Although well documented in racehorses, there is paucity in the literature regarding the prevalence of dynamic upper airway abnormalities in nonracing performance horses.To describe upper airway function of nonracing performance horses with abnormal respiratory noise and/or poor performance via exercising upper airway videoendoscopy.Medical records of nonracing performance horses admitted for exercising evaluation with a chief complaint of abnormal respiratory noise and/or poor performance were reviewed. All horses had video recordings of resting and exercising upper airway endoscopy. Relationships between horse demographics, resting endoscopic findings, treadmill intensity and implementation of head and neck flexion during exercise with exercising endoscopic findings were examined.Dynamic upper airway obstructions were observed in 72% of examinations. Head and neck flexion was necessary to obtain a diagnosis in 21 horses. Pharyngeal wall collapse was the most prevalent upper airway abnormality, observed in 31% of the examinations. Complex abnormalities were noted in 27% of the examinations. Resting laryngeal dysfunction was significantly associated with dynamic arytenoid collapse and the odds of detecting intermittent dorsal displacement of the soft palate (DDSP) during exercise in horses with resting DDSP was only 7.7%. Exercising endoscopic observations were different from the resting observations in 54% of examinations.Dynamic upper airway obstructions were common in nonracing performance horses with respiratory noise and/or poor performance. Resting endoscopy was only helpful in determining exercising abnormalities with recurrent laryngeal neuropathy.This study emphasises the importance of exercising endoscopic evaluation in nonracing performance horses with abnormal respiratory noise and/or poor performance for accurate assessment of dynamic upper airway function.
Two mature Border Leicester x Merino wethers were maintained with continuous feeding under therrnoneutral conditions. Their water balance was recorded for 2 weeks; at the beginning of each week they were given a dose of tritiated water (TOR) into the pulmonary artery or the rumen and samples were taken from both the pulmonary artery and the rumen. A four-compartment model was developed which simultaneously fitted the balance and tracer data.
A three-compartment model was developed to provide a simple kinetic description of the metabolism of copper in six sheep with liver copper concentrations of 433�51 ppm ( mean � SD dry weight). This was achieved by measuring the radioactivity in samples of blood, liver, urine and bile as a function of time after the intravenous administration of c. 1.4 mCi of 64Cu. Sizes of compartments, flow rates and rate constants were evaluated and validated experimentally by measuring the excretion of copper in urine and bile and its accumulation in the liver. The model postulates two separate mechanisms for the handling of copper by the liver, and biliary copper excretion was not related to total liver copper content. The model was tested in sheep with a wider range of liver copper concentrations, and the copper in the two compartments (C2 and C3), attributed to liver, corresponded to the actual liver copper content when this was between 30 and 70 mg. The rate constants also responded consistently to increased liver copper status. Within the 'normal' liver copper range of 50-70 mg, the three-compartment model was closed but outside this range, the undefined parameter K03 was no longer zero. This response suggests that copper is moving from C2 and C3 to either supply tissue requirements or be redistributed in an additional storage compartment.
Compartmental modelling techniques were used to measure the absorption of calcium and phosphorus in young sheep which had been fed ad libitum for 6 months on one of four diets containing 1.35 or 8.2 g calcium and 0.72 or 4.5 g phosphorus per kg dry matter. In most of the compartmental models, absorption could be represented by a primary and secondary compartment. The percentage of 45Ca absorbed increased as calcium intake decreased so that the amount of calcium absorbed was not greatly affected by changes in the dietary intake or abomasal contents of calcium. Also, there were no differences due to treatment in the amount of calcium absorbed by primary or secondary absorption. The percentage of 32P absorbed did not vary between treatments, although the percentage absorbed by primary absorption was higher in sheep on low phosphorus diets. For secondary absorption, the percentage absorbed was higher in sheep on high phosphorus diets. The amount of phosphorus absorbed by primary absorption was the same for all treatments; however, sheep on low phosphorus diets absorbed very little phosphorus by secondary absorption, whereas sheep on high phosphorus diets absorbed 2.5 times as much phosphorus as those on low phosphorus diets. The amounts of mineral absorbed by primary absorption for phosphorus and calcium, and by secondary absorption for calcium, were not altered by changes in the amount of phosphorus or calcium mixed with the tracer, indicating that primary absorption may be saturable for phosphorus and calcium and secondary absorption for calcium. The large absorption of phosphorus by the secondary compartment was proportional to the amount of phosphorus in the lower small intestine and therefore the phosphorus was probably absorbed by a non-saturable mechanism.
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The control of phosphorus excretion in sheep has been examined by constructing a kinetic model that contains a mechanistic set of connections between blood and gastrointestinal tract. The model was developed using experimental data from chaff-fed sheep and gives an accurate description of the absorption and excretion of phosphorus in feces and urine of the ruminating sheep. Simulation of the response to an intravenous phosphorus infusion by adding an inflow of 2 g/day of phosphorus into the compartment describing blood, predicted values for fecal output of phosphorus lower than found experimentally. However, by alteration of the parameters describing absorption or salivation, the predictions approached experimental values. Similarly simulation of the conditions existing when a liquid diet was infused directly into the abomasum, i.e., a decrease in salivation rate [L(4.1)] and dietary phosphorus entering compartment 5 (abomasum) instead of compartment 4 (rumen), gave incorrect predictions for plasma and urinary phosphorus, but when the parameter for urinary phosphorus was increased the predicted values approached experimental values. These results indicated the main control site for phosphorus excretion in the ruminating sheep was the gastrointestinal tract, whereas for the nonruminating sheep fed the liquid diet, control was exerted by the kidney. A critical factor in the induction of adaptation of phosphorus reabsorption by the kidney was the reduction in salivation, and since this response occurred independently of marked changes in the delivery of phosphorus to the kidney, a humoral factor may be involved in this communication between salivary gland and kidney.
A 'portable' rainfall simulator was used on alpine soils on the Bogong High Plains in Victoria, to determine the relationship of surface runoff to soil moisture, rainfall intensity, slope and the percentage of the area lacking vegetation cover (bare ground). A strong inverse relationship (R' = 0.64) existed between total runoff and antecedent soil moisture conditions. The other factors, within the range evaluated in these experiments (bare ground 0 to 33'70, rainfall intensity 37 to 97 mm/hr and slope 6 to 23%) had no significant influence on runoff. Time to runoff initiation was influenced by antecedent soil moisture, slope and rainfall intensity ( ~ ~ ~ 0 . 7 1 ) . It was found that time to runoff decreased as the soils dried, and the slope and rainfall intensity increased. The percentage of bare ground had little influence on the time to runoff initiation. These results show that differences in grassland condition, including large differences in the percentage of bare ground, had little influence on either surface runoff or on the time to runoff initiation. The single most important factor influencing runoff rates was the antecedent moisture content of the soil. This factor is generally outside management control.
Hyperinsulinemia is frequently associated with a variety of insulin-resistant states and has been implicated causally in the development of insulin resistance. This study examines the metabolic consequences of prolonged hyperinsulinemia in humans. Basally and 1 h after cessation of a 20-h infusion of insulin (0.5 mU · kg−1 · min−1, aimed at elevating plasma insulin levels to ∼30 mU/L) or normal saline, subjects were assessed for 1) glucose turnover with 3-[3H]glucose; 2) insulin sensitivity, as measured by either the euglycemic glucose-clamp technique or the intravenous glucose tolerance test (IVGTT) minimal model method of Bergman; and 3) monocyte insulin-receptor binding. Hepatic glucose production (Ra) was suppressed by >95% during each euglycemic clamp and during the 20-h insulin infusion. After the insulin infusion, Ra and glucose utilization rate returned to the initial basal level within 1 h, as did insulin levels. At that time, insulin sensitivity was significantly decreased, as measured by the “insulin action” parameter during the 40- to 80-min phase of the clamp (0.049 ± 0.003 vs. 0.035 ± 0.007 min−1 P < .05) and during the 80- to 120-min phase (0.047 ± 0.005 vs. 0.039 ± 0.007 min−1, .05 < P < .1). The IVGTT minimal model analysis revealed a fall in the rate of glucose disposal (KGTT) (2.8 ± 0.6 vs. 1.9 ± 0.2 min−1 P < .05), which was entirely explained by a decrease in insulin sensitivity (SI, 9.4 ± 0.3 vs. 3.8 ± 0.2 min−1 · μU−1 · ml−1, P < .02); there was no change in glucose-mediated glucose disposal (SG, 0.029 ± 0.004 vs. 0.029 ± 0.004 min−1) or pancreatic Ybgr;-cell responsiveness (ø1, 2.7 ± 0.4 vs. 2.6 ± 0.5 μU · ml−1 · min mg−1 · dl−1; ø2, 7.8 ± 2.4 vs. 7.8 ± 2.4 μU · ml−1 · min−2 – mg−1 · dl−1). Monocyte insulin-receptor binding was unaffected by the prolonged hyperinsulinemia. Our studies indicate that modest sustained hyperin- sulinemia may lead to decreased insulin action in the presence of normal monocyte insulin-receptor binding and normal pancreatic insulin secretion. If the monocyte reflects insulin binding in the key insulin-sensitive tissues, this defect in insulin action probably lies at a postreceptor level.
For raindrop-size distributions of the form ND = N0e−ΛD, where ND is the number of drops of diameter D per unit volume per unit increment in drop diameter, the parameters N0 and Λ cannot be specified independently as functions of rainfall rate R. A universal relationship exists between Λ and R/N0 for such distributions as established by Ulbrich and Atlas. The relationship is further examined and expanded in this paper. The results are presented graphically and the self-consistency of empirically derived drop-size distributions examined.
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