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Hypoxemic resuscitation prevents pulmonary capillary endothelial dysfunction induced by normoxemic resuscitation from hemorrhagic shock.

Abstract：

OBJECTIVE:Hypoxemic reperfusion attenuates brain injury secondary to severe cerebral ischemia, myocardial, and intestinal injury occurring in intestinal postischemic shock, and offers hemodynamic stabilization and attenuation of inflammatory response when applied in the resuscitation from hemorrhagic shock. In this study, we sought to investigate the effect of hypoxemic resuscitation on pulmonary endothelium. DESIGN:Prospective, randomized, controlled animal study. SETTING:Experimental laboratory of a university intensive care unit. SUBJECTS:Male New Zealand White rabbits weighting 3-3.5 kg. INTERVENTIONS:Hemorrhagic shock at mean arterial pressure of 40 mm Hg was induced by exsanguinations in anesthetized, mechanically ventilated animals for 60 minutes and thereafter rabbits were resuscitated by homologous blood and Ringer's lactate infusion under normoxemia (Normox-Res group, Pao2 = 95-105 mm Hg, n = 9) or hypoxemia (Hypox-Res group, Pao2 = 35-40 mm Hg, n = 7). MEASUREMENTS AND MAIN RESULTS:Using indicator-dilution techniques we measured at baseline and post resuscitation pulmonary capillary endothelial angiotensin converting enzyme activity expressed as percentage of metabolism (%M) and hydrolysis (v) of the substrate H-benzoyl-Phe-Ala-Pro. Normox-Res rabbits exhibited decreased %M (p < 0.05) and v (p < 0.05) post resuscitation as compared with baseline, while no differences occurred in the Hypox-Res group. Myeloperoxidase was measured in lung tissue and was higher in Normox-Res than Hypox-Res animals (p < 0.01). Lung injury was estimated microscopically, whereas the expression of the intercellular adhesion molecule-1 and the vascular cell adhesion molecule-1 were assessed by immunohistochemistry on sections coming from the same tissue block. Compared with Normox-Res, Hypox-Res animals exhibited lower lung injury histopathological score (p < 0.01) and lung malondialdehyde concentration (p < 0.01), and lower intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expressions in both the inflammatory cells (p < 0.01) and the blood vessels (p < 0.05). CONCLUSIONS:Normoxemic resuscitation of hemorrhagic shock is associated with pulmonary endothelial dysfunction and lung injury that may be attenuated by hypoxemic resuscitation.

journal_name

Crit Care Med

journal_title

Critical care medicine

authors

Douzinas EE,Orfanos SE,Livaditi O,Augustatou K,Villiotou V,Kavantzas N,Flevari A,Korkolopoulou P,Roussos C,Patsouris E

doi

10.1097/CCM.0b013e31819b81ec

subject

Has Abstract

pub_date

2009-03-01 00:00:00

pages

869-75

issue

eissn

0090-3493

issn

1530-0293

pii

00003246-200903000-00010

journal_volume

pub_type

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Hypoxemic resuscitation prevents pulmonary capillary endothelial dysfunction induced by normoxemic resuscitation from hemorrhagic shock.