Biomedical subjects

R J Washabau

Publications and source records attributed to R J Washabau.

At least 19 recordsLinked to original sources

PubMed1996

Serum alpha 1-antitrypsin concentration in dogs with panniculitis.

OBJECTIVE: To measure serum alpha 1-antitrypsin (alpha 1AT) concentration in dogs with histologically confirmed panniculitis to determine whether serum deficiency could cause or exacerbate panniculitis in dogs. DESIGN: Cross-sectional, descriptive study. ANIMALS: 9 dogs (5 with multiple lesions and 4 with solitary lesions). PROCEDURE: Serum samples were obtained by means of cephalic or jugular venipuncture and frozen at -20 C until assayed. Serum alpha 1AT concentration was measured by means of radial gel immunodiffusion. RESULTS: In all dogs, serum alpha 1AT concentration was within the previously established reference range. CLINICAL IMPLICATIONS: In the small number of-dogs studied, panniculitis was not associated with serum alpha 1AT deficiency.

Adipose Tissue↗

PubMed1996

Hepatic abscesses in dogs: 14 cases (1982-1994).

OBJECTIVES: To determine typical clinical signs and clinicopathologic findings in dogs with hepatic abscesses, to assess outcome of treatment, and to evaluate the role that abdominal ultrasonography has in the diagnosis of hepatic abscesses in dogs and in monitoring response to treatment. DESIGN: Retrospective case series. ANIMALS: 14 dogs with hepatic abscesses. RESULTS: Anorexia and lethargy were the most common historical complaints, followed by vomiting and diarrhea. Physical abnormalities included fever, dehydration, signs of abdominal pain, hepatomegaly, and mucosal bleeding. Hematologic abnormalities included leukocytosis with neutrophilia, mild to moderate thrombocytopenia, and mild anemia. Serum biochemical abnormalities included high alkaline phosphatase and alanine aminotransferase activities and high bilirubin concentration; hypoalbuminemia and prolonged coagulation values were also reported. Abdominal radiography revealed hepatomegaly, poor abdominal detail, a hepatic mass, or splenomegaly in 9 dogs. Thoracic radiography revealed alveolar consolidation or mixed bronchial/interstitial pulmonary patterns in 6 dogs. Hypoechoic, heteroechoic, or hyperechoic masses were identified in all dogs in which ultrasonography was performed. Escherichia coli, Clostridium sp, Klebsiella pneumoniae, Enterococcus sp, Staphylococcus epidermidis, and S intermedius were the most common bacteria isolated from hepatic abscesses. Concurrent infections were identified in the biliary tract, spleen, blood, endocardium, lung, prostate gland, peritoneum, lymph nodes, salivary gland, or brain of several dogs. Seven dogs died or were euthanatized before definitive treatment could be initiated. One dog was successfully treated with antibiotics and was alive 12 months after medical treatment. Six dogs were treated surgically (ie, full or partial liver lobectomy, drainage, abdominal lavage) and medically (ie, antibiotic administration). Five of these dogs survived and were alive 12 months after surgery. Ultrasonography was used to monitor response to treatment in several dogs. CLINICAL IMPLICATIONS: Hepatic abscesses are rare in dogs, but the clinical signs and clinicopathologic findings are similar to other inflammatory hepatic disease. Ultrasonography revealed abnormalities in all animals in which imaging studies were performed, and was successfully used to monitor response to treatment in several dogs. Medical and surgical treatments were used successfully to treat hepatic abscesses in dogs.

Animals↗

PubMed1996

Effects of cisapride on feline colonic smooth muscle function.

OBJECTIVE: To determine the effects of cisapride on feline colonic smooth muscle function. DESIGN: In vitro smooth muscle mechanical measurements. ANIMALS: Intact colon was obtained from healthy 2- or 3-year-old cats. PROCEDURE: Longitudinal smooth muscle strips from proximal and distal portions of feline colon were suspended in physiologic buffer solution (37 C. 100% O2, pH 7.4), attached to isometric force transducers, and stretched to optimal muscle length. Control responses were obtained at each muscle site with acetylcholine (10(-8) to 10(-4) M), cholecystokinin (10(-11) to 10(-7) M), substance P (10(-21) to 10(-7) M), or neurotensin (10(-11) to 10(-7) M). Muscles were then stimulated with cumulative (10(-9) to 10(-6) M) or bolus (10(-6) M) doses of cisapride in the absence or presence of tetrodotoxin (10(-5) M) and atropine (10(-6) M), nifedipine (10(-6) M), or calcium-free buffer solution. RESULTS: Cisapride stimulated contractions of longitudinal smooth muscle from proximal and distal portions of feline colon that were similar in magnitude to contractions induced by substance P and neurotensin. Cisapride contractions were only partially inhibited by tetrodotoxin (10(-6) M) and atropine (10(-6) M), suggesting that cisapride responses are only partially dependent on enteric cholinergic nerves. Nifedipine (10(-6)M) inhibited the maximal contraction to cisapride (10(-6) M) by approximately 80%. Removal of extracellular calcium did not inhibit cisapride contractions to a greater extent than did inhibition by nifedipine, indicating that calcium influx through voltage-dependent calcium channels was predominantly responsible for the dependence of the cisapride contraction on extracellular calcium. CONCLUSIONS: Cisapride-induced contractions of feline colonic smooth muscle are largely smooth muscle-mediated and dependent on calcium influx, and are only partially dependent on enteric cholinergic nerves. CLINICAL RELEVANCE: Cisapride may be useful in the treatment of feline colonic motility disorders.

Acetylcholine↗

PubMed1996

Alterations in colonic smooth muscle function in cats with idiopathic megacolon.

OBJECTIVE: To determine whether colonic smooth muscle dysfunction is involved in the pathogenesis of idiopathic megacolon in cats. DESIGN: In vitro smooth muscle mechanical measurements. ANIMALS: Colon from healthy cats and cats with idiopathic megacolon. PROCEDURE: Colonic smooth muscle strips were suspended in physiologic buffer solution, attached to isometric force transducers, and contracted with acetylcholine (ACh; 10(-9) to 10(-4)M), substance P (SP; 10(-10) to 10(-6)M), cholecystokinin (CCK; 10(-11) to 10(-8)M), potassium chloride (KCl; 10 to 80 mM), or electrical field stimulation (EFS; 25 V, 1 to 30 Hz, 0.5-millisecond duration). Isometric stress responses were compared with those obtained from healthy controls. Colonic smooth muscle strips were also evaluated histologically for neuronal and smooth muscle cell morphology. RESULTS: Passive isometric stress was not altered, but the active isometric stress responses of megacolon smooth muscle to ACh, SP, CCK, KCl, and EFS were significantly (P < 0.05) diminished, compared with healthy controls. Differences were observed in longitudinal and circular smooth muscle from proximal and distal portions of the colon. Histologic evaluation revealed few abnormalities of smooth muscle cells or of myenteric or submucosal plexus neurons. The contractile response of megacolon smooth muscle to EFS, and the inhibition of this response by tetrodotoxin, suggest that myenteric and submucosal plexus neurons in megacolon smooth muscle are functional. CONCLUSIONS: Idiopathic megacolon is a generalized dysfunction of colonic smooth muscle in cats. The diminished isometric stress responses to receptor occupancy (ACh, SP, and CCK) and membrane depolarization (KCl) further suggest that the disorder involves disturbance in the activation of smooth muscle myofilaments.

Acetylcholine↗

PubMed1995

Cisapride.

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Animals↗

PubMed1995

Canine gastric dilatation/volvulus syndrome in a veterinary critical care unit: 295 cases (1986-1992).

Two hundred ninety-five case records were included in an analysis of dogs treated by a standardized protocol for gastric dilatation/volvulus syndrome between 1986 and 1992. A breed predisposition was demonstrated for Great Danes, German Shepherd Dogs, large mixed-breed dogs, and Standard Poodles. One hundred and ninety-three dogs had gastric dilatation and volvulus (GDV) confirmed at surgery, 66 had simple gastric dilatation (GD), and 36 others had gastric dilatation but volvulus could not be proved or disproved (GD +/- V). Among dogs with GDV, the fatality rate was 15% (29/193). Twenty-six (13.5%) dogs with GDV underwent partial gastrectomy, and 8 (31%) died or were subsequently euthanatized. In comparing the group of dogs with GDV that survived to those that died, there were no statistical differences in the age of dog, time between onset of clinical signs and admission, time from admission to surgery, or duration of anesthesia. Cardiac arrhythmias were detected in 40% (78/193) of the dogs with GDV. There also was no statistical correlation between development of a cardiac arrhythmia and outcome in dogs with GDV. The causes of death in dogs with GDV were multiple and varied; presumed gastric necrosis was a common reason for intraoperative euthanasia (11 dogs). Among dogs with GD or GD +/- V, the fatality rate was 0.9% (1/102).

Animals↗

PubMed1995

GABA receptors in the dorsal motor nucleus of the vagus influence feline lower esophageal sphincter and gastric function.

Gamma-aminobutyric acid (GABA) antagonist (bicuculline methiodide, BIC; picrotoxin, PIC) or agonist (muscimol, MUS) microinjections were made into the dorsal motor nucleus of the vagus nerve (DMV), and effects on lower esophageal sphincter pressure (LESP), gastric motility, and gastric acid secretion were determined in chloralose-anesthetized cats. Right or left DMV sites were microinjected with BIC, PIC, MUS, or isotonic tonic saline (140 nl) through a glass micropipette having a tip diameter of 15-21 microns. Esophageal body, LESP, and gastric fundic pressures were measured manometrically. Circular smooth muscle contractions of the antrum and pylorus were recorded with strain-gauge force transducers. Gastric acid secretion was measured every 15 min through a gastric cannula and titrated to pH 7.0. DMV microinjection sites were verified histologically. Direct BIC microinjections (0.275 or 0.550 nmol) into the DMV primarily produced a decrease in LESP (71% of all sites tested), with mean LESP changing from 23.2 +/- 1.7 mmHg to 3.7 +/- 0.7 mmHg (p < 0.01). Tonic LESP increases and phasic LESP contractile activity occurred less frequently. BIC-induced LESP responses were abolished by vagotomy or by microinjections of MUS (0.5 to 10 nmol) into the DMV. Direct PIC microinjection (0.232 nmol) into the DMV produced a pattern of responses similar to those observed with BIC (which were also abolished by vagotomy or by MUS microinjections into the DMV). The antrum and pylorus were also responsive to DMV microinjections of both GABA antagonists. Microinjections of BIC or PIC into the DMV produced increases in gastric circular muscle activity that occurred less frequently than LESP effects, but also were eliminated by vagotomy. The high (0.550 nmol) dose of BIC increased gastric motility significantly more often than the low dose of BIC (p < 0.05). In addition, BIC (0.550 nmol) microinjections into the DMV increased gastric secretory volume (from 0.6 +/- 0.2 to 6.0 +/- 2.5 ml/15 min; p < 0.01) and total titratible acid (from 34.4 +/- 8.9 to 86.0 +/- 19.1 mEq/15 min; p < 0.01), and decreased gastric pH (from 4.63 +/- 0.44 to 3.50 +/- 0.49; p < 0.05). Vagotomy also eliminated the gastric secretory effects of DMV BIC. Direct microinjections of MUS into the DMV also blocked BIC- or PIC-induced changes in gastric motility and/or gastric acid secretion. Isotonic saline microinjected into the DMV did not increase basal or decrease stimulated gastric esophageal motility or gastric secretion. These data indicate that LESP, gastric motility, and gastric secretion are influenced by a tonic DMV inhibition mediated by GABAA receptor stimulation of the DMV. Because disinhibition of these receptors clearly activates the upper gut, future work should focus on identifying the nuclei providing this synaptic input to the DMV that might be involved in the functional regulation of upper gut motor and secretory function.

Animals↗

PubMed1995

Effects of age, sex, reproductive status, and hospitalization on serum alpha 1-antitrypsin concentration in dogs.

We performed a study to determine a reference range for serum alpha 1-antitrypsin (alpha 1AT) in dogs by specific immunoassay; to evaluate whether serum alpha 1AT concentration varied with age, sex, or reproductive status in healthy dogs; and to investigate whether the serum alpha 1AT concentration in hospitalized dogs differed from that of healthy, nonhospitalized dogs. Serum alpha 1AT was quantitated by radial gel immuno-diffusion for 60 healthy dogs and 311 hospitalized dogs. In healthy dogs, serum alpha 1AT concentration was 2.33 +/- 0.41 mg/ml (mean +/- SD), yielding a reference range (mean +/- 2 SD) of 1.51 to 3.15 mg/ml. A correlation was not found between serum alpha 1AT concentration and age in healthy dogs. The serum alpha 1AT concentration (mean +/- SEM mg/ml) was significantly higher in healthy, sexually intact females (2.64 +/- 0.1) than in healthy, spayed females (2.22 +/- 0.12; P < 0.004); healthy, sexually intact males (2.14 +/- 0.1; P < 0.0006); and healthy, and castrated males (2.25 +/- 0.14; P < 0.02). Hospitalized, sexually intact females had a lower serum alpha 1AT concentration (1.93 +/- 0.07) than healthy, sexually intact females (2.64 +/- 0.1; P < 0.0002). Likewise, the serum alpha 1AT concentration in hospitalized, sexually intact males (1.92 +/- 0.04) was less than in healthy, sexually intact males (2.14 +/- 0.1; P < 0.04). A difference in alpha 1AT concentration was not found between healthy and hospitalized, neutered dogs.

Age Factors↗

PubMed1994

Role of myosin light-chain phosphorylation in guinea pig gallbladder smooth muscle contraction.

In acetylcholine (ACh)-stimulated gallbladder smooth muscle, we have previously shown that phosphorylation of the 20,000-Da myosin light chains is necessary for the initiation of contraction, that myosin is stably phosphorylated at steady state, and that dephosphorylation of cross bridges is not necessary for the slowing of cross-bridge cycling rates during the period of steady-state isometric stress. The present studies were undertaken to determine whether 1) K+ (60 or 80 mM) or cholecystokinin (CCK, 10(-8) M) stimulation is accompanied by changes in myosin light-chain phosphorylation in gallbladder smooth muscle and 2) dephosphorylated noncycling cross bridges exist in K(+)- or CCK-stimulated gallbladder smooth muscle. Isometric stress, isotonic shortening velocity, and myosin light-chain phosphorylation were determined during contraction with K+ or CCK. Steady-state isometric stress was reached within 2.5 min of stimulation with K+ or CCK and was maintained for the duration of the stimulation. Stimulation with K+ or CCK was associated with rapid increases in myosin light-chain phosphorylation and maintenance of myosin light-chain phosphorylation during the stimulation. In contrast, isotonic shortening velocity was maximal at 1 min of stimulation with either K+ or CCK and then declined significantly to values that were only 26-32% of the peak velocity. These data, along with data from previous experiments with ACh, suggest that myosin light-chain phosphorylation is essential in the initiation of contraction in gallbladder smooth muscle, regardless of the source of Ca2+ or of the contractile agonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Beta-adrenergic agonists regulate KCa channels in airway smooth muscle by cAMP-dependent and -independent mechanisms.

Stimulation of calcium-activated potassium (KCa) channels in airway smooth muscle cells by phosphorylation-dependent and membrane-delimited, G protein actions has been reported (Kume, H. A. Takai, H. Tokuno, and T. Tomita. 1989. Nature [Lond.]. 341:152-154; Kume, H., M. P. Graziano, and M. I. Kotlikoff. 1992. Proc. Natl. Acad. Sci. USA. 89:11051-11055). We show that beta-adrenergic receptor/channel coupling is not affected by inhibition of endogenous ATP, and that activation of KCa channels is stimulated by both alpha S and cAMP-dependent protein kinase (PKA). PKA stimulated channel activity in a dose-dependent fashion with an EC50 of 0.12 U/ml and maximum stimulation of 7.38 +/- 2.04-fold. Application of alpha S to patches near maximally stimulated by PKA significantly increased channel activity to 15.1 +/- 3.65-fold above baseline, providing further evidence for dual regulatory mechanisms and suggesting that the stimulatory actions are independent. Analysis of channel open-time kinetics indicated that isoproterenol and alpha S stimulation of channel activity primarily increased the proportion of longer duration events, whereas PKA stimulation had little effect on the proportion of short and long duration events, but resulted in a significant increase in the duration of the long open-state. cAMP formation during equivalent relaxation of precontracted muscle strips by isoproterenol and forskolin resulted in significantly less cAMP formation by isoproterenol than by forskolin, suggesting that the degree of activation of PKA is not the only determinant of tissue relaxation. We conclude that beta-adrenergic stimulation of KCa channel activity and relaxation of tone in airway smooth muscle occurs, in part, by means independent of cyclic AMP formation.

Adenylyl Imidodiphosphate↗

PubMed1993

Granulomatous hepatitis in dogs: nine cases (1987-1990).

Granulomatous hepatitis (GH) is an uncommon histopathologic diagnosis in dogs. On the basis of clinical reports, fungal infections appear to be the most common cause of GH in dogs, but many other potential causes have been identified. The medical records and histopathologic findings for 9 dogs with GH were reviewed to identify additional specific causes of GH in dogs. Diseases associated with GH included intestinal lymphangiectasia (n = 2), lymphosarcoma (n = 1), histiocytosis (n = 1), dirofilariasis (n = 1), and histoplasmosis (n = 1). In 1 dog, no other disease process was identified. Of the remaining 2 dogs, 1 had concurrent granulomatous pneumonitis of unknown cause, and the other had periportal hepatitis and temporal muscle wasting. All 9 dogs with GH had clinical evidence of liver disease, such as hepatomegaly, icterus, and ascites, or had high serum alkaline phosphatase and alanine aminotransferase activity. Because of the wide variety of potential causes of GH in dogs, an accurate diagnosis should be sought so that appropriate treatment can be chosen and an accurate prognosis given.

Animals↗

PubMed1993

Control of resting membrane potential by delayed rectifier potassium currents in ferret airway smooth muscle cells.

1. In order to determine the physiological role of specific potassium currents in airway smooth muscle, potassium currents were measured in freshly dissociated ferret trachealis cells using the nystatin-permeabilized, whole-cell method, at 35 degrees C. 2. The magnitude of the outward currents was markedly increased as bath temperature was increased from 22 to 35 degrees C. This increase was primarily due to the increase in maximum potassium conductance (gK,max), although there was also a small leftward shift in the relationship between gK and voltage at higher temperatures. The maximum conductance and the kinetics of current activation and inactivation were also temperature dependent. At 35 degrees C, gating of the current was steeply voltage dependent between -40 and 0 mV. Current activation was well fitted by fourth-order kinetics; the mean time constants of activation (30 mV clamp step) were 1.09 +/- 0.17 and 1.96 +/- 0.27 ms at 35 and 22 degrees C, respectively. 3. Outward currents using the nystatin method were qualitatively similar to delayed rectifier currents recorded in dialysed cells with high calcium buffering capacity solutions. 4-Aminopyridine (4-AP; 2 mM), a specific blocker of delayed rectifier potassium channels in this tissue, inhibited over 80% of the outward current evoked by voltage-clamp steps to between -10 and +20 mV (n = 6). Less than 5% of the outward current was blocked over the same voltage range by charybdotoxin (100 nM; n = 15), a specific antagonist of large-conductance, calcium-activated potassium channels in this tissue. 4. The degree to which delayed rectifier and calcium-activated potassium conductances control resting membrane potential was examined in current-clamp experiments. The resting membrane potential of current clamped cells was -33.6 +/- 1.0 mV (n = 62). Application of 4-AP (2 mM) resulted in a 14.4 +/- 1.0 mV depolarization (n = 8) and an increase in input resistance. Charybdotoxin (100 nM) had no effect on resting membrane potential (n = 6). 5. Force measurements were made in isolated strips of trachealis muscle to determine the effect of pharmacological blockade of individual potassium conductances on resting tone. In the presence of tetrodotoxin (1 microM) and atropine (1 microM), 4-AP increased baseline tension in a dose-dependent manner, with an EC50 of 1.8 mM (n = 13); application of 5 mM 4-AP increased tone to 86.8 +/- 8.1% of that produced by 1 microM methacholine, and this tone was almost completely inhibited by nifedipine (1 microM).(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗

PubMed1991

Effect of muscle length on isometric stress and myosin light chain phosphorylation in gallbladder smooth muscle.

These experiments were designed to characterize the effect of muscle length on isometric stress, sensitivity to stimulation, and phosphorylation of the 20,000-Da myosin light chains in guinea pig gallbladder smooth muscle. Basal, active, and total isometric stress were determined in acetylcholine- or K(+)-treated (10(-4) M ACh, 80 mM KCl) muscle strips at 0.6-1.3 times the optimal muscle length (Lo) for isometric stress development. The effect of muscle length on the sensitivity to ACh and K+ was determined in cumulative dose-response experiments (10(-8) to 10(-4) M ACh, 10-80 mM KCl) at 0.7, 1.0, and 1.3 Lo. The effect of muscle length on myosin light chain phosphorylation was determined in ACh- or K(+)-treated (10(-4) M ACh, 80 mM KCl) muscle strips at 0.7, 1.0, and 1.3 Lo. In gallbladder smooth muscle, 1) active isometric stresses at 0.7 and 1.3 Lo were less than active isometric stress at 1.0 Lo; 2) the sensitivity of developed stress was similar at 1.0 and 1.3 Lo but decreased at 0.7 Lo; 3) the decline in isometric stress and sensitivity at 0.7 Lo was associated with reduced levels of phosphorylated myosin light chain; and 4) the decline in isometric stress at 1.3 Lo was not associated with reduced amounts of phosphorylated myosin light chain. These results suggest that the decline in active stress and sensitivity at short muscle lengths (L less than Lo) in gallbladder smooth muscle is due, at least in part, to decreases in the activation of the myofilaments. The decline in active isometric stress at long muscle lengths (L greater than Lo) is not due to changes in myofilament activation.

Acetylcholine↗

PubMed1991

Myosin light chain phosphorylation and contraction of guinea pig gallbladder smooth muscle.

These experiments were designed to determine 1) whether acetylcholine (ACh) stimulation is accompanied by changes in myosin light chain phosphorylation in gallbladder smooth muscle and 2) whether dephosphorylated noncycling cross bridges (latch bridges) exist in gallbladder smooth muscle. Isometric stress, isotonic shortening velocity, and myosin light chain phosphorylation were determined under conditions of contraction and relaxation in ACh-stimulated guinea pig gallbladder smooth muscle. Unstimulated muscle contained 6.8 +/- 2.0% phosphorylated myosin light chain. ACh stimulation (5 x 10(-5) or 10(-4) M) was associated with a rapid increase in myosin light chain phosphorylation to a value that was maintained throughout the tonic contraction. In contrast, isotonic shortening velocity was maximal at 30 s of stimulation and then declined over time to a steady-state level that was 25-30% of the peak velocity. Upon agonist washout (relaxation), dephosphorylation of the myosin light chain occurred at about the same rate as the decline in shortening velocity and preceded the decline in isometric stress. These data suggest that ACh stimulation is accompanied by changes in myosin light chain phosphorylation but that dephosphorylation of cross bridges is not necessary for the slowing of cross-bridge cycling rates in gallbladder smooth muscle.

Acetylcholine↗

PubMed1986

Use of pulmonary hydrogen gas excretion to detect carbohydrate malabsorption in dogs.

Pulmonary H2 excretion was measured in 10 healthy dogs, in 6 dogs with pancreatic exocrine insufficiency, and in 6 dogs with chronic small intestinal disease. Concentration of expired H2 in fasted healthy dogs was 0.9 +/- 0.1 ppm (mean +/- SEM) and peak H2 concentration of 1.4 +/- 0.2 ppm was detected up to 8 hours after feeding. Dogs with pancreatic exocrine insufficiency had fasting expired H2 concentrations of 3.3 +/- 0.9 ppm, which increased to a mean peak H2 concentration of 28.8 +/- 2.0 ppm 6.5 hours after feeding. Following xylose administration, expired H2 concentrations increased from fasting concentrations of 3.6 +/- 0.9 ppm to peak at 19.0 +/- 2.0 ppm in 1.5 hours. Blood xylose concentrations were diagnostic for carbohydrate malabsorption in 4 of 6 dogs with pancreatic exocrine insufficiency. Plasma p-aminobenzoic acid concentration identified bentiromide maldigestion in all dogs with pancreatic exocrine insufficiency. In 3 pancreatic exocrine insufficient dogs tested, pancreatic enzyme replacement therapy partially corrected carbohydrate malabsorption. Fasting expired H2 concentration was 5.3 +/- 1.3 ppm in dogs with chronic small intestinal disease and increased to a peak H2 of 72.2 +/- 18.0 ppm 7 hours after feeding. Following administration of xylose to dogs with chronic small intestinal disease, fasting expired H2 concentration increased from 3.0 +/- 1.0 ppm to a peak of 35.5 +/- 7.2 ppm at 2 hours. Blood xylose concentration was abnormal in only 2 of 6 dogs with chronic small intestinal disease. Results of these studies indicate that expired H2 analysis can identify carbohydrate malabsorption in dogs with pancreatic exocrine insufficiency or chronic small intestinal disease, and that pulmonary H2 testing is more sensitive than xylose absorption testing for the identification of carbohydrate malabsorption.

Animals↗

PubMed1986

Serum thyroxine concentrations after radioactive iodine therapy in cats with hyperthyroidism.

Thirty-one cats with hyperthyroidism were given one dose of radioactive iodine (131I) IV. Serum thyroxine (T4) concentrations were measured before treatment in all cats, at 12-hour intervals after treatment in 10 cats, and at 48-hour intervals after treatment in 21 cats. Serum T4 concentrations also were measured one month after 131I therapy in 29 cats. Activity of 131I administered was 1.5 to 6.13 mCi, resulting in a dose of 20,000 rads to the thyroid. Serum T4 concentrations before 131I administration were 5.3 to 51.0 micrograms/dl, with a median T4 concentration of 11.0 micrograms/dl. Serum T4 decreased most rapidly during the first 3 to 6 days after treatment. Sixteen cats (55%) had normal serum thyroxine concentrations by day 4 after 131I administration, and 23 cats (74%) were euthyroxinemic by day 8 after treatment. One month after administration of 131I, the 29 cats evaluated were clinically improved, and 24 (83%) of the 29 cats evaluated had normal serum T4 concentrations, 3 cats (10%) remained hyperthyroxinemic, and 2 cats (7%) were hypothyroxinemic. Therefore, administration of 131I was a safe and effective method to quickly decrease serum T4 concentrations in hyperthyroid cats.

Animals↗

PubMed1986

Digestion of bentiromide and absorption of xylose in healthy cats and absorption of xylose in cats with infiltrative intestinal disease.

The digestion of bentiromide and the absorption of D-xylose was measured in 17 clinically healthy cats. The plasma xylose concentrations of the healthy cats were compared with values from 9 cats with diffuse infiltrative intestinal disease. The cats were administered 16.7 mg of bentiromide/kg and 0.5 g of xylose/kg via a stomach tube. Plasma samples were obtained before administration and 30, 60, 90, and 120 minutes after administration. The maximum mean plasma p-aminobenzoic acid concentration occurred at 60 minutes, with a value of 386 +/- 134 micrograms/dl (mean +/- SD). The maximum mean plasma xylose concentration also occurred at 60 minutes, with a value of 26.0 +/- 9.2 mg/dl. Plasma concentrations of p-aminobenzoic acid and xylose were lower in healthy cats than those reported for healthy dogs. There was no significant difference between xylose concentrations in healthy cats and cats with infiltrative intestinal disease.

4-Aminobenzoic Acid↗

PubMed1986

Evaluation of intestinal carbohydrate malabsorption in the dog by pulmonary hydrogen gas excretion.

Breath H2 was measured for the assessment of intestinal carbohydrate absorption in healthy, fasted dogs before and after the ingestion of carbohydrate test meals. The dogs were fed lactulose, xylose, glucose, a hypoallergenic diet, or the hypoallergenic diet supplemented with rice, corn, or wheat flour. Breath samples for H2 analysis were collected by an interval-sampling technique during tidal breathing and were analyzed by thermal conductivity gas chromatography. Pulmonary H2 excretion in fasted dogs never exceeded 1 part per million (molecules of H2 per 10(6) molecules of air). Breath H2 excretion after the ingestion of 12.5 g of glucose, a completely absorbed monosaccharide, was not significantly different (P greater than 0.05) from that during fasting; however, ingestion of 12.5 g of xylose, an incompletely absorbed pentose, significantly increased (P less than 0.001) breath H2 excretion. After ingestion of 12.5, 25, or 50 g of lactulose, a nonabsorbable disaccharide, pulmonary H2 excretion increased significantly (P less than 0.001) over fasting amounts and the increases were different (P less than 0.001) from one another. Increases in breath H2 excretion correlated (r = 0.97) with increases in lactulose dose. Breath H2 excretion after the ingestion of the hypoallergenic diet did not significantly (P greater than 0.05) differ from that after fasting. The addition of rice flour to this diet did not significantly (P greater than 0.05) increase H2 production. However, the addition of wheat or corn flour to this diet significantly (P less than 0.001) increased breath H2 excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗