Search PubMed⌕ Search

Biomedical subjects

A Wald

Publications and source records attributed to A Wald.

At least 163 records · Page 9Linked to original sources
PubMed1981

Comparative sensitivity of eight- and 24-hour bile acid breath tests and Schilling test in ileopathies.

The conventional eight-hour bile acid breath test ("acute measurements"), was compared with a modified, extended, 24-hour breath test ("ratio measurements") and the Schilling test to assess relative sensitivity in detecting ileal dysfunction. Sixty-four patients with ileopathies were studied. The presence or absence of bile acid malabsorption was documented by fecal excretion studies of bile acid labels. The sensitivity of the "acute measurements" in the breath test was not significantly different from that of the "ratio measurements" in the ileopathies, regardless of whether or not bile acid malabsorption was present. The "acute measurements" were positive in 49 (77%), the "ratio measurements" in 54 (84%) and the Schilling test in 49 (77%) of the patients. In about 30%, bile acid breath test and Schilling test were not positive in the same patient. A combination of "acute measurements" (breath test) and Schilling test increased the percentage of cases with at least one positive test to 91%. The results of the study show: 1. The sensitivity of the bile acid breath test does not increase if 14CO2 measurements are carried out beyond eight hours. 2. Although the breath test and Schilling test are of similar sensitivity in ileopathies, they are frequently not positive in the same patient. Therefore, it would be clinically useful to combine both tests in order to increase the likelihood of diagnosing ileal dysfunction.

Bile Acids and Salts↗
PubMed1978

Evidence for the movement of fluid, macromolecules and ions from the brain extracellular space to the CSF.

This report examines the effect of decreasing serum osmolality on movement into the ventricular system of fluid and of test material injected into the brain. Trace quantities of 22NaCl and 125I-labeled cat serum albumin (CSA) were injected into cerebral white matter of cats. The rates of cerebrospinal fluid volume flow, and appearance of 22Na and 125I-CSA were measured in the effluent fluid using ventriculocisternal perfusion before and while serum osmolality was acutely decreased by the intravenous infusion of a 60 mOsm sucrose solution. As compared to the control period, at the end of the infusion serum osmolality decreased from 321 +/- 4.2 mOsm to 283 +/- 4.0 mOsm and CSF volume flow increased from 21.8 +/- 2.3 microliter/min to 54.9 +/- 4.1 microliter/min (means +/- S.E.). The slope of the regression line describing 22Na influx went from 1.04 to 1.79, while for 125I the slope went from 0 to 1.38. These results suggest that a common pathway may exist for the movement, through the brain and into the ventricular system, of water, ions and large molecules.

Animals↗
PubMed1978

Kaolin-induced hydrocephalus impairs CSF secretion by the choroid plexus.

CSF volume flow and sodium (Na+)-influx rates in normal and kaolin-induced hydrocephalic cats were measured during ventricular perfusion with anisotonic sucrose solutions. When ventricular fluid osmolality was 120 mOsm, CSF volume flow ceased for both groups of cats. As ventricular fluid osmolality was increased, the CSF volume flow rate of normal cats increased to 70 microliter per minute, and in hydrocephalic cats to 40 microliter per minute. In normal cats, for ventricular fluid osmolality between 50 and 350 mOsm, Na+-influx was constant and thought to occur by diffusion; while for higher osmolalities, Na+-influx increased. In hydrocephalic cats, Na+-influx increased over the entire range of ventricular osmolality but was less than in normal cats. Acetazolamide decreased the CSF volume flow in normal cats by 40 percent, but was ineffective in hydrocephalic cats. These results suggest that CSF secretion by the choroid plexus of cats with kaolin-induced hydrocephalus is impaired.

Animals↗
PubMed1978

Suppressed murine mammary tumor virus (MuMTV) expression in RIII female mice treated neonatally with goat antiserum to MuMTV.

Passive immunization of newborn inbred RIII (R3) mice with the globulin fraction of goat antiserum to murine mammary tumor virus (MuMTV) successfully suppressed MuMTV expression in the milk of some of the treated mice throughout nine successive lactations. No mammary tumors developed in the MuMTV-suppressed mice during the first 9 months, whereas all untreated R3 female breeders expressed MuMTV in the milk of the third lactation, and all developed tumors before 9 months of age (mode and median: 189 days).

Animals↗
PubMed1977

Sodium exchange between blood, brain, and CSF in normal and hydrocephalic cats.

The exchange of sodium between blood, brain, and cerebrospinal fluid was studied in normal and kaolin-induced hydrocephalic cats. The ventricles were perfused to measure fluid formation and Na+ exchange rates. 22Na was added to the perfusion fluid or injected intravenously as a tracer for Na+ movement. Na+ and 22Na were also measured in cortical gray and white matter. Na+ relative specific activities were calculated for brain, effluent fluid, and serum. With 22Na in the perfusion fluid, Na+ exchange was not different from nascent Na+ influx for both normal and hydrocephalic cats. Na+ relative specific activities of cortical gray and white matter were 10 times greater in hydrocephalic than in normal cats. This difference in Na+ relative specific activity for brain may be due to a higher diffusion constant or to a lower brain capillary permeability. When 22Na was given intravenously, the Na+ diffusional exchange for normal cats was less than that measured when 22Na+ was in the perfusion fluid. In hydrocephalic cats, the Na+ diffusional exchange was effectively zero. Na+ relative specific activities of cortical gray and white matter were the same for normal and hydrocephalic cats. These findings suggest that the impaired Na+ diffusional exchange may be due to pathological changes in the choroid plexus.

Animals↗
PubMed1977

Effect of indomethacin on cholera-induced fluid movement, unidirectional sodium fluxes, and intestinal cAMP.

Cholera enterotoxin (CT) produces intestinal secretion associated with an elevation of intestinal cyclic AMP (cAMP). Indomethacin, a potent inhibitor of prostaglandin (PG) synthesis, decreases CT-induced secretion, although a role for PG in this process has not been demonstrated. The purpose of this study was to measure the effects of indomethacin on net fluid movement and unidirectional Na fluxes in rabbit jejunal loops exposed to CT and to correlate these findings with intestinal cAMP levels. In untreated animals (no indomethacin), CT loops secreted 0.37 ml per cm per 4 hr compared to absorption in control loops of 0.23 ml per cm per 4 hr (P less than 0.001). In indomethacin-treated animals, there was a striking reduction of secretion in CT loops (0.07 ml per cm per 4 hr, P less than 0.001). Absorption in control loops in indomethacin animals was greater than in untreated animals (0.42 ml per cm per 4 hr, P less than 0.02). Unidirectional Na fluxes were greatly depressed in indomethacin animals at 1 h in both CT and control loops. This effect disappeared by 4 hr. Intestinal cAMP levels in CT loops, although not elevated at 1 hr despite the onset of secretion, were significantly elevated at 4 hr. Indomethacin did not alter cAMP levels at 1 and 4 hr in either cholera or control loops. These studies support the view that PG synthesis is not involved in CT-induced elevation of intestinal cAMP. Indomethacin may depress intestinal secretion by inhibiting a PG-mediated step beyond the generation of cAMP or by acting on some other, as yet unidentified, biological mechanism involved in intestinal secretion.

Animals↗
PubMed1976

The effects of ventricular fluid osmolality on bulk flow of nascent fluid into the cerebral ventricles of cats.

The effects of ventricular fluid osmolality on the bulk flow of nascent fluid into the cerebral ventricles of anesthetized cats was measured during ventriculocisternal perfusion. This nascent fluid consists of both cerebrospinal fluid (CSF) and fluid which results from an osmotic gradient between ventricular fluid and the blood and/or brain. Perfusions were carried out with both mock CSF and with solutions containing either sucrose, urea, or NaCl. Differences between the normal bulk flow rate of nascent CSF and bulk flow rate measured during perfusion with anisotonic solutions were linearly related to corresponding differences in osmolality of the effluent fluid from the ventricles. The coefficients of somotic flow using sucrose (0.231 mul/min per mOsm) and NaCl (0.224) were similar, and greater than that using urea (0.156). During perfusion with sucrose when effluent osmolality increased by 200 mOsm (63% of normal), bulk flow rate of nascent fluid increased by 50 mul/min (200% of normal). Flow was undetectable when the effluent osmolality was 190 mOsm (decrease of 135 mOsm), although osmotically active particles continued to enter the ventricular system. Intravenous injection of acetazolamide reduced these coefficients to similar values of 0.0963 for NaCl, and 0.0955 for urea. In all experimental conditions no changes were found in cerebral water content. These results suggest that the increased bulk flow which occurs during perfusion with hypertonic solutions originates from the choroid plexus.

Acetazolamide↗
PubMed1976

The sink action of cerebrospinal fluid volume flow. Effect on brain water content.

Effects of changes in serum osmolarity on volume flow of fluid into the cerebral ventricles of cats were measured by ventriculocisternal perfusion with mock cerebrospinal fluid (CSF), mock CSF containing acetazolamide, or a 30 mOsm/liter sucrose solution. Serum osmolarity was altered by intravenous infusion of a sucrose solution ranging between 10 and 650 mOsm/liter changing volume flow. For all perfusion fluids, regression lines relating volume flow to infused solution osmolarity were parallel. After infusion of a 10 mOsm/liter solution, brain water content increased. One hour after infusion, volume flow returned to normal, although serum was still hypotonic. Gray matter water content was still elevated; white matter returned to normal. The results suggest that the source of increased volume flow is the brain, and that the CSF acts as a sink, limiting excess water accumulation during water intoxication.

Animals↗
PubMed1976

On the movement of fluid through the brain of hydrocephalic cats.

The effects of changes in serum osmolality on the volume flow of fluid into the cerebral ventricles and on brain water content was examined in cats with kaolin-induced hydrocephalus. Slopes of the regression lines relating volume flow and serum osmolality for both normal and hydrocephalic cats are the same. The constant difference in flow rates between the two lines, 7 mul per minute, is probably due to impaired choroid plexuow rates between the two lines, 7 mul per minute, is probably due to impaired choroid plexus function of the hydrocephalic cats. The osmotic pressure gradient that causes the flow of fluid is therefore probably between blood and brain. Under these conditions changes in brain water content of hydrocephalic cats were smaller than in normals and can be related to the edema present in this disorder. Despite the inflammatory response to kaolin, the blood-brain barrier remains intact. From the calculated filtration coefficient, it can be inferred that the flow of water from serum through brain and into cerebrospinal fluid is limited by the resistance of fluid flow through the brain.

Animals↗
PubMed1976

Effect of caffeine on the human small intestine.

Methylxanthines produce intracellular accumulation of cyclic 3'5'-AMP (cAMP) by inhibition of phosphodiesterase and mucosal cAMP accumulation. Cyclic AMP is thought to mediate small intestinal secretion caused by some enterotoxins, hormones, and methylxanthines. These studies were designed to evaluate the effect of caffeine on small intestinal net fluid movement and transit times. The administration of caffeine in amounts ordinarily contained in many beverages and medications (75 to 300 mg) resulted in striking net secretion in the jejunum which lasted at least 15 minutes. This occurred in six of seven studies. Baseline net absorption of 0.5 ml per cm per hr was reversed to net secretion of 6.0 +/- 2.2 ml per cm per hr after oral caffeine ingestion (P less than 0.01). Net secretion also occurred in the ileum in seven of eight studies, but the onset of secretion appeared 35 min later than in the jejunum. These patterns of secretion correlated best with the passage of the intestinal bolus of caffeine rather than plasma caffeine levels. In contrast to other net secretory conditions, which increase the speed of transit, small intestinal transit times, as determined by dye dilution methods, were unchanged by caffeine. It is possible that methylxanthine-induced small intestinal secretion may play a role in the symptoms experienced by some patients with functional diarrhea.

Administration, Oral↗