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Biomedical subjects

K Phaosawasdi

Publications and source records attributed to K Phaosawasdi.

7 recordsLinked to original sources
PubMed1989

Understanding idiopathic chronic constipation: an understated problem.

Constipation is a common problem and is frequently taken for granted by both the lay and medical populations. Although sometimes easily resolved it can prove to be a lifelong, debilitating problem, both medically and sociologically. Most frustrating is the category of idiopathic chronic constipation, a problem without identifiable etiology and diagnosed by exclusion. This paper takes an in-depth view of chronic and more specifically, idiopathic chronic constipation, discussing etiology, diagnosis and treatment. Two case histories are presented illustrating opposite ends of the spectrum in terms of severity. The objective of this paper is to enhance the reader's knowledge about a "common" problem and to increase the future appreciation for patients experiencing this alteration in bowel functioning.

Adult↗
PubMed1986

Carbon dioxide-insufflated colonoscopy: an ignored superior technique.

Colonoscopy and barium enema are complementary studies in the diagnosis of the cause of lower intestinal bleeding. The air usually insufflated during colonoscopy often makes it impossible to perform a good barium enema on the same day. As a possible solution to this problem, we studied the quality of barium enemas performed immediately following carbon dioxide-insufflated colonoscopy. All 15 patients who underwent unsuccessful total colonoscopies using carbon dioxide insufflation were able to have barium enemas performed the same day in contrast to only one out of 15 patients who had air-insufflated colonoscopy. In a survey of all hospitals in Illinois with 150 beds or more, we found only 15 of 146 hospitals used carbon dioxide for colonoscopy insufflation. We recommend the routine use of carbon dioxide for colonoscopic insufflation not only for greater safety and comfort for the patient, but also for the convenience and cost savings.

Adult↗
PubMed1982

Hormonal effects on the pylorus.

The control mechanisms of pyloric pressure responses have not been elucidated clearly. The purposes of this study were twofold: 1) to determine the dose-related pressure responses of the pylorus to exogenous glucagon, secretin, and cholecystokinin, and 2) to correlate changes in pyloric pressure with serum concentrations of these hormones. Pyloric pressures were measured by infusion manometry, and the serum concentrations of glucagon and secretin were quantitated using radioimmunoassays. Each of the hormones tested, glucagon, secretin, and cholecystokinin, increased the pyloric pressure significantly. The lowest active dosages tested for each of these peptide hormones were 2 micrograms.kg-1.h-1, 2 U.kg-1.h-1, and 1 U.kg-1.h-1, respectively. The maximal pyloric pressure responses recorded were 8.7 +/- 1.1 (P less than 0.05), 12.6 +/- 2.1 (P less than 0.02), and 14.8 +/- 1.7 (P less than 0.02) mmHg, respectively. The pyloric pressure responses to insulin hypoglycemia, duodenal acidification, and intraduodenal olive oil were 11.3 +/- 1.5, 13.4 +/- 1.4, and 11.3 +/- 1.4 mmHg, respectively. The serum concentrations of immunoreactive glucagon during infusion of the lowest active dosage of glucagon and insulin hypoglycemia were 801 +/- 55 and 322 +/- 12 pg/ml, respectively. The serum concentrations of immunoreactive secretin during infusion of the lowest active dosage of secretin and during duodenal acidification were 980 +/- 60 and 110 +/- 7.0 pg/ml, respectively. Although pyloric contraction can be induced by administration of exogenous glucagon, secretin, and cholecystokinin, these studies suggest that these effects may have no physiological relevance.

Cholecystokinin↗
PubMed1981

Pyloric pressure response to insulin-induced hypoglycemia in humans.

The pyloric pressure response to insulin-induced hypoglycemia was studied. Studies were performed in 102 experiments on 38 normal subjects. During insulin-induced hypoglycemia, pyloric pressure increased from 5.5 +/- 1.2 to 10.8 +/- 1.1 mmHg (P less than 0.02). This increase in pyloric pressure ws not due to a direct effect of insulin, duodenal acidification, or the release of corticosteroids or growth hormone. Glucagon doses of 2 and 5 micrograms . kg-1 . h-1 increased pyloric pressure from 4.7 +/- 1.1 to 6.7 +/- 0.5 mmHg (P less than 0.05) and from 4.7 +/- 1.1 to 8.5 +/- 1.1 mmHg (P less than 0.02), respectively. Pyloric pressures were increased to 10.8 +/- 0.9 (P less than 0.01) and 13.0 +/- 1.4 mmHg (P less than 0.01) at 0.1 and 0.2 micrograms . kg-1 . min-1 of epinephrine, respectively. Neither cholinergic blockade nor alpha-adrenergic blockade significantly affected the pyloric pressure response to insulin hypoglycemia. beta-Adrenergic blockade abolished the pyloric pressure responses to both insulin hypoglycemia and epinephrine. Neither beta- nor alpha-adrenergic stimulation altered the basal pyloric pressure. In contrast, the combination of isoproterenol and phenylephrine increased the pyloric pressure significantly from 4.2 +/- 0.8 to 12.0 +/- 1.7 mmHg ( P less than 0.01). These observations suggest that insulin hypoglycemia increases pyloric pressure by an adrenergic mechanism that requires stimulation of both alpha- and beta-receptors.

Atropine↗
PubMed1981

Cholinergic effects on esophageal transit and clearance.

Modern manometric and scintigraphic techniques were employed in an effort to determine the relationships between esophageal contractions and esophageal transit and clearance. The effects of direct cholinergic stimulation with bethanechol and blockade with atropine were evaluated in a total of 20 normal subjects and 13 patients with symptomatic gastroesophageal reflux. Bethanechol increased the amplitudes of deglutition-induced and distention-induced esophageal contractions, but diminished their propagation velocities. Both esophageal transit and clearance were decreased in patients with reflux, but both were improved after bethanechol. Atropine sulfate decreased the amplitudes of contractions, accelerated their propagation velocities, and delayed esophageal transit and clearance. Both transit and clearance were diminished significantly when reflux patients were compared with normal subjects. The amplitudes of esophageal contraction were significantly lower in patients with reflux than in normal subjects. Neither bethanechol nor atropine affected the incidence of deglutition-induced esophageal contractions. These studies suggest that the efficiency of esophageal emptying may be determined by the amplitudes of esophageal contractions.

Adult↗
PubMed1979

Effects of alcohol on the pyloric sphincter.

The effects of an intoxicating dose of alcohol (79 g of 100 proof alcohol) on pyloric sphincter function were studied in 12 normal subjects using an infused manometric system. Alcohol had no effect on resting pyloric sphincter pressure. Intraduodenal administration of olive oil and hypertonic amino acids increased pyloric sphincter pressure significantly to 10.8 +/- 1.4 and 10.2 +/- 2.0 mm Hg, respectively. These responses were not affected by the administration of alcohol. In contrast, alcohol decreased the pyloric pressure response to duodenal acidification from 12.0 +/- 2.1 to 8.0 +/- 1.3 mm Hg (P less than 0.05). These results suggest that an intoxicating dose of alcohol may interfere with the normal function of the pyloric sphincter.

Adult↗