Search PubMed⌕ Search

Biomedical subjects

C C Chou

Publications and source records attributed to C C Chou.

At least 163 records · Page 9Linked to original sources

Relative contribution of fat, protein, carbohydrate, and ethanol to intestinal hyperemia.

The relative contribution of dietary fat, protein, carbohydrate, and ethanol to postprandial intestinal hyperemia was assessed by comparing the vascular and metabolic effects of luminal placement of various solutions prepared from standard high -fat, high-protein, and high-carbohydrate test diets, corn oil, and ethanol in the jejunum of anesthetized dogs. The high-fat diet (45% fat, 18% protein, 29% carbohydrate) produced the greatest hyperemia (+30.4% of control), followed by high-protein (22% fat, 64% protein, 4% carbohydrate) (+24.1%) and high-carbohydrate (8% fat, 18% protein, 68% carbohydrate) (+18.2%) diets. When the fat content of the high-carbohydrate diet was raised to equal that of the high-protein diet, the two diets produced the same degree of hyperemia. All three diets produced a significantly greater hyperemia than the solutions containing the same amount of fat. All these dietary solutions increased intestinal oxygen consumption. Ethanol, however, increased blood flow without altering oxygen consumption. Thus, on weight basis, fat produces the greatest hyperemia, but the contribution of protein and carbohydrate to postprandial intestinal hyperemia cannot be considered as insignificant. The hyperemia results from a synergistic effect of all three dietary components.

Animals↗

Prostaglandin synthesis inhibition and postprandial intestinal hyperemia.

The effect of prostaglandin synthesis inhibition on the postprandial intestinal hyperemia was examined in the jejunum of anesthetized dogs. Both intravenous and intra-arterial infusion of the cyclooxygenase inhibitors indomethacin and mefenamic acid reduced resting jejunal blood flow and markedly enhanced the food-induced jejunal hyperemia. The jejunal vascular response to food did not change after either intravenous or intra-arterial infusion of the carrier solutions or intra-arterial infusion of angiotensin II. The enhancement of the jejunal hyperemia was associated with an increase in the food-induced increase in jejunal oxygen consumption. Infusion of the cyclooxygenase inhibitors increased the mean amplitude of the monophasic intestinal contractions; however, this did not appear to play a role in the enhancement of the food-induced hyperemia. The study indicates that inhibition of prostaglandin synthesis has a marked effect on the postprandial intestinal hyperemia and that this may be due to its enhancement of the jejunal metabolic response to food. The prostaglandins involved and their mechanism of action are unknown.

Animals↗

Role of histamine H1- and H2-receptors in postprandial intestinal hyperemia.

Studies were conducted in anesthetized dogs to assess whether histamine H1- and/or H2-receptors play a role in post-prandial intestinal hyperemia. The vascular and metabolic responses of jejunal segments to intra-arterial infusion of histamine and luminal placement of food before and after administration of tripelennamine, an H1-receptor antagonist, metiamide, an H2-receptor antagonist, and the combination of both antagonists were compared. Administration of the antagonists had no effect of jejunal blood flow and intestinal oxygen uptake (VO2). Tripelennamine or metiamide alone attenuated while the combination of both blocked the histamine-induced increases in blood flow and VO2. Metamide alone had no effect on the food-induced increases in flow and VO2. Tripelennamine significantly attenuated the food-induced increase in flow and blocked the increase in VO2. A 30% increase in flow was reduced to 15% after tripelennamine. The effects of tripelennamine plus metiamide were statistically the same as those of tripelennamine alone. It is concluded that endogenous histamines may play a role in postprandial intestinal hyperemia, and the effect is primarily mediated by the H1-receptors.

Animals↗

Blood flow and intestinal motility.

The effect of motility on blood flow varies with the nature of the motility and the initiating stimulus, and the mechanical compressing effect on contractions can be modified by intricate local regulatory mechanisms. Although rhythmic contractions usually decrease instantaneous arterial inflow and increase instantaneous venous outflow, mean blood flow may increase, decrease, or remain unchanged. A decrease in mean flow may indicate the predominance of the mechanical effects whereas an increase may be due to an active muscular hyperemia. Both tonic contractions and gut distention decrease total wall blood flow if mechanical compression overrides compensatory mechanisms; the effect is more pronounced on mucosal than on muscularis flow. Oxygen consumption and the capillary filtration coefficient may increase, decrease, or remain unchanged, depending on the degree of distention. The effects of chemicals depend on the interplay and predominance of their vascular, metabolic, and motility actions. When drawing conclusions regarding the effect of motility on blood flow, one must consider the role of local neural and chemical factors, alterations in the metabolic activity of different layers of the gut wall, collateral blood flow, and the mechanical effects of contractions and increased lumen pressure. Increased blood flow has little effect on motility, but severe or total ischemia and hypoxia produce a transient rise in motility followed by a prolonged paralysis.

Animals↗

Contribution of bile to postprandial intestinal hyperemia.

The role played by bile in postprandial intestinal hyperemia was examined by comparing the vascular effects of luminal placement of various nutrients with and without bile in situ jejunal segments of anesthetized dogs. The bile concentration was either 10 or 33% of that in the gallbladder. At these concentrations, bile per se in the jejunal lumen does not alter local blood flow. In the absence of bile, only glucose increased flow (+5% above control). With 10% bile, glucose and oleic acid increased flow by 10 and 24%, whereas with 33% bile, glucose, oleic acid, caproic acid, and amino acids increased flow by 22, 21, 12, and 12% above control, respectively. Triolein increased flow only after digestion by pancreatic enzymes and mixing with bile. Dipeptides did not alter flow with or without bile. Thus, bile plays an important role in postprandial intestinal hyperemia because it potentiates the glucose-induced hyperemia and because only in its presence can oleic acid, amino acids, caproic acid, and digested triolein increase intestinal blood flow.

Amino Acids↗

Regional blood flow during digestion in the conscious dog.

Blood flows to the major organs of the resting conscious dog were measured prior to and 30 and 90 min after feeding using the radioactive microsphere technique. Mean systemic arterial pressure, heart rate, and arterial PO2, PCO2, and pH, as well as blood flow to the brain, heart, adrenals, skeletal muscle, hepatic artery, and gastric antrum were not significantly changed following the meal. Pancreatic and duodenal and jejunal blood flows increased at both 30 and 90 min, whereas ileal blood flow increased only at 90 min after feeding. Flow to the gastric body increased in only half of the fed animals, but it increased in all of the animals treated with histamine. In all cases where there was an increase in total wall flow the increase was confined to the mucosa-submucosal layer. Blood flow to the colon was unchanged except for a decrease in the distal colon at 30 min. Thus, the cardiovascular response to feeding appears to be limited to those organs and tissues actively involved in digestion.

Animals↗

Motility and blood flow distribution within the wall of the gastrointestinal tract.

In anesthetized dogs, the effects of a gentle manipulation of the gut wall, increasing the lumen pressure to 20 mmHg by distention, or an intravenous infusion of physostigmine on blood flow distribution within the wall of the gastrointestinal tract were studied with radioactive microspheres. Manipulation and distension produced rhythmic contractions and increased flow to the distended and manipulated segments. The increased flow was confined to the muscularis serosa; the mucosa-submucosa flow was unchanged. Physostigmine produced a sustained tonic contraction and decreased flow to the whole wall of the stomach, duodenum, jejunum, ileum, and colon. The decreased flow was confined to the mucosa-submucosa; the muscularis serosa flow was unchanged. Thus, the muscularis serosa vasculatures escape the effects of a fall in vascular transmural pressure during the tonic contraction. Manipulation, distention, and physostigmine all increase the percentage of total wall flow perfusing the muscularis serosa. These studies suggest that active hyperemia, similar to exercise hyperemia in skeletal muscles, occurs in the muscularis of gut wall during intestinal contractions.

Animals↗

Constituents of chyme responsible for postprandial intestinal hyperemia.

While local venous outflow was measured in anesthetized dogs, various constituents of intestinal chyme were placed in the jejunal lumen to identify those responsible for postprandial intestinal hyperemia. Digested food and its supernatant increased local blood flow, whereas its precipitate, undigested food, and pancreatic enzymes did not. In the jejunum bile alone had no effect, but it markedly enhanced the hyperemic effect of digested food. Bile in the ileal lumen, however, increased local blood flow. At physiological postprandial concentrations in the jejunum, glucose, and micellar solutions of oleic acid and monoolein increased flow, but taurocholate and 16 common dietary amino acids did not. The hyperemic effect of lipids required the presence of taurocholate. Of the 16 amino acids, only Glu and Asp increased flow at 10 times the physiological concentrations (28 and 20 mM, respectively). The study indicates that the constituents of chyme responsible for postprandial intestinal hyperemia are the hydrolytic products of food, especially those of carbohydrates and fats and that bile plays an important role in the hyperemia.

Amino Acids↗

Comparison of vascular effects of gastrointestinal hormones on various organs.

Vascular effects of raising local arterial concentration of pentagastrin (2-1,500ng/ml), secretin (0.2-150mU/ml), and cholecystokinin (0.2-150mU/ml) in the duodenum, jejunum, heart, kidney, forelimb, spleen, and the skin and muscle of the forelimb were studied in 54 anesthetized dogs. Secretin produced similar vasodilation in all organs. The minimal increment in local blood secretin concentration for vasodilation ("concentration requirement") was between 7 and 32 mU/ml. Pentagastrin produced vasodilation only in the duodenum and jejunum and the concentration requirement was between 25 and 50 ng/ml. Cholecystokinin did not affect vascular resistance of the forelimb, skin, or muscle. In the heart, kidney, and spleen, cholecystokinin produced vasodilation but the concentration requirement was above 21-33 mU/ml. In contrast, vasodilation in the duodenum and jejunum appeared when cholecystokinin concentration was increased by only 2.5 mU/ml. Furthermore, almost all its vasodilating effect occurred below an increment of 10 mU/ml. Comparison of our data with the reported cardiovascular adjustments and blood concentration of gastrointestinal hormones following a meal suggests that cholecystokinin may contribute to postprandial intestinal hyperemia.

Animals↗

Radioactivity in urine and feces of mink (Mustela vison) treated with [14C] aflatoxin B1.

Excretion of radioactivity by mink (Mustela vison) during 7 days after intraperitoneal injection of two different amounts of aflatoxin B1 was studied. Male mink that received a single dose of 25 mug aflatoxin B1/kg body weight excreted an average of 89.5% of administered radioactivity (56.8% via feces, 32.7% via urine); whereas female mink excreted an average of 85% (63.6% via feces, 21.4% via urine) of administered radioactivity during the 7-day period. Male and female mink given 150 mug aflatoxin B1/kg body weight excreted an average of 76.9-80.1% of administered radioactivity during the 7 days that followed treatment with toxin. These mink excreted somewhat more of the administered radioactivity in their urine than did the mink that received the lower dose of aflatoxin (37.2 vs. 32.7% for males and 32.7 vs. 21.4% for females). Regardless of sex and dosage of toxin, most of the radioactivity ultimately excreted either through feces or urine appeared in the first 24 h after toxin was administered to mink.

Aflatoxins↗

Distribution of aflatoxin B1 in tissues of mink (Mustela vison).

Seven female mink (Mustela vison) were injected intraperitoneally with a single dose of 100 mug aflatoxin B1 (14 C-label and unabeled). They were sacrificed 1, 2, 4, and 24 h after dosing. Liver, instestines, stomach, lung, kidney, brain, pancrease, spleen, urinary bladder, uterus, and bile were removed and examined for the retained radioactivity. 1 h after dosing, intestines and their contents retained the largest amount of 14C-radioacivity (18.9% of the amount that was administered) which was followed by liver (13.2%) and the bile (10.8%). At this time all other tissues retained less than 1% of the administered radioactivity. Generally, the amount of radioactivity retained in all tissues declined with time. Only 1.2 and 0.6% of the administered radioactivity was found in testines and bile, respectively, 24 h after dosing; however, the liver still contained 6.6% of the initial radioactivity. Examination of subcellular fractions of liver revealed that at all time intervals most of the radioactivity was associated with the micrososmal supernatant fluid.

Aflatoxins↗

Studies on glucose isomerase from a Streptomyces species.

Production and properties of glucose isomerase from a Co2+-sensitive Streptomyces species were studied. After 4 days of shaking cultivation at 30 degrees C and 200 rpm, a maximum of 1.1 enzyme units per ml of broth was obtained. Cell-free glucose isomerase, obtained from mycelia heat-treated in the presence of 0.5 mM Co2+, showed a 3.5-fold increase in specific activity over enzyme obtained from untreated mycelia. The optimum pH and temperature for the glucose isomerase were 7 to 8 and 80 degrees C, respectively. The Michaelis constant for fructose was 0.40 M. Mg2+ was found to enhance the glucose isomerase activity, whereas the effect of Co2+ on enzyme activity depended on the manner in which the enzyme was prepared. This glucose isomerase was quite heat stable, with a half-life of 120 h at 70 degrees C.

Carbohydrate Epimerases↗

Localization of mesenteric hyperemia during digestion in dogs.

For localization of the site of post-prandial mesenteric hyperemia, low-fat, low-protein food was placed in either the stomach, duodenum, or jejunum while blood flow was measured in the celiac artery, superior mesenteric artery (SMA), or jejunal vein of anesthetized dogs. Distribution of flow in the jejunal wall was also measured. After intragastric placement of food, celiac arterial flow increased within 5 min and remained elevated for 30-60 min; SMA flow increased within 30 min and stayed up for at least 3 h. Intra-duodenal infusion of digested food increased SMA flow but did not alter celiac flow or flow to an isolated jejunal segment. Placement of digested food into one jejunal segment increased flow to that segment did not affect flow was localized to the mucosal layer. These studies indicate that during digestion, blood flow increases in the mucosa of the intestine when exposed to chyme and is not changed in other areas of the gastrointestinal tract. Postprandial mesenteric hyperemia induced by low-fat, low-protein food is a local phenomenon.

Animals↗

Contribution of luminal concentration of nutrients and osmolality to postprandial intestinal hyperemia in dogs.

Intestinal blood flow is increased during digestion. This study assesses if the concentration of nutrients and/or osmolality of chyme in the intestinal lumen are factors determining the hyperemia. Six digested food mixtures containing different concentrations of nutrients and/or having different osmolalities were placed into the jejunal lumen, and their effects on local venous outflow compared. The 100% (999 mOsm/kg), 33% (291 mOsm/kg), and 20% (183 mOsm/kg) food mixtures all increased flow, but the 10% food mixture (94 mOsm/kg) did not. The hyperemic effect of 33 and 20% food was similar, but 100% food produced a greater increase in flow than did 33 or 20% food. Luminal placement of a 30% solution of a nonabsorbable substance polyethylene glycol (1000 mOsm/kg) did not alter flow. Also, the vascular effects of 20 or 10% food mixtures were not altered when these mixtures were made isotonic by the addition of NaCl. These studies indicate that lumen osmolality, within a range of 180 to 1000 mOsm/kg, is not a significant factor contributing to the local hyperemia occurring when nutrients are in the gut lumen. However, the concentration of nutrients in the lumen is a factor determining the local hyperemia.

Animals↗