CONICET | Buscador de Institutos y Recursos Humanos

Sarcopenia and heart failure are common features of chronic liverdisease (CLD). The loss of skeletal muscle (SM) and its functioncontributes to morbidity and mortality. Its prevalence in patients withCLD is estimated at 40-70%. Hepatic encephalopathy (HE) has asimilar prevalence and, in addition, there is a correlation betweenthe two. The CLD decreases the detoxification capacity of ammonia,so SM and astrocytes become the main route of ammonia, mainlythrough glutamine synthetase (GS). We hypothesized that a modelof subclinical hepatic encephalopathy (MHE) showing moderatehyperammonemia and almost normal liver could show a point for early events in myocardial (HM) damage. The Wistar ratswere divided into 2 groups, (i) simulated surgery and (ii) group withstenosed portal vein, MHE. GS, oxygen consumption, nitric oxideproduction, high resolution light microscopy (HRLM) and electrontransmission microscopy (ETM) were evaluated, after 14 days ofsurgery, in left HM. The results showed a significant increase in GS(p <0.01) in the MHE group with reduced oxygen consumption and asignificant decrease in nitric oxide. HRLM showed that the HM triad(sarcolemma, T-tubes and sarcoplasmic reticulum) was widely dilatedwith a convergent structure. This membrane traffic system wasundulated with an increased surface, to the detriment of the fibrillarstructure. ETM, confirmed these, showing subcellular edema, withdetachment of fibrillar structures, swollen mitochondria with loss ofridges and matrix density, disruption of the nuclear membrane andan increase in the number and size of subsarcolemal vacuoles. Thetriad was also altered showing the dilatation of this system and thefocal interruption. The most relevant ETM data were focal myofibrillolysis.These results suggest that under these conditions, in earlystages of HE, hyperammonemia could induce myocardial cell damage,with or without CLD.