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Biomedical subjects

H Westergaard

Publications and source records attributed to H Westergaard.

At least 19 recordsLinked to original sources
PubMed1992

[In-hospital day for patients connected with the District Psychiatric Center in Svendborg. A controlled study].

As of 31.12.1990, the employment of bed-days and admissions was calculated for patients who had been connected with a district psychiatric centre for more than three years. A before-and-after comparison revealed a percentage reduction in the employment of bed-days as compared with a control group. This corresponds to the findings in other investigations. In the before-and-after analysis, various reductions are described according to the diagnostic groups. The reduction in bed-day employment consisted mainly of fewer readmissions and reduction in the group of long-term hospitalisations. A reduction also occurred in the group of patients who could characterized as least ill. In this group, a marked percentage reduction in bed-days was observed as compared with the control group and this was probably due to the good and continuous treatment after discharge offered by the district psychiatric centre. This investigation revealed that the employment of bed-days for a patient population receiving district psychiatric treatment after discharge can be reduced. Nevertheless, the most severely ill patients will still require periodic admission to hospital. The value of treatment after discharge of the "Svendborg Model" type does not provide scientifically valid arguments that hospital admission can be avoided where the most severely ill patients are concerned.

Adult↗
PubMed1989

Intestinal glucose transport using perfused rat jejunum in vivo: model analysis and derivation of corrected kinetic constants.

1. The transport model that best describes intestinal glucose transport in vivo remains unsettled. Three models have been proposed: (1) a single carrier, (2) a single carrier plus passive diffusion, and (3) a two-carrier system. The objectives of the current studies were to define the transport model that best fits experimental data and to devise methods to obtain the kinetic constants, corrected for diffusion barrier resistance, with this model. 2. Intestinal glucose uptake was measured during perfusion of rat jejunum in vivo over a wide range of perfusate concentrations and diffusion barrier resistance was determined under identical experimental conditions. The data were fitted to the transport equations that describe the three models with appropriate diffusion barrier corrections, and the kinetic constants were derived by non-linear regression techniques. The fit of each model to the data was assessed using six statistical tests, five of which favoured a model described by a single carrier and passive diffusion. 3. The main conclusions of these studies are: (1) kinetic constants uncorrected for diffusion barrier resistance are seriously in error; (2) values for the derived kinetic constants are strongly dependent on the transport model selected for the data analysis which underscores the need for rigorous model analysis; (3) corrected kinetic constants may be obtained by either non-linear regression or by a simpler graphical analysis once the correct transport model has been selected and diffusion barrier resistance determined; (4) only corrected kinetic constants should be used for inter-species comparisons or to study the effect of specific interventions on intestinal glucose transport.

Animals↗
PubMed1989

Insulin modulates rat intestinal glucose transport: effect of hypoinsulinemia and hyperinsulinemia.

The current studies were designed to evaluate the role of plasma insulin and glucose as regulators of intestinal glucose transport in vivo. Initially, rats received either intravenous glucose infusion or intraperitoneal streptozotocin to induce sustained hyperglycemic hyperinsulinemia or hyperglycemic hypoinsulinemia. Net jejunal uptake rates of glucose were measured in vivo at several perfusate concentrations, and the kinetic constants, corrected for diffusion barrier resistance, were derived. Maximal velocity (Jmax) was increased 1.8-fold by hyperglycemic hyperinsulinemia and 2.6-fold by hyperglycemic hypoinsulinemia compared with controls, whereas Km and passive permeability of glucose were unchanged. The rate of L-proline uptake at saturation conditions was not increased by these experimental interventions. The corrected kinetic constants for jejunal glucose transport in streptozotocin diabetic rats kept normoglycemic and normoinsulinemic with insulin were similar to controls. Finally, induction of normoglycemic hyperinsulinemia by intravenous glucose-insulin infusion increased Jmax 1.8-fold, similar to hyperglycemic hyperinsulinemia, but induction of hyperglycemic normoinsulinemia by intravenous glucose-somatostatin infusion did not change Jmax. In conclusion, changes in plasma insulin but not glucose concentration cause a specific and reversible increase in Jmax of intestinal glucose transport. Hypoinsulinemia is a more potent signal than hyperinsulinemia. The membrane level, microvillus or basolateral, at which insulin induces an increased number of glucose transporters in intestinal epithelial cells remains to be defined.

Animals↗
PubMed1987

Laser photocoagulation for the treatment of acute peptic-ulcer bleeding. A randomized controlled clinical trial.

We tested the hypothesis that therapeutic endoscopy using the Nd:YAG (neodymium:yttrium-aluminum-garnet) laser would benefit patients with acute peptic-ulcer bleeding. Over 43 months, 174 patients with active bleeding (n = 32) or stigmata of recent bleeding (n = 142) due to peptic ulcers were randomly assigned during endoscopy to either standard treatment with laser photocoagulation or therapy without photocoagulation. There were no significant differences in a number of outcomes between the group treated with laser photocoagulation and the control group. Continued bleeding or rebleeding was observed in 22 percent of the laser-treated group and in 20 percent of the control group. Urgent surgery was necessary in 16 percent of the laser-treated patients and in 17 percent of the controls. Laser-treated patients spent a mean of 41 hours in the intensive care unit, and controls spent a mean of 32 hours. The mean hospital stay was 12 days in the laser-treated group and 11 days in the control group. One death occurred in each group. When patients with active bleeding were analyzed separately, there was no significant difference in outcome, even though laser photocoagulation stopped active bleeding in 88 percent of cases. Among patients with visible vessels, rebleeding occurred in 5 of 14 (36 percent) who received laser treatment and 2 of 15 (13 percent) who did not. Laser treatment precipitated bleeding in four patients and duodenal perforation in one. We conclude that Nd:YAG-laser photocoagulation does not benefit patients with acute upper gastrointestinal bleeding from peptic ulcers.

Acute Disease↗
PubMed1987

The passive permeability properties of in vivo perfused rat jejunum.

The polarity of the microvillus membrane of rat and rabbit jejunum, determined in vitro by the incremental free energy changes associated with the addition of -CH2 groups to fatty acids or -OH groups to bile acids, has been found to be more polar than other biological membranes. The reason for the difference in polarity is unexplained but could be due to artifacts caused by the in vitro conditions. In the current studies the apparent permeability coefficients were determined for a homologous series of fatty acids and bile acids in in vivo perfused rat jejunum. The true permeability coefficients were derived by correction for diffusion barrier resistance. The incremental free energy changes associated with the addition of a -CH2 group to a fatty acid and a -OH group to a bile acid were -619 and +2069 cal/mol, respectively. These values correspond to values determined in other biological membranes such as erythrocytes and adipocytes. Thus, the rat microvillus membrane is more nonpolar than previously observed in vitro. The reason for the discrepancy between the in vivo and in vitro results is most likely due to an underestimation of the permeability coefficients in the in vitro studies.

Animals↗
PubMed1986

Measurement of resistance of barriers to solute transport in vivo in rat jejunum.

Assessment of intestinal absorptive function requires techniques for correcting transport constants for diffusion barrier resistance. These studies were done to develop such techniques for use in vivo. In one method the functional thickness of the unstirred water layer (d) in rat jejunum was quantitated electrically, and its minimal surface area (Sw) was measured directly. From these values the diffusion barrier resistance (d/Sw) decreased from 0.041 to 0.022 as the perfusion rate of the intestine was increased from 1.5 to 15 ml/min. In the second method apparent passive permeability coefficients (*P) were measured for a series of saturated fatty acids, and these increased with chain length. However, at the longest chain lengths tested, *P became proportional to their free diffusion coefficients, indicating that uptake was limited by the rate of diffusion up to the microvillus surface. From the rates of uptake of such diffusion-limited probes, the diffusion barrier resistance was again calculated and found to decrease from 0.041 to 0.022 as the rate of perfusion was increased from 1.5 to 15 ml/min. Over this same range of perfusion rates, the apparent Michaelis constant (*Km) for D-glucose transport decreased from 18.2 to 10.0 mM. Using either set of resistance terms and these apparent Km values, the true Km value for glucose transport in vivo was found to equal 0.8 mM when the barrier resistance was extrapolated to zero. Thus these data indicate that diffusion-limited probes can be utilized to measure unstirred layer resistance in the intestine of a live animal so that absolute transport parameters can be determined in vivo in experimental animals and, presumably, in humans.

Animals↗
PubMed1985

The sprue syndromes.

The sprue syndromes, tropical and nontropical sprue, were both described as disease entities in the 1880s and share similar morphological features with varying degrees of villus atrophy of the small intestinal mucosa, and both present clinically with malabsorption. Recent cell kinetic studies of the turnover of the intestinal epithelium in sprue have convincingly demonstrated that the flat mucosa is caused by increased efflux (cell death) with compensatory crypt hyperplasia. The pathogenetic insult in tropical sprue appears to be a persistent overgrowth of the small intestine by enteric pathogens after a bout of turista. The pathogenesis of nontropical sprue is determined by both genetic factors, demonstrated with a strong association with certain HLA haplotypes (B8, DR3, DR7 and DC3) and presumably also environmental events (virus infection?), which render the mucosa susceptible to gluten. The cause of the malabsorption syndrome is multifactorial and results from both intraluminal and cellular events. The digestion of proteins, carbohydrates, and lipids is compromised due to decreased pancreatic and biliary secretion. The absorption of the digestive products is also severely affected due to decreased activity of microvillus enzymes (dipeptidases and disaccharidases) and a presumed reduction in the number of transport carriers. The clinical presentation is identical and the distinction between tropical and nontropical sprue is based on the history (ie, exposure to a tropical environment) and the response to treatment. Tropical sprue is cured by treatment with tetracycline and folic acid, whereas nontropical sprue responds to a gluten-free diet. Nontropical sprue is associated with dermatitis herpetiformis by common genetic and morphological features, and the skin lesions in dermatitis herpetiformis are also responsive to a gluten-free diet. Finally, there appears to be an increased incidence of intestinal malignancies (lymphoma, adenocarcinoma) in nontropical sprue.

Celiac Disease↗
PubMed1977

Duodenal bile acid concentrations in fat malabsorption syndromes.

Meal-stimulated duodenal bile acid concentrations were measured in 38 control subjects and in 138 patients with various gastrointestinal diseases with or without fat malabsorption. In controls, the duodenal bile acid concentrations were normally distributed after Iogarithmic transformation, with a mean of 10.8 mM/1 (range: 5.4-21.5 mM/1). In general, the lower normal limit, 5.4 mM/1, discriminated well between patients with or without steatorrhea in whom other causes of fat malabsorption had been ruled out. The combination of intraluminal bile acid deficiency and steatorrhea was most often encountered in patientswit h hepatic disease, ileal disorders, and in the stagnant loop syndrome. Measurements of duodenal bile acid concentrations may serve to detect disorders of bile acid metabolism and thereby elucidate the pathogenesis of fat malabsorption syndromes.

Adult↗
PubMed1976

The mechanism whereby bile acid micelles increase the rate of fatty acid and cholesterol uptake into the intestinal mucosal cell.

Studies were undertaken to define the mechanism whereby bile acid facilitates fatty acid and cholesterol uptake into the intestinal mucosal cell. Initial studies showed that the rate of uptake (Jd) of several fatty acids and cholesterol was a linear function of the concentration of these molecules in the bulk phase if the concentration of bile acid was kept constant. In contrast, Jd decreased markedly when the concentration of bile acid was increased relative to that of the probe molecule but remained essentially constant when the concentration of both the bile acid and probe molecule was increased in parallel. In other studies Jd for lauric acid measured from solutions containing either 0 or 20 mM taurodeoxycholate and saturated with the fatty acid equaled 79.8+/-5.2 and 120.8+/-9.4 nmol.min(-1).100 mg(-1), respectively: after correction for unstirred layer resistance, however, the former value equaled 113.5+/-7.1 nmol.min(-1).100 mg(-1). Maximum values of Jd for the saturated fatty acids with 12, 16, and 18 carbons equaled 120.8+/-9.4, 24.1+/-3.2, and 13.6+/-1.1 nmol.min(-1).100 mg(-1), respectively. These values essentially equaled those derived by multiplying the maximum solubility times the passive permeability coefficients appropriate for each of these compounds. The theoretical equations were then derived that define the expected behavior of Jd for the various lipids under these different experimental circumstances where the mechanism of absorption was assumed to occur either by uptake of the whole micelle, during interaction of the micelle with an infinite number of sites on the microvillus membrane or through a monomer phase of lipid molecules in equilibrium with the micelle. The experimental results were consistent both qualitatively and quantitatively with the third model indicating that the principle role of the micelle in facilitating lipid absorption is to overcome unstirred layer resistance while the actual process of fatty acid and cholesterol absorption occurs through a monomer phase in equilibrium with the micelle.

Animals↗
PubMed1974

Delineation of the dimensions and permeability characteristics of the two major diffusion barriers to passive mucosal uptake in the rabbit intestine.

THE RATE OF PASSIVE ABSORPTION INTO THE INTESTINAL MUCOSAL CELL IS DETERMINED BY AT LEAST TWO MAJOR DIFFUSION BARRIERS: an unstirred water layer and the cell membrane. This study defines the morphology and permeability characteristics of these two limiting structures. The unstirred water layer was resolved into two compartments: one behaves like a layer of water overlying the upper villi while the other probably consists of solution between villi. The superficial layer is physiologically most important during uptake of highly permeant compounds and varies in thickness from 115 to 334 mum as the rate of mixing of the bulk mucosal solution is varied. From data derived from a probe molecule whose uptake was limited by the unstirred layer, the effective surface area of this diffusion barrier also was determined to vary with stirring rate and equaled only 2.4 cm(2).100 mg(-1) in the unstirred condition but increased to 11.3 cm(2).100 mg(-1) with vigorous mixing. This latter value, however, was still only 1/170 of the anatomical area of the microvillus membrane. With these values, uptake rates for a number of passively absorbed probe molecules were corrected for unstirred layer resistance, and these data were used to calculate the incremental free energy changes associated with uptake of the -CH(2)- (-258 cal.mol(-1)), -OH (+564), and taurine (+1,463) groups. These studies, then, have defined the thickness and area of the unstirred layer in the intestine and have shown that this barrier is rate-limiting for the mucosal uptake of compounds such as fatty acids and cholesterol; in addition, the lipid membrane of the microvillus surface has been shown to be a relatively polar structure.

Action Potentials↗