Endothelial dysfunction in trauma patients: a preliminary communication.

Global ischemia, followed by reperfusion during resuscitation, leads to cellular damage by generating toxic reactive metabolites that includes, but is not exclusive to, superoxide radical. Superoxide decreases the bioavailability of nitric oxide (NO) via its reaction that yields peroxynitrite. The observation of decreased bioavailability of NO, and attenuated endothelium-dependent relaxation have been observed in animal models of trauma and resuscitation. However, it remains unknown whether endothelium-mediated vasodilation is impaired in humans after traumatic hemorrhage followed by crystalloid resuscitation. Based on these previously established precepts, we hypothesized that endothelium-dependent relaxation is impaired in trauma patients despite adequate fluid resuscitation with crystalloid solutions. Baseline characteristics such as age, body mass index, and blood pressure being similar in both groups, NO-mediated, endothelium-dependent flow-mediated dilation (FMD) of the brachial artery was examined in resuscitated trauma victims (n = 13) and compared in normal controls (n = 12). Baseline brachial artery diameter, endothelium-dependent FMD induced by reactive hyperemia and endothelium-independent dilation induced by administration of sublingual nitroglycerin were measured. Brachial artery diameter measured at baseline in trauma patients and in control subjects were not dissimilar. In conclusion, brachial artery FMD, a surrogate for NO-mediated endothelial function, was significantly impaired in trauma patients despite fluid resuscitation resulting in stable hemodynamics (0.8 +/- 1.7 mm vs. 5.7 +/- 0.8 mm, respectively; P < 0.05) However, endothelium-independent dilation induced by nitroglycerin was not significantly different between trauma patients and controls.