Pulmonary function after hemorrhagic shock and resuscitation in a porcine model

Abstract

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, PaO2 /FiO2 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: In the hemorrhage groups, wet/dry ratio increased significantly compared with the sham groups. PaO2 /FiO2 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.