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Biomedical subjects

O R Koch

Publications and source records attributed to O R Koch.

At least 37 records · Page 2Linked to original sources
PubMed1979

[Hepatic function in vivo and in the isolated liver of rats poisoned with parathion].

Enzyme determinations and hepatic histological studies were carried out in normal rats and in rats intoxicated with the organophosphorus pesticide parathion. No significative evidence of hepatocellular damage was seen in parathion -- intoxicated rats as responsible of the impaired bile flow and sulfobromophthalein biliary excretion that were previously reported. On the contrary, the isolated perfused rat liver from normal and intoxicated rats showed a similar behavior when the perfusate flow through the liver was maintained at a similar rate. We conclude that altered hepatic blood flow may be a factor determinant of an impairment of bile flow and of biliary excretion of several organic anions like sulphobromopthalein that were observed in parathion -- intoxicated rats.

Alanine Transaminase↗
PubMed1978

Effects of quinestrol on hepatic function in the rat.

Hepatic function in female rats given 200 microgram of quinestrol every 15 days for up to 210 days was studied. Prolonged treatment with quinestrol affected liver weight, serum cholestrol levels, biliar flux, and bromosulphthalein test, but these parameters tended toward control levels after 30 days of treatment. Quinestrol failed to affect alkaline phosphatase, oxalacetic and pyruvic transaminases and the concentration of bilirubin in serum and bile. The effects of quinestrol on hepatic function are similar to the effects of other estrogen derivatives.

Alkaline Phosphatase↗
PubMed1978

Ultrastructural and biochemical aspects of liver mitochondria during recovery from ethanol-induced alterations. Experimental evidence of mitochondrial division.

To study the morphologic and biochemical changes occuring in liver mitochondria during recovery from ethanol-induced injury, rats fed a 6-month high-alcohol regimen plus a nutritionally adequate diet which did not induce fatty liver were compared with isocalorically fed controls. After this period the alcohol-fed animals displayed striking ultrastructural changes of liver mitochondria and a decreased respiratory activity with succinate or malate-glutamate as substrate. On the contrary, the respiratory rate with I-glycerophosphate was 50% increased. Regression changes were studied after alcohol was withdrawn from the diet. Enlarged mitochondria rapidly disappeared (in 24 hours), although a few megamitochondria were still present after 8 days of abstinence. A similar recovery was observed for the functional alterations. At the end of the experimental period, only a slight decrease of the maximal respiratory rate using malate-glutamate as a substrate was noted. The ultrastructural findings and the morphometric data suggest that the way in which mitochondrial normalization takes place is based on partition of these organelles.

Animals↗