INVESTIGADORES
LORES ARNAIZ Silvia
congresos y reuniones científicas
Título:
Experimental portal hypertension and hippocampal mitochondrial dysfunction.
Autor/es:
PERAZZO, JC; LORES ARNAIZ, S.; PRESTIFILIPPO, J.P.; LAGO, N.; D´AMICO, G.; CZERNICZYNIEC, A.; BUSTAMANTE, J.; BOVERIS, A.; LEMBERG, A.
Lugar:
Solingen
Reunión:
Congreso; 12th International Symposium on Hepatic Encephalopathy and Nitrogen Metabolism.; 2005
Resumen:
Portal hypertension is a major
complication of human cirrhosis that frequently leads to central nervous system
dysfunction. In our study, rats with prehepatic portal hypertension developed
hippocampal mitochondrial dysfunction as indicated by decreased respiratory
rates, respiratory control and mitochondrial nitric oxide synthase (mtNOS)
activity in mitochondria isolated from the whole hippocampus.
Succinate-dependent respiratory rates decreased by 29 % in controlled state 4
and by 42 % in active state 3, and respiratory control diminished by 20 %.
Portal hypertensive rats showed a decreased mtNOS activity of 46 %. Hippocampal
mitochondrial dysfunction was associated with ultrastructural damage in the
mitochondria of hippocampal astrocytes and endothelial cells. Swollen
mitochondria, loss of cristae and rupture of outer and inner membrane was
observed in astrocytes and endothelial cells of the blood-brain barrier in
parallel with the ammonia gradient. The moderate increase in plasma ammonia
that followed portal hypertension was the potential primary cause of the
observed alterations.