Hemorrhagic shock (HS) induces a compensatory endocrine and cytokine response which aims to restore homeostasis. This response can be modulated by general anesthetics. To our knowledge, no studies have evaluated if etomidate modulates this response in experimental HS. After being premedicated with buprenorphine (0.05 mg/kg subcutaneously), male Wistar rats were anaesthetized with 5% isoflurane and divided into three groups: G1 (control, n = 16), G2 (n = 13), and G3 (n = 14). G2 and G3 were subjected to HS by collecting 30% of their blood volume and resuscitated 90 min later with the collected blood and normal saline, in a 1:3 ratio, respectively. G3 received etomidate (1 mg/kg IV) before HS. Blood gas analysis, adrenocorticotropic hormone (ACTH), corticosterone, and plasma levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10 and of TNF-α, IL-6, and IL-10 mRNA obtained through real-time polymerase chain reaction (RT-PCR) were measured at 0, 90, 150, and 240 min after HS induction. Compared with G2, etomidate-treated animals had significantly lower corticosterone, PO2, PO2/FiO2, base excess and HCO3, and higher TNF-α, IL-6, IL-10, and TNF-α mRNA levels (P <0.05). Etomidate-treated rats showed impaired adrenal and increased cytokine response to HS and evidence of worse tissue oxygenation and lung dysfunction. Based on these results, and until further studies are performed to confirm if these findings occur in clinical patients, we suggest that etomidate should be used cautiously in HS.
- adrenocorticotropic hormone (ACTH)
- hemorrhagic shock
- tumor necrosis factor (TNF)-α