Acute traumatic coagulopathy (ATC) may trigger sympathoadrenal activation associated with endothelial damage and coagulation disturbances. Overexcitation of sympathetic nerve in this state would disrupt sympathetic-vagal balance, leading to autonomic nervous system dysfunction. The aim of this study was to evaluate the autonomic function in ATC and its influence on
inflammation, endothelial and coagulation activation. Male Sprague-Dawley rats were randomly assigned to
sham, ATC control (ATCC) and ATC with
sympathectomy by
6-hydroxydopamine (ATCS) group.
Sham animals underwent the same procedure without
trauma and
bleeding. Following
trauma and
hemorrhage, rats underwent heart rate variability (HRV) test, which predicts autonomic dysfunction through the analysis of variation in individual R-R intervals. Then, rats were euthanized at baseline, and at 0, 1 and 2 h after
shock and blood gas, conventional coagulation test and markers of
inflammation, coagulation, fibrinolysis, endothelial damage and
catecholamine were measured. HRV showed an attenuation of total power and high frequency, along with a rise of low frequency and low frequency : high frequency ratio in the ATC rats, which both were reversed by
sympathectomy in the ATCS group. Additionally,
sympathetic denervation significantly suppressed the increase of proinflammatory
cytokines,
tumor necrosis factor-α and the fibrinolysis markers including
tissue-type plasminogen activator and
plasmin-
antiplasmin complex. Serum
catecholamine, soluble
thrombomodulin and
syndecan-1 were also effectively inhibited by
sympathectomy. These data indicated that autonomic dysfunction in ATC involves both sympathetic activation and parasympathetic inhibition. Moreover,
sympathectomy yielded anti-inflammatory, antifibrinolysis and endothelial protective effects in rats with ATC. The role of autonomic neuropathy in ATC should be explored further.