Biomedical subjects
R J Washabau
Publications and source records attributed to R J Washabau.
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).
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.
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.
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.
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.
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.
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.
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.
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)
The post-prandial intestinal hyperaemic response.
Explore the source record for details and available documents.
Hiatal hernia repair by restoration and stabilization of normal anatomy. An evaluation in four dogs and one cat.
Clinical signs of esophageal hiatal hernia in four dogs and one cat included regurgitation, vomiting, hematemesis, hypersalivation, dysphagia, and dyspnea. Thoracic radiographs, esophagram, and fluoroscopy were used to demonstrate cranial displacement of the esophagogastric junction and part of the stomach through the esophageal hiatus. Other findings included megaesophagus, esophageal hypomotility, gastroesophageal reflux, and pneumonia. Medical therapy failed to resolve the clinical signs. Reduction in size of the esophageal hiatus, fixation of the esophagus to the diaphragmatic crus (esophagopexy), and a left fundic gastropexy were performed. Surgical results were considered good to excellent.