are significantly higher than group S during the ischemia period(P < 0.001, P < 0.001, respectively). The arterial oxygen pressure of group LE was significantly higher than group IR (P = 0.003), the arterial carbon dioxide pressure of group LE were lower than that of group IR (P = 0.005). The concentration of plasma interleukin-6, tumor necrosis factor-α and malondialdehyde in group LE were significantly lower than group IR (P < 0.001, P = 0.009 and 0.029, respectively). The plasma superoxide dismutase activity in group LE was significantly higher than group IR (P = 0.029). The myeloperoxidase activity in lung tissues of group LE was significantly less than group IR (P = 0.046). Both muscle and lung in group IR were damaged seriously, whereas lipid emulsion (Intralipid) effectively reversed the damage. In summary, Intralipid administration resulted in several beneficial effects as compared to group IR, such as the pulmonary gas exchange and inflammatory.ConclusionsThe ischemic/reperfusion injury of limb muscles with resultant inflammatory damage to lung tissue can be mitigated by administration of a lipid emulsion (Intralipid, 20%, 5 ml/kg). The mechanisms attenuating such a physiological may be attributed to reduction of the degree of limb injury through a decrease in the release of local inflammatory mediators, a reduction of lipid peroxidation, and a blunting of the subsequent remote inflammatory response.

Highlights

  • Limb ischemia/reperfusion causes inflammation and elicits oxidative stress that may lead to local tissue damage and remote organ such as lung injury

  • Shih et al [1] have suggested that tumor necrosis factor-α (TNF-α), IL-1β, IL-6 in limb tissues after limb ischemia/reperfusion lead to the activation of polymorphonuclear leukocytes (PMNs) and increase the expression of cell adhesion molecules (CAMs) on both neutrophils and endothelial cells, resulting in local tissue injury and downstream damage to the lungs

  • We found that Intralipid administration resulted in several beneficial effects as compared to group IR

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Summary

Introduction

Limb ischemia/reperfusion causes inflammation and elicits oxidative stress that may lead to local tissue damage and remote organ such as lung injury. Reperfusion of the acutely ischemic limb may cause significant local tissue damage and release of toxic metabolites [2] that initiate a cascade of events that may result in single or multiple organ dysfunction [3, 4]. Yassin et al [2] reported increased tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels are associated with vascular obstruction, and activation and infiltration of neutrophils in the lung after limb ischemia/reperfusion. Shih et al [1] have suggested that TNF-α, IL-1β, IL-6 in limb tissues after limb ischemia/reperfusion lead to the activation of polymorphonuclear leukocytes (PMNs) and increase the expression of cell adhesion molecules (CAMs) on both neutrophils and endothelial cells, resulting in local tissue injury and downstream damage to the lungs. Wang et al [5] reported that Shenmai can improve secondary lung dysfunction after limb ischemia/reperfusion by attenuating inflammatory and oxidative response

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