Argon attenuates multiorgan failure following experimental aortic cross-clamping

Abstract

Aims

Argon was shown to prevent ischemic injuries in several situations of regional ischemia. We determined whether it could provide a systemic effect in a model of multiorgan failure (MOF) induced by aortic cross-clamping.

Methods

Anesthetized rabbits were submitted to aortic cross-clamping (30 min) and subsequent reperfusion (300 min). They were either ventilated with oxygen-enriched air throughout protocol (FiO₂=30%, Control group) or with a mixture of 30% oxygen and 70% argon (Argon groups). In a first group treated with Argon (Argon-Total), its administration was started 30 min before ischemia and maintained throughout protocol. In the two other groups, the administration was either started 30 min before ischemia (Argon-Pre) or at the onset of reperfusion (Argon-Post), for a total duration of two hours. Cardiovascular, renal and inflammatory endpoints were assessed throughout protocol.

Results

As compared to Control, shock was significantly attenuated in Argon-Total and Argon-Pre but not Argon-Post groups (e.g., cardiac output = 62±5 vs 29±5 mL.min^-1.kg^-1 in Argon-Total and Control at the end of the follow-up). Shock and renal failure were reduced in all Argon vs Control groups. Histopathological examination of the gut showed attenuation of ischemic lesions in all Argon vs Control groups. Blood transcription levels of Interleukin (IL)-1β, IL-8, IL-10, and hypoxia-inducible factor-1α were not significantly different between groups.

Conclusion

Argon attenuated clinical and biological modifications of cardiovascular, renal and intestinal systems, but not inflammatory response after aortic cross-clamping. The window of administration was crucial to optimize organ protection.

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