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Biomedical subjects

E A Carter

Publications and source records attributed to E A Carter.

At least 91 records · Page 5Linked to original sources
PubMed1981

Use of hydrogen gas (H2) analysis to assess intestinal absorption. Studies in normal rats and in rats infected with the nematode, Nippostrongylus brasiliensis.

The in vitro and in vivo production of hydrogen gas (H2) from various carbohydrates or proteins has been examined in normal rats and in rats infected with the nematode Nippostrongylus brasiliensis. Normal rat fecal homogenates were capable of producing H2 in vitro from glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate. Direct injection of glucose, sucrose, xylose, lactulose, bovine serum albumin, or casein hydrolysate into the cecum of normal rats resulted in approximately twice as much H2 production in vivo than when these same carbohydrates or proteins were administered to the normal rats by gavage. Partial small intestinal villous atrophy was produced by infecting rats with the nematode N. brasiliensis. Impaired small intestinal cell function and evidence of malabsorption in the nematode-infected rats included: (a) decreased activity of intestinal cell lactase (-43%), sucrase (-33%), and alkaline phosphatase (-46%); (b) decreased gut sac uptake of 3-O-(methyl-3H]-D-glucose (-21%) or 1-[carboxyl-14C]-aminocyclopentane-1-carboxylic acid (-28%); and (c) increased (+ 64%-561%) 14CO2 production after D-[U-14C]xylose administration. These rats produced approximately twice as much H2 after gavage administration of glucose, sucrose, xylose, bovine serum albumin, or casein hydrolysate compared with normal rats. The present study suggests that H2 analysis may be useful in the evaluation of small intestinal malabsorption states in rats.

Animals↗
PubMed1980

Effect of acute and chronic ethanol intoxication on hepatic regeneration.

We studied the effects of acute and chronic ethanol feeding on hepatic regeneration in rats following partial hepatectomy and toxic liver injury produced by D-galactosamine. Ethanol, when administered as a single dose (6 gm/kg), inhibited 3H-thymidine incorporation into hepatic DNA; this effect depended in part on the time of ethanol feeding following partial hepatectomy. Multiple ethanol feedings produced an even greater inhibition, which persisted for at least 48 hr after partial hepatectomy. Rats chronically fed ethanol for 30 days also failed to achieve a hepatic proliferative response to either partial hepatectomy or D-galactosamine induced hepatitis comparable to isocaloric pair-fed controls. These investigations suggest that there may be a certain metabolic state in the hepatocyte cell cycle which is most susceptible to the action(s) of ethanol; inhibition of liver regeneration by acute or chronic ethanol consumption may result in delayed recovery from prior or coincident liver injury.

Alcoholic Intoxication↗
PubMed1979

Inhibition of hepatic regeneration in rats by acute and chronic ethanol intoxication.

We studied the effects of acute and chronic ethanol feeding on hepatic regeneration in rats after partial hepatectomy and toxic liver injury produced by D-galactosamine. Ethanol, when administered as a single dose (6 g/kg), inhibited 3H-thymidine incorporation into hepatic DNA; this effect depended in part on the time of ethanol feeding after partial hepatectomy. Multiple ethanol feedings produced an even greater inhibition, which persisted for at least 48 hr after partial hepatectomy. Rats chronically fed ethanol for 30 days also failed to achieve a hepatic proliferative response to either partial hepatectomy or D-galactosamine-induced hepatitis, comparable with isocaloric pair-fed controls. These investigations suggest that there may be a certain metabolic state in the hepatocyte cell cycle that is most susceptible to the action(s) of ethanol; inhibition of liver regeneration by acute or chronic ethanol consumption may result in delayed recovery from prior or coincident liver injury.

Alcoholic Intoxication↗
PubMed1978

Plasma alpha-amino-n-butyric acid to leucine ratio: nonspecificity as a marker for alcoholism.

Recent studies suggest that the ratio of plasma alpha-amino-n-butyric acid to leucine is increased specifically by chronic heavy alcohol consumption. To test this hypothesis, we determined this ratio in normal controls and (1) currently drinking chronic heavy alcoholics; (2) currently abstaining chronic alcoholics; (3) patients with nonalcoholic liver disease; (4) chronically alcohol-fed rats and mice; (5) mice infected with murine hepatitis virus; and (6) mice exposed to carbon tetrachloride. Mean ratios in control persons, drinking alcoholics, abstaining alcoholics, and nonalcoholic liver disease patients were not statistically different. Of 5 drinking alcoholics followed serially from the beginning of abstinence, 1 had an elevated ratio on admission and a persistently elevated ratio even 2 weeks later; another had a ratio more elevated after 2 weeks of abstinence, than on admission; and 3 had ratios in the normal elevated after 2 weeks of abstinence than on admission; and 3 had ratios in the normal range. Compared to control rats, chronically alcohol-fed rats had a significantly elevated mean ratio after 1 month and an even higher ratio after 2 months (P less than 0.001). In control, alcohol-fed and carbon tetrachloride-treated mice, alpha-amino-n-butyric acid was undetectable, but in two sets of mice with severe murine hepatitis virus infection, elevated ratios were found. We conclude that because the ratio of alpha-amino-n-butyric acid to leucine is not necessarily elevated in chronic heavy alcoholics but can be elevated in acute experimental liver cell injury, it does not appear to be a specific marker for the detection of alcoholism.

Alcoholism↗
PubMed1977

Familial hemochromatosis. Physiologic studies in the precirrhotic stage of the disease.

We studied 12 members of a family with precirrhotic hemochromatosis to define the physiologic abnormalities in the asymptomatic phase of the disease. Six of 12 had increased iron stores; the mode of inheritance was consistent with an autosomal dominant trait. Serum ferritin levels were no more predictive of tissue iron levels than measurements of serum iron, transferrin saturation or chelatable iron excretion. In three affected family members intestinal iron content was normal. Liver proline hydroxylase activity and urinary hydroxyproline excretion did not correlate with tissue iron content, suggesting that, in addition to the possible role of tissue iron, hepatic fibrosis may involve other factors. "Borderline diabetes mellitus" was present in three affected family members, but extensive studies revealed that pituitary dysfunction is uncommon in early hemochromatosis. Increased levels of liver iron proved to be the most reliable marker for the disease.

Adolescent↗
PubMed1971

Ethanol stimulates triglyceride synthesis by the intestine.

In vivo ethanol given acutely or chronically by two dietary means resulted in significant increases in [1-(14)C]palmitate incorporation into triglyceride by intestinal slices or microsomes derived from intestinal slices. In vitro, 2.6 percent ethanol, an amount comparable to that found in t..e intestinal lumen of social drinkers, also resulted in significant increases in [1-(14)C]palmitate incorporation into triglyceride. Pyrazole, an inhibitor of alcohol dehydrogenase, diminished the stimulatory effect of ethanol both in vivo and in vitro. These data may provide a new insight into the effects of alcohol, and specifically on the possible contribution of intestinal triglyceride synthesis to alcoholic hyperlipemia and the alcohol-induced fatty liver.

Administration, Oral↗