Pulmonary function after hemorrhagic shock and resuscitation in a porcine model

Background Hemorrhagic shock may trigger an inflammatory response and acute lung injury. The combination adenosine, lidocaine ( AL ) plus Mg 2+ ( ALM ) has organ‐protective and anti‐inflammatory properties with potential benefits in resuscitation.The aims of this study were to investigate: (1) pulmonary function and inflammation after hemorrhagic shock; (2) the effects of ALM / AL on pulmonary function and inflammation. Methods Pigs (38 kg) were randomized to: sham + saline ( n  = 5); sham +  ALM / AL ( n  = 5); hemorrhage control ( n  = 11); and hemorrhage +  ALM / AL ( n  = 9). Hemorrhage animals bled to a mean arterial pressure ( MAP ) of 35 mmHg for 90 min, received resuscitation with Ringer's acetate and 20 ml of 7.5% NaCl with ALM to a minimum MAP of 50 mmHg, after 30 min shed blood and 0.9% NaCl with AL were infused. Hemorrhage controls did not receive ALM / AL . Primary endpoints were pulmonary wet/dry ratio, PaO 2 / FiO 2 ratio (partial pressure of arterial oxygen to the fraction of inspired oxygen), cytokine and protein measurements in bronchoalveolar lavage fluid ( BALF ) and lung tissue, neutrophil invasion and blood flow in lung tissue. Results I n the hemorrhage groups, wet/dry ratio increased significantly compared with the sham groups. PaO 2 / FiO 2 ratio decreased during shock but normalized after resuscitation. BALF did not indicate significant pulmonary inflammation, oxidative stress or increased permeability. Intervention with ALM caused a temporary increase in pulmonary vascular resistance and reduced urea diffusion across the alveolar epithelia, but had no effect on wet/dry ratio. Conclusion Hemorrhagic shock and resuscitation did not cause acute lung injury or pulmonary inflammation. The question whether ALM / AL has the potential to attenuate acute lung injury is unanswered.