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Biomedical subjects

A Chung

Publications and source records attributed to A Chung.

At least 109 records · Page 6Linked to original sources
PubMed1977

Dietary cholesterol affects chenodeoxycholic acid action on biliary lipids.

Chenodeoxycholic acid (CDC) decreases biliary saturation and dissolves gallstones in one-half of the treated patients. Dietary cholesterol also affects biliary lipids and is a possible factor explaining unsuccessful CDC therapy. The aim of this investigation was to study the effect of high and low dietary cholesterol on the CDC-induced decrease of biliary saturation and activity of hepatic hydroxymethylglutaryl coenzyme A reductase (HMG-CoAR). Seventy two hamsters in six groups were fed for 1 month one of three diets: 0.8 mg of cholesterol per g of food, 2.4 mg of cholesterol per g, or cholesterol-free. On each diet hamsters received no CDC or CDC 30 mg per kg per day. When animals were killed, biliary lipids were determined and the activity of hepatic HMG-CoAR was assayed. CDC administration decreased the saturation index (SI)(P less than 0.01) in hamsters on the high cholesterol and standard diets but not on the cholesterol-free diet. The SI in CDC-treated hamsters on the high cholesterol (0.78 +/- 0.03) and cholesterol-free (0.68 +/- 0.02) diets were greater (P less than 0.02) than in CDC-treated hamsters on the standard diet (0.48 +/- 0.03). CDC decreased (P less than 0.01) HMG-CoA reductase activity on each diet. In comparison to HMG-CoAR activity (190 +/- 7.6 pmoles per mg per min) in CDC-treated hamsters on the standard diet, the activity in CDC-treated hamsters on the high cholesterol diet (176 +/- 5.8 pmoles per mg per min) was decreased ( less than 0.05), whereas the activity on the cholesterol-free diet (495 +/- 11.5 pmoles per mg per min) was greater (P less than 0.01). It is concluded that: (1) dietary cholesterol is necessary for optimum CDC inhibition of HMG-CoAR; (2) high cholesterol and cholesterol-free diets prevent maximum CDC decrease of the biliary saturation index; (3) dietary cholesterol alterations may therefore be one cause of the failure of CDC dissolution of gallstones.

Animals↗
PubMed1976

Localization of angiotensin converting enzyme (kininase II). I. Preparation of antibody-hemeoctapeptide conjugates.

Antibodies to pig lung angiotensin converting enzyme (kininase II) were conjugated to a heme-octapeptide (8-microperoxidase, 8-MP) derived from cytochrome c. 8-MP, which has only one reactive amine, was coupled to antibody in a two-step procedure using a bifunctional active ester, bis-succinyl succinate. In the first-step, 8-MP-succinyl succinate, a stable compound which can be stored. In a second step, the remaining active ester was used for coupling to reactive amines of the antibody. The conjugate consists of 1.6-2.3 8-MP moieties per antibody. Using these procedures, the formation of complex polymers is avoided. Each molecule of conjugate possesses both immunoreactivity and peroxidatic activity. The conjugate has been used to localize angiotensin converting enzyme along the plasma membrane and associated caveolae of pig aortic endothelial cells in culture.

Antibodies↗
PubMed1976

Inhibition by propranolol of bile acid stimulation of rabbit colonic adenylate cyclase in vitro.

UNLABELLED: Bile acids, especially unconjugated deoxycholic acid, cause diarrhea by inducing colonic mucosal secretion of water and electrolytes. This effect has been shown to be mediated by adenylate cyclase (AC). Propranolol, a beta-adrenergic blocking agent which inhibits AC, may then prevent this action of bile acids on colonic mucosa. The aim of this study was to determine the effect of bile acids, catecholamines, and propranolol on AC activity in colonic mucosa. The in vitro effects of deoxycholic acid, taurocholic acid, NaF, epinephrine, norepinephrine, and propranolol on AC in rabbit colonic mucosa were determined. NaF, 10(-4) M, increased AC activity to 220% of control (P less than 0.01). Deoxycholic acid, 10(-4) M, increased AC activity to 178% of control (P less than 0.01). Lesser but significant (P less than 0.01) stimulation of AC occurred at both higher and lower concentrations of deoxycholic acid, with no effect at 10(-10) M. Taurocholic acid, 10(-4) M, and epinephrine and norepinephrine, 10(-2) M, 10(-4) M, 10(-6) M, and 10(-8) M, had no effect on AC. Propranolol, 10(-6) M, caused a 60% decrease (P less than 0.01) in the stimulated AC activity induced by 10(-4) M deoxycholic acid. Propranolol, 10(-4) M, decreased basal AC by 30% (P less than 0.01). IN CONCLUSION: (1) Deoxycholic acid, but not taurocholic acid, epinephrine, or norepinephrine, stimulates colonic AC activity. (2) Propranolol inhibited this deoxycholic acid stimulation of AC. (3) Catecholamines are not intermediaries in this action of propranolol on colonic mucosal AC activity.

Adenylyl Cyclase Inhibitors↗
PubMed1976

Propranolol inhibits adenylate cyclase and secretion stimulated by deoxycholic acid in the rabbit colon.

Bile acids cause diarrhea by inducing colonic secretion, probably mediated through the cyclic AMP system. The aim was to determine the effects of an adenylate cyclase inhibitor, propranolol, on deoxycholic acid (DCA) stimulation of net secretion and the cyclic AMP system in the colon. In each of 30 New Zealand white rabbits, 0.9% NaC1 as control and 6 mM and 8 mM DCA were injected in random sequence into three colonic loops in situ. Propranolol, 4 mg per kg was administered intravenously to 12 of the 30 rabbits 1/2 hr before preparation of the loops, i.e., 5 1/2 hr before the rabbits were killed. In the 18 untreated animals, 6 and 8 mM DCA significantly stimulated colonic net secretion and mucosal adenylate cyclase activity; 6 mM DCA caused no change in mucosal phosphodiesterase activity, whereas 8 mM DCA caused a 25% decrease (P less than 0.01). In propranolol-treated animals compared to untreated animals, the volume of luminal fluid in controls was not different, with 6 mM DCA it was 88% less (P less than 0.01), and with 8 mM DCA it was 45% less (P less than 0.01); adenylate cyclase activity in controls was 43% less (P less than 0.01), with 6 mM DCA it was 67% less (P less than 0.01), and with 8 mM DCA it was 65% less (P less than 0.01); phosphodiesterase activity in controls and with 6 mM DCA was not different and with 8 mM DCA it was 38% greater (P less than 0.02). In conclusion, propranolol prevented DCA stimulation of colonic net secretion and inhibited the cyclic AMP system. Propranolol, therefore, warrants investigation as therapy for diarrhea caused by bile acids in the colon.

Adenylyl Cyclase Inhibitors↗
PubMed1975

Treatment of gallstones with chenodeoxycholic acid and phenobarbital.

In a controlled trial, 36 patients with asymptomatic radiolucent gallstones were treated with chenodeoxycholic acid, 750 mg per day, phenobarbital, 180 mg per day, combination of both drugs, and placebo. After one year, chenodeoxycholic acid, phenobarbital and the combination, but not placebo, significantly decreased biliary cholesterol saturation. The effect was significantly greater with chenodeoxycholic acid and the combination than with phenobarbital. Gallstones size decreased more than 50 per cent in nine of 20 patients receiving chenodeoxycholic acid, either alone or combined with phenobarbital, but in no patient receiving only phenobarbital or placebo. Gallstones disappeared completely in tow patients. Abnormalities in liver-function tests in thriee of 36 patients and in five of 16 liver biopsies, occured with equal frequency in the four treatment groups. Thus, after one year, phenobarbital alone was ineffective in gallstone dissolution. Chenodeoxycholic acid alone or combined with phenobarbital, however, offered a partially effective and safe treatment for asymptomatic radiolucent gallstones.

Adult↗
PubMed1975

Subcellular localization of pulmonary antiotensin-converting enzyme (kininase II).

Goat antibodies to pig lung angiotensin-converting enzyme (kininase II) were conjugated to microperoxidase. Rat lung tissue, previously incubated with non-immune goat serum, was incubated with the antibody-microperoxidase conjugate and then with H2O2 and 3,3-diaminobenzidine. Electron microscopy revealed reaction product on the plasma membrane and caveolae of endothelial cells, especially those of capillaries and venules. These results support the hypothesis that angiotensin I and bradykinin are metabolized by enzymes on the luminal surface of pulmonary endothelial cells.

Angiotensin II↗
PubMed1975

Cardiac glycogen in long-evans rats: diurnal pattern and response to exercise.

The 24-h pattern of cardiac glycogen was determined in normally active, caged male Long-Evans rats. Relatively small fluctuation was observed during a 24-h cycle with maximal difference between mean values ranging from 3.41 +/- 0.28 (dark room) to 5.15 +/- 0.19 (light room) mg glycogen/g wet wt heart, suggesting that the substantial diurnal variation of cardiac glycogen reported in Wistar rats is not a universally observed phenomenon. Cardiac glycogen during and following a single bout of moderate running was compared to a bout of strenuous running in fed male Long-Evans rats. Moderate continuous running at 20 m/min for 30 min did not decrease cardiac glycogen below the average control level (4.09 +/- 0.10 mg glycogen/g heart) but did cause a short period of supercompensation, which reached a peak of 6.27 +/- 0.19 mg/g heart at 2 h postexercise. Strenuous running in bouts at 30 m/min over a 2-h period for a distance of 1,413 m caused a significant decrease in cardiac glycogen to 2.66 +/- 0.20 mg/g heart followed by an extended period of supercompensation, which reached a peak of 9.01 +/- 1.41 mg/g heart at 4 h postexercise and remained significantly elevated during the next 13 h. Thus, the severity of exercise in normal, fed rats determines not only the extent of cardiac depletion, but also the supercompensation pattern of glycogen repletion following exercise.

Animals↗