Hypothalamus-pituitary-adrenal (HPA) axis is involved in the modulation of the innate immune response. The purpose of this study was to evaluate the dynamic relationship between plasma
corticosterone and
interleukin-6 in the hypothalamus-destroyed rats after
blast injury. A total of 105 Sprague-Dawley rats were divided randomly into normal control (normal),
sham operated (
sham),
blast injury plus
sham operated (
blast injury) and
blast injury plus hypothalamus destruction groups. Symmetric electrolytic bilateral destruction of the hypothalamus was performed for the deeply
anesthetic rats under sterile conditions. Seven days after the destruction of the hypothalamus, the animals were succumbed to moderate
blast injury using a BST-I bioimpact machine. Plasma
corticosterone and
IL-6 levels were determined by radioimmunoassay and
enzyme-linked
immunosorbent assay, respectively. After
blast injury, the
corticosterone level in the hypothalamus-destroyed rats was significantly lower than that in the rats without destruction of hypothalamus at 3h (P<0.01) or from 5 to 8h (P<0.05). Reduction of
corticosterone may be intrinsically correlated with the severe tissue injury and increased mortality (4/15 vs. 0/15, P<0.05). Circulating
IL-6 level was markedly elevated in response to
blast injury and hypothalamus destruction further increased
IL-6 secretion (P<0.05). We concluded that elevation of pro-inflammatory
IL-6 secretion might compensate the impaired HPA axis function after the
trauma occurred in the hypothalamus-destroyed rats. These results also suggested that release of hypothalamus
hormones is necessary to maintain certain magnitude of innate immunity after
trauma.