Trabecular bone remodeling and bone mineral density in the adult cat during chronic dietary acidification with ammonium chloride.

Ammonium chloride (NH4Cl) is used as a urinary acidifier in the treatment and prevention of feline urologic syndrome. It is reported to cause alterations in calcium and bone metabolism in humans, dogs, and rats. Adult cats with normal renal function were fed 1.5% NH4Cl for 6 months to study the effects of chronic dietary acidification on trabecular bone remodeling of the iliac crest and bone mineral density (BMD) of lumbar vertebral trabecular bone and femoral cortex. Histomorphometric analyses of iliac crest biopsies were performed before and after treatment. Static and dynamic parameters of bone resorption and formation were determined. Single-energy quantitative computed tomography (SEQCT) was used to measure lumbar trabecular and femoral cortical BMD. There were no significant treatment effects in iliac crest trabecular bone remodeling or BMD of the vertebrae and femora. Bone remodeling activity decreased with time in both acidotic and control cats. Vertebral BMD increased with time in both groups of cats, whereas no change was seen in the femora. Thus, chronic dietary acidification for 6 months with therapeutic levels of NH4Cl produced no significant changes in trabecular bone remodeling or bone mineral density in adult cats.

Practical and clinical nutritional concerns during spaceflight.

Experience with space exploration to date has raised more questions regarding nutritional requirements for astronauts than it has answered. As mission lengths continue to increase, nutrient imbalances due to alterations in intake, dietary requirements, bioavailability, or excretion, may become more important. Factors adversely affecting intake include those as straightforward as stress and as complex as space-adaptation syndrome. Metabolic alterations induced by shifts in fluid and electrolyte balance, neuroendocrine function, and changes in hepatic protein synthesis and skeletal muscle type that result in nutrient partitioning to different biochemical pathways may also affect dietary requirements. Food processing effects on nutrient stability and digestibility, which apply to limited quantities of our usual diet on Earth, may become more important for diets that contain little fresh food during extended-length missions. Whereas nutrient and water recycling through ecosystems is taken for granted on Earth, specific effects of trace contaminant accumulation will require greater attention for prolonged space flights. Human factors, esthetics, and user-friendly operations will be necessary to facilitate the psychological as well as physiological health of the astronauts.

The effect of glutathione depletion by buthionine sulphoximine on 1-cyano-3,4-epithiobutane toxicity.

The effect of glutathione (GSH) depletion by buthionine sulphoximine (BSO) on the nephrotoxicity and GSH-enhancing effect of the naturally occurring, crucifer-derived nitrile 1-cyano-3.4-epithiobutane (CEB), was investigated. Male Fischer 344 rats were administered 50 or 125 mg CEB/kg body weight by gavage with or without prior ip treatment with 550 mg/kg body weight L-BSO. One group of control animals was treated with water only by gavage, while another group was pretreated with BSO and then given water by gavage. Liver and kidney samples were taken 48 hr after CEB treatment for GSH determinations and histological examination. The high-dose CEB without BSO resulted in increased GSH in liver and kidney, marked karyomegaly in the pars recta of renal proximal tubules and tubular epithelial necrosis, which was limited to a few renal tubules. The low-dose CEB alone resulted in increased hepatic GSH and mild karyomegaly. Pretreatment with BSO abrogated the tubular necrosis and karyomegaly induced by either CEB dose. BSO pretreatment inhibited low-dose CEB-induced GSH enhancement in the liver. The combined BSO and high-dose CEB treatment still resulted in increased hepatic GSH, although the increase was less than that observed with high-dose CEB alone. In the kidney, BSO pretreatment abrogated the high-dose CEB-induced increase in GSH, but GSH content was not significantly different from that with high- or low-dose CEB alone. These results provide evidence that CEB conjugation may be a bioactivation reaction with the conjugate involved in nephrotoxicity. The conjugate may also be involved in increasing renal and hepatic GSH.

Selective pancreato-toxicity in the rat induced by the naturally occurring plant nitrile 1-cyano-2-hydroxy-3-butene.

The acute toxicity of 1-cyano-2-hydroxy-3-butene (CHB), a nitrile derived from many cruciferous plants, was investigated. Young male CDF (F-344/CrlBr) rats were treated by gavage once daily with 200 mg (2.1 mmol) CHB/kg body weight for 0-4 days and killed 24 hr after the final dose. Lesions were confined to the exocrine pancreas and characterized by individual acinar cell death, inflammation and acinar atrophy and disorganization. Ultrastructural alterations included dilation of cisternae of the acinar cell endoplasmic reticulum, acinar cell death resembling apoptosis, macrophage phagocytosis of acinar cell debris and regenerative changes in remaining acinar cells. Pancreatic, hepatic and renal non-protein thiol concentrations were elevated, suggesting an enhancement of tissue glutathione concentrations and an alteration in glutathione metabolism. Urinary thiocyanate (SCN-) excretion was modestly elevated, indicating some in vivo cyanide release from this nitrile. The results of this study indicate that CHB is a selective pancreatotoxin, inducing changes consistent with apoptosis. CHB is also a possible inducer of tissue glutathione in the liver and kidneys as well as in the pancreas, even at toxic doses.

Sequential changes in hepatic and renal glutathione and development of renal karyomegaly in 1-cyano-3,4-epithiobutane toxicity in rats.

The effect of 1-cyano-3,4-epithiobutane (CEB) on glutathione (GSH) metabolism was investigated in rat liver, kidney and pancreas. Male Fischer 344 rats were gavaged with a single dose (125 mg/kg body weight or 50 mg/kg body weight) of CEB. Tissue samples were taken for histological examination, determination of GSH and oxidized glutathione (GSSG) concentrations and gamma-glutamyl transpeptidase (GGT) and glutathione S-transferase (GST) activities. Urine samples were analysed for non-protein thiol (NP-RSH) content. The high dose of CEB induced hepatic GSH depletion followed by increased GSH. The low dose of CEB induced elevated hepatic GSH by 12 hr without depletion. Renal GSH was increased with both doses without an observed depletion phase. Renal tubule epithelial cell death was observed only with the high dose of CEB, but both doses caused renal proximal tubule karyomegaly. Pancreatic GSH content was unaffected. No alterations of GSSG were observed. GST activity was unaffected in any tissue. Renal GGT activity was decreased at 12 hr with both doses and at 24 and 48 hr with the high dose. Urinary NP-RSH excretion was increased with both doses. Depletion of hepatic GSH concurrent with increased urinary NP-RSH excretion suggests that conjugation with GSH is a significant pathway in CEB metabolism.

Comparative toxicities of the naturally occurring nitrile 1-cyano-3,4-epithiobutane and the synthetic nitrile n-valeronitrile in rats: differences in target organs, metabolism and toxic mechanisms.

Toxic but sublethal oral doses of 125 mg/kg (1.1 mmol/kg) of the cruciferous nitrile, 1-cyano-3,4-epithiobutane (CEB), or 175 mg/kg (2.1 mmol/kg) of its synthetic saturated analogue, n-valeronitrile (VN), were given by gavage to male CDF (F-344/CrlBr) rats once daily for 1, 2 or 3 days, in order to compare target tissues and to observe structure-activity relationships between the nitriles. CEB-induced changes included degeneration and necrosis of the pars recta of the renal proximal tubules, ulceration and necrosis in the forestomach, a mild increase (4.5-fold) in daily urinary thiocyanate (SCN-) excretion (only in rats treated for 3 days) and 1.5- to 2.4-fold increases in hepatic and pancreatic non-protein thiol (RSH) concentrations (in all CEB-treated groups). In VN-treated rats, there were no consistent histological changes but 95- to 170-fold increases in daily urinary SCN- excretion, delayed clinical signs of cyanide toxicity and minimal effects on tissue RSH concentrations. These results indicate different toxic mechanisms for VN and CEB. The nephrotoxic effects of CEB were very similar to those of 1-cyano-2-hydroxy-3,4-epithiobutane, suggesting a role for the epithio group in the nephrotoxicity of these nitriles. The relatively low SCN- excretion in CEB-treated rats also suggested that cyanide played only a minimal role in CEB toxicity, while the high SCN- excretion, clinical signs of cyanide poisoning and lack of histological changes imply a greater role for metabolically-derived cyanide in VN toxicity. The enhancement of tissue RSH by CEB treatment with indications of enhanced tissue glutathione concentrations suggested the involvement of glutathione in the detoxication of CEB and/or its reactive metabolites.

Effects of Escherichia coli on iron, copper, and zinc metabolism in chicks.

The present report describes the effects of Escherichia coli endotoxin and infection on kinetic changes of copper (Cu), iron (Fe), and zinc (Zn) levels in the transport (serum), storage (liver), and immune organs (spleen and bursa of Fabricius) of the chicken. During infection and endotoxin challenge, increased serum and bursal Cu were noted. Infection and endotoxin both led to a redistribution of Fe with a decrease in serum and an increase in the spleen. Infection decreased serum Zn and concomitantly increased hepatic and splenic Zn. Seven days postinfection, when recovery was well underway, hepatic and splenic Cu and splenic Zn were elevated. Hepatic Fe decreased with recovery, whereas splenic Fe increased. Endotoxin and infection changed trace element kinetics. The endotoxin produced tissue elemental alterations similar to the early stages of infection. This indicated that in early infection, some of the disease responses may be due to endotoxin, whereas the later responses may be due to other aspects of infection such as stress.

Effects of neutering on bodyweight, metabolic rate and glucose tolerance of domestic cats.

Few controlled studies have been made of the possible mechanisms and physiological consequences of weight gain after cats have been neutered. In this study, six male and six female cats were gonadectomised and compared with five entire male and six entire female cats, before they were neutered and one and three months later. The neutered males gained significantly more weight (mean [SEM] per cent) than the entire males (30.2 [5.2] v 11.8 [2.3]) and the entire females gained 40.0 (7.3) v 16.1 (3.3) per cent, (P < 0.05). The castrated males gained more weight as fat than the sexually intact males (22.0 [3.3] v 8.8 [4.5] per cent, P < 0.05). There was a significant increase (P < 0.05) in daily food intake after neutering. Spayed females underwent a significant decrease in fasting metabolic rate (83.7 [5.5] v 67.2 [2.3] kcal/kg bodyweight0.75/day P < 0.05). Gonadectomy had minimal effects on serum thyroid hormone concentrations, the resting or fasting metabolic rates in males, or on indices of glucose tolerance.

Effects of weight gain and loss on metabolic rate, glucose tolerance, and serum lipids in domestic cats.

Weight gain is a common problem in domestic cats, but little is known about its metabolic effects. The purpose of this study was to determine the effects of diet-induced weight gain and subsequent weight loss on metabolic rate, body composition, and glucose tolerance. Gain of approximately 20 per cent body weight (divided approximately equally between fat and fat-free mass) over three months resulted in insulin resistance in females, indicated by increases in basal insulin concentration (68.2+/-7.9 to 119+/-16.5 pmol litre(-1), P<0.05), insulin peak response to glucose (241.1+/-31.6 to 315.0+/-23.0 pmol litre(-1), P<0.05), and deltaI/deltaG (14.2+/-2.6 to 18.1+/-1.3 pmol mmol(-1), P<0.05) compared with pre-gain values. The same numerical trend was noted in male cats, however, changes were not significant (P>0.05). Alterations in serum lipids included significant (P<0.05) elevations in triglyceride concentrations in male cats and decreased beta-lipoprotein concentrations in both genders. Weight loss over three months normalised basal insulin, insulin response to glucose, and serum triglyceride concentrations, and resulted in significant (P<0.05) decreases in serum concentrations of beta- and prebeta-lipoproteins, cholesterol, and triiodothyronine. Diet-induced weight gain of three months' duration, followed by three months' maintenance of increased body weight did not affect fasting or resting metabolic rate. Development and severity of impaired glucose tolerance, insulin resistance, and other changes may be affected by duration and possibly severity of weight gain.

Platelet hyperfunction in dogs with malignancies.

In vitro platelet aggregometry was performed on whole blood samples from 59 dogs with malignancies and 24 control dogs. Three reagents were used for the aggregation studies: collagen, arachidonic acid, and adenosine diphosphate (ADP). The parameters measured to evaluate response to collagen included delay in the aggregation response, slope of the aggregation curve, maximum aggregation, and adenosine triphosphate (ATP) secretion. The platelets of dogs with malignancies exhibited significantly (P < .05) shorter delays in the aggregation response, higher maximum aggregation, and higher ATP secretion when compared to control dogs. For the weaker reagents, ADP and arachidonic acid, the lowest concentration resulting in aggregation was determined. Platelets of dogs with malignancies tended to aggregate in response to lower concentrations of ADP than did those of controls (P < .05). The response of platelets to the concentrations of arachidonic acid employed in this study was poor, with few samples achieving measurable aggregation. The findings of this study suggest that dogs with malignancies have hyperaggregable platelets.

Serum bile acid concentrations in dairy cattle with hepatic lipidosis.

This study was designed to evaluate serum bile acid measurements as indicatory, of liver function and/or hepatic fat infiltration in dairy cattle. Serum bile acid concentrations were measured in healthy dairy cattle at different stages of lactation after fasting or feeding. Bile acid concentrations were compared with liver fat content and sulfobromophthalein (BSP) half-life (T 1/2). Serum bile acid concentrations were higher in cows in early lactation and with higher daily milk production. Compared with prefasting values, bile acid concentrations were decreased at 8, 14, and 24 hours of fasting. Blood samples from fed cows at 1- to 2-hour intervals had wide and inconsistent variations in bile acid concentration. Because serum bile acids correlated well with BSP T 1/2, it is suggested that both measurements evaluate a similar aspect of liver function. Neither bile acids nor BSP T 1/2 correlated with differences in liver fat content among cows. Because of large variability in serum bile acid concentrations in fed cows and the lack of correlation of measured values with liver fat content, bile acid determinations do not appear useful for showing changes in hepatic function in fed cows with subclinical hepatic lipidosis nor serve as a screening test for this condition.

Hepatic lipidosis in anorectic, lactating holstein cattle: a retrospective study of serum biochemical abnormalities.

The association between hepatic lipidosis (HL) and disease in 59 anorectic, ketotic, lactating Holstein heifers and cows was investigated. Severe HL, as determined by histologic evaluation of liver tissue, was present in 46 animals; only half of these animals required intensive treatment for ketosis, and only half had serum biochemical evidence of liver disease, as determined by the presence of a last value of 2-fold or greater than the upper limit of the reference ranges for at least 2 of the 4 serum tests: gamma-glutamyl transferase, aspartate aminotransferase, and sorbitol dehydrogenase activities and bile acid concentrations. Most cattle with biochemical evidence of liver disease and severe HL had been lactating for 14 or more days. Cows that required intensive treatment inconsistently had serum biochemical evidence of liver disease. Although cattle with severe HL had significantly higher serum bilirubin concentrations and aspartate aminotransferase and sorbitol dehydrogenase activities than cattle with less severe lipidosis, the specificity of abnormally high serum sorbitol dehydrogenase activity or bilirubin concentration for severe lipidosis was only 8%. Abnormally high serum aspartate aminotransferase activity was 83% sensitive and 62% specific for severe lipidosis. Serum glucose and total carbon dioxide concentrations were significantly lower in cattle with severe lipidosis than in those with mild or moderate lipidosis, and low serum glucose or total carbon dioxide concentrations were rare in cattle without severe lipidosis. From these data, we conclude that the use of a single biochemical or histopathologic criterion to define severity of disease or degree of liver compromise in anorectic, ketotic cows results in the misidentification of many animals.

Platelet function in dogs treated for lymphoma and hemangiosarcoma and supplemented with dietary n-3 fatty acids.

A prospective randomized, double-blind clinical trial was performed to test the hypothesis that dogs with malignancies that are supplemented with n-3 fatty acids do not have clinical or laboratory evidence of coagulation disorders or altered platelet function when compared with unsupplemented dogs with similar malignancies. Thirteen dogs with hemangiosarcoma and 66 dogs with lymphoma were evaluated. Coagulation status of the dogs with lymphoma and hemangiosarcoma was evaluated with prothrombin time, partial thromboplastin time, platelet count, and in vitro platelet aggregometry using the whole-blood method. These tests were performed at 5 time points: before beginning the diet (week 0), at weeks 3, 15, and 21, and at 1 year or when progressive disease was evident. Alterations in platelet function in dogs receiving a diet supplemented with dietary n-3 fatty acids were not identified when compared to dogs fed a control diet. Dietary n-3 fatty acid supplementation using this dosage and ratio in dogs with lymphoma or hemangiosarcoma did not induce clinically significant hemorrhage in these animals. Therefore, supplementation with n-3 fatty acids did not result in clinical or laboratory evidence relating to uncontrolled hemorrhage in these dogs.

Exacerbation of hyperlactatemia by infusion of lactated Ringer's solution in dogs with lymphoma.

Blood lactate concentrations and acid-base status of six dogs with lymphoma were compared statistically with those from six healthy control dogs before, during, and after a 6-hour infusion of lactated Ringer's solution (LRS). Blood lactate concentrations in dogs with lymphoma were significantly (P less than 0.05) higher immediately before, and at the 1-, 2-, 4-, and 6-hour time periods after infusion when compared with controls. Blood lactate concentrations increased significantly (P = 0.016) after the first hour of infusion in dogs with lymphoma but did not increase in the control dogs. The increase in blood lactate concentrations over baseline values after 1 hour of LRS infusion was significantly (P = 0.008) greater in dogs with lymphoma when compared with controls. Blood lactate concentrations returned to baseline levels after 2 hours of infusion in dogs with lymphoma, suggesting that dogs with lymphoma have a transient inability to handle increased lactate loads when compared with controls. However, the potential to augment lactate use, clearance, or both is present and does occur over time. Blood gas values were not significantly altered within the lymphoma or control dog groups after 6 hours of LRS infusion. Blood bicarbonate concentrations in dogs with lymphoma were significantly decreased before and after LRS infusion when compared with controls.

Identification of matrix metalloproteinases in canine cutaneous mast cell tumors.

Presence of matrix metalloproteinases has been associated with tumor invasion and metastasis in human neoplasia. The presence of matrix metalloproteinase 2 and matrix metalloproteinase 9 was determined in canine mast cell tumor tissue and normal stromal tissue from 24 dogs with spontaneously occurring cutaneous mast cell tumors. Seventeen of the mast cell tumors were of histologic grade 2, and 7 were of histologic grade 3. Gelatin zymography and computer assisted densitometry image analysis were used to quantify matrix metalloproteinase concentration. Bands from canine tissues migrated in the same location as human proenzyme and active enzyme matrix metalloproteinase 2 and matrix metalloproteinase 9 standards. A semiquantitative value for each patient sample was obtained by comparing the optical assessment density of each unknown band to the optical density of the human standard. The presence of matrix metalloproteinase 2 and matrix metalloproteinase 9 in histologic grade 2 mast cell tumors and histologic grade 3 mast cell tumors was compared, as was presence of matrix metalloproteinases in tumor and stromal tissue. There was dramatically more proenzyme matrix metalloproteinase 9 activity in histologic grade 3 mast cell tumors when compared to grade 2 tumors (P = .03). There was also dramatically more active enzyme matrix metalloproteinase 2 and active enzyme matrix metalloproteinase 9 activity in tumor tissue compared to stromal tissue (P = .02, P < .0001). This study demonstrates that the proenzyme and active enzyme forms of matrix metalloproteinase 2 and matrix metalloproteinase 9 are present in canine mast cell tumors. This appears to be related to the degree of histologic malignancy, although histologic grade 1 tumors were not evaluated.

Estimation of quantitative enzymuria in dogs with gentamicin-induced nephrotoxicosis using urine enzyme/creatinine ratios from spot urine samples.

The correlation between 24-hour urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) and gamma-glutamyl transferase (GGT) with urine NAG and GGT/creatinine ratios was assessed in dogs with gentamicin-induced nephrotoxicosis. Eighteen 6-month-old male Beagles with normal renal function were randomly divided into 3 groups of 6. Each group was fed a different concentration of protein (high protein, 27.3%; medium protein, 13.7%; and low protein, 9.4%) for 21 days. After dietary conditioning, gentamicin was administered at a dose of 10 mg/kg IM tid for 8 days and each group was continued on its respective diet. Endogenous creatinine clearance and 24-hour urinary excretion of NAG and GGT were determined after dietary conditioning (day 0) and on days 2, 4, 6, and 8 of gentamicin administration. In addition, urine NAG and GGT/creatinine ratios (IU/L divided by mg/dL) were determined from catheterized spot urine samples obtained between 7 and 10 AM on the same days. The correlation between 24-hour urinary enzyme excretion and urine enzyme/creatinine ratio in the spot urine samples was evaluated by simple linear regression analysis. Spot sample urine enzyme/creatinine ratios were significantly correlated with 24-hour urinary enzyme excretion through day 4 for dogs on low dietary protein, through day 6 for those on medium protein, and through day 8 for those on high dietary protein. Mean +/- SD baseline values for urine NAG/creatinine ratio and 24-hour urinary NAG excretion were 0.06 +/- 0.04 and 0.19 +/- 0.14 IU/kg/24 hr, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations in lipoprotein profiles in dogs with lymphoma.

After a 12-hour fast, blood samples were obtained from 31 dogs with previously untreated lymphoma. Blood samples were also collected from 16 of these dogs after up to 5 treatments with doxorubicin (30 mg/m2 intravenously every 3 weeks). All 16 dogs underwent complete remission. Five dogs were re-evaluated after relapse and after overt signs of cancer cachexia had become clinically apparent. Samples were assayed for 8 quantitative parameters: total cholesterol (T-CH) and total triglyceride (T-TG) concentrations, and the concentration of cholesterol and triglyceride in each of the three major lipoprotein fractions, very-low-density lipoprotein (LDL-CH and LDL-TG), and high-density lipoprotein (HDL-CH and HDL-TG). The results were compared with those from 20 healthy control dogs of similar weight and age before and 3 weeks after being given one dose of doxorubicin (30 mg/m2 intravenously). The administration of doxorubicin to control dogs resulted in a significant (P < .05) decrease in T-CH, LDL-CH, and HDL-CH, as well as a significant increase in VLDL-TG and HDL-TG. When compared with untreated controls, untreated dogs with lymphoma had significantly higher concentrations of VLDL-CH, T-TG, VLDL-TG, LDL-TG, and HDL-TG, and significantly lower concentrations of HDL-CH. HDL-TG and VLDL-TG concentrations from dogs with lymphoma were significantly increased above pretreatment values after relapse and development of overt signs of cancer cachexia.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of dobutamine infusion to exercise as a cardiac stress test in healthy horses.

This study was done to determine whether administration of dobutamine would produce echocardiographic and electrocardiographic alterations comparable to those induced by treadmill exercise in healthy horses. Fourteen horses received maximal treadmill exercise and, separately, intravenous dobutamine infusion up to a maximum rate of 50 microg/kg/min. Ten of the 14 horses were euthanized, and the myocardial tissues were examined grossly and histopathologically. No significant differences were found in the chronotropic effects of dobutamine and exercise (P = .905). Dobutamine induced greater interventricular septal thickening during systole (dobutamine = 4.78 cm, exercise = 4.03 cm; P = .004). and greater left ventricular diameters during diastole (dobutamine = 9.73 cm, exercise = 9.26 cm; P = .037), than did exercise treatment. Horses exhibited transient signs of sweating and restlessness during infusion of moderate to maximum doses of dobutamine. Ventricular ectopy seen in 11 of 14 horses was attributed to the arrhythmogenic properties of dobutamine, as well as to increased vagal tone present at low dobutamine doses. Myocardial lesions characteristic of catecholamine myotoxicity were present in 2 of the 10 horses examined. Although dobutamine induces chronotropic and inotropic changes similar to those induced by exercise, the use of high-dose dobutamine as a cardiac stressor in horses cannot be advocated because of potential development of arrhythmias or myotoxicity.

Treatment of neonatal calf diarrhea with an oral electrolyte solution supplemented with psyllium mucilloid.

Dairy calves under 14 days of age with naturally occurring, uncomplicated diarrhea were treated for 3 days with a hypertonic oral electrolyte solution with (n = 15) or without (n = 12) psyllium. Clinical response and clinical pathology data were compared between the 2 groups. Glucose absorption was evaluated on days 1 and 3 by measurement of plasma glucose and lactate and serum insulin concentrations for 4 hours after formula administration. On day 1, glucose, lactate, and insulin concentrations were lower in psyllium-fed calves than in control calves, with significant differences noted in glucose and lactate concentrations at several time points (P < 0.05). Plasma lactate concentrations were higher at several times in both treatment groups on day 3 than on day 1 (P < 0.05). Fecal consistency was markedly different in psyllium-fed calves as compared with control calves within 24 hours of psyllium supplementation. Fecal percent dry matter content was lower in psyllium-fed calves than in control calves at least once a day during supplementation and on day 3 compared with day 0 in the psyllium-fed calves (P < 0.05). There were no significant differences in clinical performance scores, hydration status, arterial blood gas, serum anion gap, electrolyte, or total CO2 concentrations. Addition of psyllium to an oral electrolyte solution resulted in immediate alterations in glucose absorption without impairing rehydration in diarrheic calves, but differences were transient and did not affect clinical outcome.

Alterations in carbohydrate metabolism in canine lymphoma.

Following an overnight fast, blood samples were obtained from 14 dogs with previously untreated lymphoma before and 5, 15, 30, 45, 60, and 90 minutes following an intravenous challenge with 500 mg/kg dextrose. Samples were assayed for glucose, lactate, and insulin concentrations and compared statistically with ten control dogs of similar weight and age undergoing an identical dextrose challenge. Dogs with lymphoma had similar glucose tolerance curves when compared with controls. Lactate concentrations were significantly higher (P less than 0.001) at baseline and all time periods of the glucose tolerance test in dogs with lymphoma when compared with controls. Rise in lactate concentrations over baseline levels in the first 30 minutes of the glucose tolerance test were significantly higher in dogs with lymphoma (P = 0.011). Insulin concentrations were significantly higher (P less than 0.001) at baseline and at the 5-, 45-, 60-, and 90-minute time periods of the glucose tolerance test in dogs with lymphoma. Rise in insulin concentrations over baseline in the first 5 minutes of the glucose tolerance test were also significantly greater in dogs with lymphoma (P = 0.021). These results indicate carbohydrate metabolism is altered in dogs with lymphoma. Many of these alterations parallel those observed in human patients suffering from cancer cachexia making canine lymphoma a potential model for further study of the pathogenesis and therapy of cancer cachexia.