OBJECTIVE: To explore the relationship between plasma levels of carbon monoxide and blood-brain permeability in cirrhotic rats. METHODS: We measured mean arterial pressure (MAP), heart rate, plasma levels of carbon monoxide and amount of Evans blue in the brain tissue taken as the index of blood-brain permeability in cirrhotic rats (n=10) and controls (n=10). RESULTS: Cirrhotic rats showed significant increases in plasma carbon monoxide and amount of Evans blue in brain tissue compared with controls [(18.37 +/- 1.79) micromol/L,(18.52 +.- 1.39) ng/mg vs (10.27 +/- 1.21) micromol/L, (15.08 +/- 1.06) ng/mg; P< 0.01]. Carbon monoxide levels in cirrhotic rats correlated positively with blood-brain barrier permeability and inversely with MAP (r=0.72, P< 0.01; r= -0.67, P< 0.05). CONCLUSIONS: Carbon monoxide, involving in the occurrence of hypotension and the increase of blood-brain barrier permeability, may play a role in the development of hepatic encephalopathy.
OBJECTIVE: To explore the relationship between plasma levels of carbon monoxide and blood-brain permeability in cirrhotic rats. METHODS: We measured mean arterial pressure (MAP), heart rate, plasma levels of carbon monoxide and amount of Evans blue in the brain tissue taken as the index of blood-brain permeability in cirrhotic rats (n=10) and controls (n=10). RESULTS: Cirrhotic rats showed significant increases in plasma carbon monoxide and amount of Evans blue in brain tissue compared with controls [(18.37 +/- 1.79) micromol/L,(18.52 +.- 1.39) ng/mg vs (10.27 +/- 1.21) micromol/L, (15.08 +/- 1.06) ng/mg; P< 0.01]. Carbon monoxide levels in cirrhotic rats correlated positively with blood-brain barrier permeability and inversely with MAP (r=0.72, P< 0.01; r= -0.67, P< 0.05). CONCLUSIONS:Carbon monoxide, involving in the occurrence of hypotension and the increase of blood-brain barrier permeability, may play a role in the development of hepatic encephalopathy.