• José L Pascual, Kosar A Khwaja, Prosanto Chaudhury, and Nicolas V Christou.
• Division of General Surgery, McGill University Health Center, Montreal, Quebec, Canada. jose.pascual@mail.mcgill.ca
• J Trauma. 2003 May 1;54(5 Suppl):S133-40.

AbstractThe systemic inflammation that occurs in shock states is believed to promote overexuberant microcirculatory activation, the release of toxic proteases and oxygen radicals causing microvascular damage, and subsequent tissue and organ injury. Although shock-associated microvascular failure is often unresolved after standard resuscitation, hypertonic saline (HTS) appears to reduce microvascular collapse, restoring vital nutritional blood flow. In addition, hypertonic fluids tend to blunt the up-regulation of leukocyte and endothelial adhesion molecules that occurs with isotonic resuscitation of shock. Recently, direct evaluation by intravital microscopy has shown that HTS resuscitation dampens the interactions between leukocytes, platelets, and endothelium found with Ringer's lactate resuscitation. Furthermore, fewer cellular interactions have been correlated with attenuation in microvascular wall permeability after resuscitation with HTS. Better characterization of microcirculatory effects by hypertonic saline may provide mechanisms for improved morbidity and mortality associated with hypertonic resuscitation.

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