Argon reduces the ET-1 induced increase of segmental PVR and the generation of lung edema

Introduction: Argon exerts neuroprotection [1] and might improve the outcome of patients after cardiopulmonary resuscitation, intracerebral bleeding or traumatic brain injury. In patients suffering from left heart disease (LHD) and pulmonary hypertension (PH), limited data for the effect of argon on the pulmonary vascular resistance (PVR) are available. Recently, Neyrinck et al. showed that argon does not alter total PVR in pigs. Aims and objectives: To study if argon alters segmental PVR, we used the isolated perfused lung (IPL). Methods: Rat IPLs have been prepared as described [2].Tidal volume (TV), compliance (C), resistance (R), pulmonary arterial (P PA ) and left atrial pressure (P LA ) were continuously recorded. The pulmonary capillary pressure (P cap ) was determined by double occlusion and the pre- (R pre ) and postcapillary resistance (R post ) were calculated. PVR was increased by 20 nM ET-1 or remained unchanged. Both groups have been ventilated with argon (argon 74%, CO 2 5%, O 2 21%). Controls have been ventilated with room-air or air-mix (N 2 74%, CO 2 5%, O 2 21%). Finally, the wet-dry ratio (W/D) was determined. Statistics was performed by a „linear mixed model“ (SAS 9.3) or by the Mann-Whitney U test (GraphPad5). Results: In controls, argon did not alter P cap , R pre , R post or R, but increased TV and C. If P cap , R pre , R post were increased by ET-1 (p cap , R post and the W/D (p Conclusions: Argon might be beneficial in case of increased P cap and R post , as it occurs in LHD or PH due to LHD. Further, argon exerts bronchodilation. References: 1) Hollig, A. et al. Int J Mol Sci 2014; 15:18175-96; 2) Uhlig, S. et al. J Pharmacol Toxicol Methods 1994; 31(2):85-94.