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Biomedical subjects

J B Watkins

Publications and source records attributed to J B Watkins.

At least 91 records · Page 5Linked to original sources
PubMed1983

Nonnutritive sucking during gavage feeding enhances growth and maturation in premature infants.

The effects of nonnutritive sucking (NNS) by means of a pacifier during gavage feeding were studied in 30 premature infants whose birth weight was less than 1,500 g. The addition of NNS accelerated the maturation of the sucking reflex, facilitating a more rapid transition from gavage to oral feedings. Additionally, NNS decreased intestinal transit time and caused a more rapid weight gain despite comparable caloric intake resulting in a shortened hospital stay. Although the physiologic mechanisms resulting from this form of oral stimulation remain to be investigated, our data suggest that NNS may be an important factor to consider in the feeding of premature infants.

Body Weight↗
PubMed1983

Depletion of hepatic uridine diphosphoglucuronic acid decreases the biliary excretion of drugs.

Hepatic levels of uridine diphosphoglucuronic acid (UDPGA) in rats decreased substantially (greater than 80%) 40 min after galactosamine (GAL) (600 mg/kg i.p.) or after 1 hr of diethyl ether (DE) narcosis. Biliary excretion of several cholephils requiring glucuronidation before excretion was reduced by GAL 76, 62, 92, 90 and 97% for bilirubin, diethylstilbestrol, iopanoic acid, phenolphthalein and valproic acid, respectively. GAL treatment caused delayed plasma clearances of the parent compounds and reductions in plasma concentrations and biliary excretions of glucuronide conjugates. The degree of this reduction was related to the maximal excretion rate of the individual compounds. For phenolphthalein glucuronide and phenol-3,6-dibromphthalein disulfonate, which do not undergo conjugation, GAL had no effect on their biliary excretion. DE-induced UDPGA depletion had no effect on phenolphthalein glucuronide excretion but reduced that of phenol-3,6-dibromphthalein disulfonate 25%. DE did not affect the plasma elimination or biliary secretion of phenolphthalein. Of the other cholephils requiring conjugation, DE reduced the excretion of bilirubin, diethylstilbestrol, iopanoic acid and valproic acid by 41, 29, 76 and 28%, respectively. DE decreased the plasma elimination of the parent compounds and the appearance of the conjugates in both plasma and bile. Reduction of glucuronide excretion into bile was less pronounced at higher doses of the cholephilic anions. Neither treatment reduced in vitro hepatic UDP-glucuronosyltransferase activity toward these substrates or substantially altered extrahepatic UDPGA concentrations. Thus, both GAL and DE decreased UDPGA to similar concentrations, but the biliary excretion of compounds requiring glucuronidation before secretion was depressed to a greater extent by GAL.

Animals↗
PubMed1983

Choleretic effect of structural analogs of valproic acid in the rat.

A comparison of structure-choleretic activity relationship has been made for several branched- and straight-chain carboxylic acids including valproic acid. Cumulative bile flow was 13.8, 23.8, 29.4 and 14.9 ml/4hr/kg body weight for dimethyl-, diethyl-, dipropyl- (valproic acid), and dibutyl-acetic acid, respectively, after iv administration of approximately equimolar doses (1100 mumoles/kg). Except for dibutylacetic acid, maximal bile flow increased from control rates of 50-60 to 120-140 microliters/min/kg. Administration of higher doses of 2,2-dimethylbutanoic acid and 2-ethylbutanoic acid did not increase maximal bile flow above 125-140 microliters/min/kg but did prolong the duration of choleresis. Maximal and cumulative bile flows increased with length of carboxylic acid chain for 2,2-dimethyl substituted acids (2,2-dimethylacetic acid to 2,2-dimethylbutanoic acid). If the two methyl groups were on C-3 (3-methylbutanoic acid), no change in bile flow was observed. Straight-chain acids from C-5 to C-11 and pent-4-enoic acid did not alter bile flow. Thus, the effectiveness of several branched-chain carboxylic acids as choleretics parallel their ability as anticonvulsants. In contrast, the straight-chain acids which cause central nervous system depression have no choleretic activity.

Animals↗
PubMed1983

Feeding the low-birth weight infant: V. Effects of taurine, cholesterol, and human milk on bile acid kinetics.

This study was conducted to compare the influence of diet on the physiologic changes in bile acid kinetics, intraluminal bile acid concentrations, conjugation patterns, and nutrient lipid absorption, which occur postnatally. Preterm infants, 31-35 wk gestation, were fed one of four diets: (a) human milk pasteurized at 62 degrees C for 30 min, 55% from a pooled source, 35% from the infant's own mother, with the remainder (approximately 10%) being fresh human milk; (b) an adapted infant formula (F1); (c) F1 supplemented with taurine, 30 mumol/dl, (F2); and (d) F1 with both taurine, 30 mumol/dl, and cholesterol, 9.6 mg/dl, to a total of 12.7 mg/dl, the levels found in human milk (F3). In all infants, the bile acid pool size increased nearly twofold between 11 and 35 days, irrespective of dietary regimens. Taurine conjugation of bile acids predominated in all infants at 11 days of age and at 35 days in those infants fed human milk or the taurine-supplemented formulas. In taurine-supplemented formulas, the conjugation pattern did not influence bile acid kinetics. However, the bile acid pool and intraluminal bile acid concentrations were significantly greater in infants fed human milk at all ages, suggesting that human milk feeding, per se, uniquely influences intestinal and possibly hepatic function independent of developmental factors.

Bile Acids and Salts↗
PubMed1982

Congenital esophageal atresia: lipase activity is present in the esophageal pouch and stomach.

Lipolytic activity was studied in aspirates from the esophageal pouch and from the stomach of eight infants with congenital esophageal atresia. Lipolytic activity, tested with doubly labeled ([3H]glyceryl, [14C]fatty acid) long-chain triglyceride was present in esophageal and gastric aspirates. The activity in esophageal aspirates was in the range of 2.7-130 nmol/min/ml aspirate and that in gastric aspirates was in the range of 2.9-40.4 nmol/min/ml aspirate. The reaction products of lipolytic activity in esophageal and gastric aspirates were a mixture of mono- and diglycerides, glycerol, and free fatty acids. The lipolytic activity at the two sites--esophagus and stomach--varied with respect to pH optimum (5.0-7.6 and 6.0-6.5, respectively) and reaction products (glycerol 41.6 +/- 20% and 7.3 +/- 4.6%, respectively). These findings confirm the earlier observations that digestion of dietary fat is initiated in the stomach and suggest that the lipolytic activity present in gastric contents originates concomitantly from the oral-esophageal area as well as from the stomach. These studies do not exclude the possibility that the lipolytic activity in the stomach of infants with esophageal atresia could originate in regurgitated intestinal contents.

Esophageal Atresia↗
PubMed1982

Determination of hepatic uridine 5'-diphosphoglucuronic acid concentration by conjugation with diethylstilbestrol.

A sensitive and reliable assay for uridine 5'-diphosphoglucuronic acid (UDPGA) was developed that involved conjugation of diethylstilbestrol (DES) in vitro. This conjugation reaction is solely dependent upon UDPGA concentration. The assay uses 0.13 M Tris-HCl, pH 7.4, 6.7 mM MgCl2, 0.05% Brig 58, 0.25 mg guinea pig liver microsomal protein, 0.13 mM 3H-DES (0.2 microCi/ml), and 200 microliters of boiled 10% liver homogenate in a total volume of 0.5 ml. After a 60-min incubation at 37 degrees C, unconjugated DES is extracted into 5 ml of chloroform and the residual metabolized 3H-DES in the aqueous phase is determined by liquid scintillation spectrometry. After addition of beta-glucuronidase to the aqueous phase, about 90% of the radioactivity could be extracted into chloroform, demonstrating the DES-glucuronic acid is the primary metabolite. Thus, this method easily permits quantitation of UDPGA in rat liver in the 1-10 nmol range.

Animals↗
PubMed1982

Attenuated pressure natriuresis in hypertensive rats.

We studied the isolated blood-free perfused nonclipped kidneys from the 2-kidney Goldblatt hypertensive rat model (GHR) to evaluate intrinsic excretory responses to changes in perfusion pressure. We examined kidneys from 10 control rats (in vivo systolic BP 110 +/- 3.6 mm Hg), from 9 rats with nonmalignant hypertension (HBP) (in vivo systolic BP 158 +/- 6.5 mm Hg), and from 5 rats with malignant HBP (in vivo systolic BP 183 +/- 6.4 mm Hg). We found that at all levels of perfusion pressure, the renal vascular resistances were significantly higher and glomerular filtration rate (GFR) lower in kidneys from hypertensive rats than in kidneys from control rats. Kidneys from hypertensive rats had lower urinary excretion of sodium (UNaV) and urine flow than kidneys from control rats at all levels of pressure above 100 mm Hg. The most striking differences in all functional parameters were noted in kidneys from rats with malignant HBP. Kidneys from both hypertensive and control rats failed to show changes in vascular resistance in response to Saralasin. We conclude that the nonclipped kidney in GHR exhibits a blunted natriuresis in response to elevated perfusion pressure which occurs in the absence of angiotensin II (AII) and renin substrate. This diminished pressure natriuresis may be caused partly by the lower GFR and by reduced pressure transmission due to greater renal vascular resistance and thus may be partially responsible for the maintenance of the hypertensive state.

Animals↗
PubMed1982

Pleural effusion and ascites: unusual presenting features in a pediatric patient with vitamin A intoxication.

The usual presenting features of vitamin A intoxication are pseuotumor cerebri, skeletal pain, desquamative dermatitis, and hepatic inflammation. Our patient was a nine-year-old female who had increasing cough, dyspnea, and abdominal distention for a short time prior to admission. She was said to have been treated with 10,000 units of vitamin A per day for skin rashes. Radiographic studies revealed a very large right sided pleural effusion, ascites, demineralized bones, and retarded skeletal maturation. The diagnosis of hypervitaminosis A was made. More detailed medical history confirmed that the child had, in actuality, received up to 300,000 units/day of vitamin A plus desiccated liver pills and carrot juice for the previous year. Clinical symptoms completely abated following acute medical treatment for ascites and cessation of vitamin A intake. Several months later, a sample of liver, obtained and preserved at the time of exploratory laparotomy, was homogenized and extracted with ethanol/hexane. The retinyl palmitate level was significantly elevated and consistent with vitamin A poisoning.

Age Determination by Skeleton↗
PubMed1982

Effect of inducers and inhibitors of glucuronidation on the biliary excretion and choleretic action of valproic acid in the rat.

Valproic acid (VPA) induces an immediate choleresis in the rat which may be attributable to the osmotic properties of VPA-glucuronic acid conjugates in bile. The influence of inducers and inhibitors of glucuronidation of VPA on the biliary excretion and choleretic effect of VPA was studied. Hepatic UDP-glucuronyltransferase activity toward VPA was determined in vitro. Pretreatment with phenobarbital (75 mg/kg/day for 4 days) enhanced VPA glucuronidation; borneol (750 mg/kg) decreased VPA conjugation; 3-methylcholanthrene (20 mg/kg/day for 4 days) and galactosamine (600 mg/kg) had no effect on glucuronidation of VPA in vitro. Hepatic UDP-glucuronic acid content was decreased by borneol and galactosamine administration and was enhanced by phenobarbital and 3-methylcholanthrene pretreatment. The enzyme inducers increased the plasma disappearance of VPA in vivo but did not augment its biliary excretion or choleretic effect. Borneol and galactosamine, which inhibited the conjugation and plasma disappearance of VPA, decreased its biliary excretion and inhibited the VPA-induced increase in bile flow. Thus, the bile flow rate after VPA administration is closely related to the excretion of VPA-glucuronic acid. These data support the conclusion that the choleretic effect of VPA is due to the osmotic activity of VPA conjugates in bile.

Animals↗
PubMed1982

Diagnosis and differentiation of fat malabsorption in children using 13C-labeled lipids: trioctanoin, triolein, and palmitic acid breath tests.

Three substrates labeled with nonradioactive 13C have been employed to establish a trilogy of noninvasive breath tests to detect fat malabsorption in children and then to differentiate the etiology of the steatorrhea. Administration of 17 mg/kg of (13C)triolein Lipomul (The Upjohn Co., Kalamazoo, Mich.) resulted in a peak excretion rate of 13CO2 greater than 2.7% dose/h in 10 normal subjects (mean value 4.96 +/- 2.2% dose/h) whereas all 17 subjects with fat malabsorption were below this value (mean value, 0.75% +/- 0.63% dose/h); p less than 0.001). For the detection of fat malabsorption, the discriminative value of (13C)triolein was superior, 100% sensitive, and 89% specific, while the use of (13C)palmitic acid (17 mg/kg) or (13C)trioctanoin (7.5 mg/kg) alone yielded both false-positive and false-negative results. In 6 out of 6 cases, pancreatic insufficiency could be differentiated from mucosal disease (7 patients) or bile salt deficiency (4 patients) by the presence of abnormal triolein or trioctanoin breath tests, or both but normal palmitic acid breath tests. However, further differentiation of mucosal disorders from bile salt disorders could not be achieved using either a single- or a multiple-substrate breath test. The use of the single triolein breath test in children offers an attractive, sensitive alternative to conventional fecal fat measurements to establish the presence of steatorrhea, and when using 12C-lipid with multiple substrates, the tests are capable of providing additional insight into the mechanism of fat malabsorption.

Adolescent↗
PubMed1981

Successful treatment of achalasia in childhood by pneumatic dilatation.

Ten consecutive patients (ages 10 to 17) with achalasia of the esophagus diagnosed by radiographic, manometric, and endoscopic criteria were treated by forceful dilatations of the lower esophageal sphincter. A good to excellent response was seen in eight of the ten patients, manifested by disappearance of vomiting, improvement in dysphagia, and weight gain. A decrease in resting gastroesophageal sphincter pressure was documented in four patients tested. Short-term complications of fever or chest pain were seen following three of 18 procedures; however, barium swallow was negative for perforation and symptoms resolved spontaneously without treatment. Our findings suggest that pneumatic dilatation may produce similar results as surgical esophagomyotomy (Heller procedure) without the immediate operative morbidity, cost, and potential long-term effects.

Adolescent↗
PubMed1981

Effect of repeated oral administration on taurocholate on hepatic excretory function in the rat.

The effect of repeated administration of taurocholate on bile acid pool size, biliary composition and biliary excretory capacity for bile acids and two xenobiotics was determined. The bile acid pool was increased 50 to 60% by oral administration of sodium taurocholate (300--900 mg/kg, 10 ml/kg) every 12 hr for 2 days to male Sprague-Dawley rats. Bile flow, biliary excretion of bile acids, cholesterol and phospholipid and the concentrations of phospholipid and bile acids in bile were increased in rats treated with 750 mg of taurocholate per kg. No effect was observed on Na+,K+ or Cl- levels. The biliary transport maximum for taurocholate was increased by 30% in rats treated with 750 mg/kg. In contrast, the plasma disappearance and biliary excretion of phenol-3,6-dibromphthalein and ouabain were not affected by taurocholate administration.

Animals↗
PubMed1981

Mucosal function and breath hydrogen excretion: comparative studies in the clinical evaluation of children with nonspecific abdominal complaints.

To evaluate the role of the lactose breath hydrogen test for the detection of lactose malabsorption in children with chronic nonspecific abdominal complaints, breath hydrogen excretion was measured in 131 children with recurrent abdominal pain (n = 75) or chronic nonspecific diarrhea (n = 56) following a lactose load (2 gm/kg; maximum 50 gm). The data were compared to those obtained from lactose tolerance tests (n = 113) and symptom response following a lactose load (n = 109) performed simultaneously with the lactose breath hydrogen test, and with results from small bowel biopsies obtained in 31 children to determine dissacharidase activity and mucosal histology. The results indicate that an increase in breath hydrogen of greater than 10 ppm above base line values (delta ppm) by 120 minutes ("early increase" response) completely discriminates between biopsy-proven isolated lactase-insufficient and lactase-sufficient children. A similar increase after 120 minutes ("late increase" response) is consistent both with normal mucosal function and partial lactase insufficiency due to mucosal injury. Breath hydrogen responses predicted assayed lactase activity in all patients with isolated lactase insufficiency, but were "falsely negative" in four of ten children whose lactase insufficiency was secondary to mucosal injury. In both clinical groups, lactose malabsorbers report significantly more symptoms than absorbers (P less than .001), but neither symptom reports nor tolerance tests are accurate methods for distinguishing lactose malabsorbers from absorbers. Although the lactose breath hydrogen test provides objective documentation of lactose malabsorption, it is equally predictive of assayed lactase activity in all clinical groups.

Abdomen↗