RESUMO
BACKGROUND: Acute brain injury is associated with a bimodal hypermetabolic state probably caused by cytokine secretion and high hormone and catecholamine concentrations. In a first stage, the brain would produce these substances and afterwards, another production source, most probably the splanchnic territory, would perpetuate the hypermetabolic state. AIM: To investigate the cytokine production source and to assess intestinal permeability in acute brain injury in the absence of cerebral ischemia and systemic oxygen deficit. PATIENTS AND METHODS: Arterial systemic and cerebral venous bulbar interleukin 1 beta and interleukin 6 levels were measured during the first seven days of evolution in 15 patients with acute brain injury. Serum lactate, the oxygen/lactate ratio, gastric intramucosal pH and intestinal permeability using the lactulose/mannitol test were also assessed in the same period. RESULTS: High arterial and venous interleukin 1 beta and interleukin 6 levels were detected. A positive gradient for interleukin 6 levels was detected throughout the study period with normal intramucosal pH, lactate and oxygen/lactate ratio. There was also an early impairment of intestinal permeability in these patients. CONCLUSIONS: High arterial and venous cytokine concentrations were detected in patients with acute brain injury. The positive gradient for interleukin 6 suggests a brain origin for this cytokine. Intestinal permeability is also altered in these patients.
