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Biomedical subjects

M Bergeron

Publications and source records attributed to M Bergeron.

108 records · Page 6Linked to original sources
PubMedDate not supplied

Monitoring of the effects of dysprosium shift reagents on cell suspensions.

The effects of two widely used paramagnetic shift reagents for cationic NMR, dysprosium tripolyphosphate [Dy(PPP)2(7-)] and dysprosium triethylenetetramine hexaacetate [Dy(TTHA)3-], on the cell structure of dog and human erythrocytes, dog kidney cortical tubules and rat hepatocytes were investigated. The effect of shift reagents on cell integrity was monitored by measuring the hematocrit values for erythrocytes, by measuring the lactate dehydrogenase (LDH) release and by electron microscopy for cortical tubules and hepatocytes. The quantitation of the dyprosium penetration inside cells was accomplished by atomic absorption, atomic emission and neutron activation. More severe effects were observed with Dy(PPP)2(7-) than with Dy(TTHA)3-, and were dependent on the divalent cation concentration and on the shift reagent concentration. Very serious cell damage was observed after 60 min incubation in the presence of 10 mumol Dy(PPP)2(7-)/mL suspension at low or high divalent cation concentration. The situation was improved at 5 mumol Dy(PPP)2(7-)/mL suspension especially at high divalent cation concentration (2.5 mM). Incubation with Dy3+, PPP5- or Dy(TTHA)3- caused little or no structural effects but dysprosium was found to penetrate slowly inside tubules with Dy(TTHA)3-. Both Dy3+ and Dy(PPP)2(7-) penetrated rapidly inside cells. Dysprosium was found to bind to the isolated cytosol but not to isolated membranes, eliminating the possibility of extracellular membrane binding.

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PubMedDate not supplied

Cerebral GABA-ergic and glutamatergic function in hepatic encephalopathy.

Measurement of amino acids in brain tissue obtained at autopsy from cirrhotic patients dying in hepatic coma revealed a threefold increase in glutamine and a concomitant decrease in brain glutamate. The GABA levels were found to be unaltered. Studies using an animal model of portal-systemic encephalopathy gave similar results. Glutamic acid decarboxylase (GAD) activities were within normal limits, both in the brains of cirrhotic patients and portocaval-shunted rats. A previous study reported normal [3H]GABA binding to synaptic membrane preparations from cerebral cortex in these animals. Taken together, these findings suggest that cerebral GABA function is not impaired in hepatic encephalopathy associated with chronic liver disease and portal-systemic shunting. On the other hand, there is evidence to suggest that the releasable pool of glutamate may be depleted in brain in hepatic encephalopathy. Data consistent with this hypothesis include: Reduction in the evoked release of endogenous glutamate by superfusion of hippocampal slices with pathophysiological levels of ammonia; ammonia-induced reduction of glutamatergic neurotransmission; and an increase in the number of [3H]glutamate binding sites in synaptic membrane preparations from hyperammonemia rats and from rats with portocaval shunts. Such neurochemical changes may be of pathophysiological significance in hepatic encephalopathy.

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