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  • Author or Editor: Walter E. Hoffmann x
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SUMMARY

The effects of whole-body potassium depletion induced by food deprivation on plasma, erythrocyte, and middle gluteal muscle K concentrations was quantified in 16 healthy, adult horses before, during, and at the end of a 7-day period of food deprivation during which water and sodium chloride were available ad libitum. Potassium concentrations were determined by atomic absorption spectroscopy.

Plasma K concentration remained constant (3.49 ± 0.09 mM K/L of plasma; mean ± sem) throughout the study. Erythrocyte potassium concentration decreased from 93.10 ± 1.94 mM K/L of erythrocytes on day 0 to 88.63 ± 2.39 mM K/L of erythrocytes on day 2 (decrease of 4.8%; P < 0.05) and thereafter did not change. The K concentration of the middle gluteal muscle decreased from 91.06 ± 2.96 μM K/g of muscle (wet weight) to 79.61 ± 2.09 μM K/g of muscle (decrease of 12.6%; P < 0.05) on day 4 and decreased further on day 7 to 73.62 ± 1.85 μM K/g of muscle (decrease of 19.2%; P < 0.05). There was no correlation between the plasma and erythrocyte K concentrations (r = −0.066), the erythrocyte and middle gluteal muscle K concentrations (r = 0.167), or the plasma and middle gluteal muscle potassium concentrations (r = −0.018). The water content of the middle gluteal muscle remained constant (73.23 ± 0.36%) throughout the study.

Erythrocyte membrane potential did not change (−99.26 ± 0.87 mV) during the study, whereas the magnitude of the membrane potential of the middle gluteal muscle decreased from −105.84 ± 1.67 mV on day 0 to −100.93 ± 2.10 mV on day 7 (P < 0.05).

Free access
in American Journal of Veterinary Research

Abstract

Objective—To evaluate the influence of a 1,4- butanedisulfonate stable salt of S-adenosylmethionine (SAMe) administered orally on clinicopathologic and hepatic effects induced by long-term administration of prednisolone in dogs.

Animals—12 healthy dogs.

Procedure—Following a pilot study (4 dogs), 2 groups of 4 dogs received prednisolone (2.2 mg/kg) orally once daily (84-day trial). One group received SAMe (20 mg/kg/d divided in 2 doses) for 42 days and then a placebo for 42 days; the other group received treatments in the reverse order. Before and during the trial, numerous variables were monitored, including serum total alkaline phosphatase (ALP) and glucocorticoid- induced ALP (G-ALP) activities, serum haptoglobin concentration, and total and oxidized glutathione (TGSH and GSSG) and thiobarbiturate-reacting substances (TBARS) concentrations in erythrocytes and liver tissue (days 0, 42, and 84). Hepatic specimens also were examined microscopically.

Results—The stable salt of SAMe was biologically available; plasma concentrations of SAMe or prednisolone were not affected by coadministration. Compared with baseline values, serum ALP and GALP activities and haptoglobin concentrations increased and erythrocyte GSSG and TBARS concentrations decreased with both treatments. Erythrocyte TGSH concentration decreased with the prednisolone- placebo treatment. Administration of SAMe appeared to conserve erythrocyte TGSH values and did not inhibit hepatocyte glycogen vacuolation but increased hepatic TGSH concentration and improved the hepatic tissue GSSG:TGSH ratio.

Conclusions and Clinical Relevance—In dogs, administration of 20 mg of SAMe/kg/d may mitigate the apparent pro-oxidant influences of prednisolone but did not block development of classic clinicopathologic or histologic features of vacuolar hepatopathy. (Am J Vet Res 2005;66:330–341)

Full access
in American Journal of Veterinary Research

Summary

High serum alkaline phosphatase (alp) activity is considered a sensitive marker of cholestasis in most mammalian species, including dogs. Induction of high serum alp activity in association with cholestasis is dependent on high hepatic bile acids concentrations. Treatment of dogs with glucocorticoids also results in high serum alp activity. The possible causal relation between serum alp activity and bile acids concentration was investigated in dogs treated with glucocorticoids. The relation of glucocorticoid treatment to changes in the activity of individual alp isoenzymes, alanine transaminase (alt) and γ-glutamyltransferase (ggt) also was investigated.

Eight conditioned dogs were given 4 mg of prednisone/kg of body weight, im, daily for 10 days. Blood samples were taken prior to treatment and on treatment days 3, 5, 7, and 10. Liver tissue was then taken from each dog. Serum total alp activity was significantly (P < 0.05) high at day 3 in prednisone-treated dogs. Isoenzyme analysis indicated that this increase was attributable to an increase in the liver alp isoenzyme (LALP). Significant increases in serum corticosteroid-induced alp (calp) and bone alp were first observed on days 7 and 10, respectively. Serum alt and ggt activities were significantly increased by day 5. Increased serum or hepatic tissue bile acids concentrations were not observed in prednisonetreated dogs, compared with values in 8 clinically normal (control) dogs, but were high in 3 dogs with complete bile duct ligation.

Hepatic activities of LALP, calp, and ggt were higher in prednisone-treated dogs than values in controls, indicating probable increased hepatic synthesis of these enzymes. Hepatic alt activity was not increased. The ratio of serum to tissue lalp activity was increased in prednisone-treated dogs, compared with values in controls, indicating that lalp may have been preferentially released into serum. There was no difference in the ratio of serum to liver ggt activity between prednisone-treated dogs and controls. The lalp and ggt ratios were increased in bile duct-obstruction dogs.

It was concluded that, although lalp is the principal alp isoenzyme in serum during the first 10 days of prednisone treatment, hepatic bile acid concentrations are not increased and, therefore, are not likely to be responsible for induction and release of alp into serum. Prednisone may, therefore, be directly responsible for induction of alp activity in dogs treated thusly.

Free access
in American Journal of Veterinary Research

SUMMARY

Assay procedures for determining serum haptoglobin concentration and ceruloplasmin oxidase activity in dogs were validated, and reference values were established. Serum haptoglobin concentration is reported as milligrams per deciliter of cyanmethemoglobin binding capacity, whereas serum ceruloplasmin oxidase activity was determined by use of p-phenylenediamine as substrate. Both assays were used to analyze serum samples from 288 dogs. In each dog’s case record, clinical history and final diagnosis were evaluated to determine whether the dog had an inflammatory condition. Complete blood cell counts were performed in 265 dogs, using simultaneously collected blood samples. Plasma fibrinogen concentration was determined for 161 dogs. A positive correlation (P < 0.01) was found for serum haptoglobin concentration and for ceruloplasmin oxidase activity, compared with wbc counts, segmented neutrophil and band neutrophil counts, and plasma fibrinogen concentration. Ceruloplasmin oxidase activity and haptoglobin concentration were up to 6 times more sensitive than fibrinogen concentration or leukocyte counts in detecting inflammation. Specificity of ceruloplasmin oxidase activity was comparable to fibrinogen concentration and leukocyte counts, whereas haptoglobin concentration was found to be slightly less specific. Specificity of haptoglobin concentration improved slightly (from 0.82 to 0.88) when dogs with a history of glucocorticoid administration were excluded from analysis. Predictive value of a negative test result (haptoglobin concentration < 125 mg/dl; ceruloplasmin oxidase activity < 20 IU/L) and predictive value of a positive test result for haptoglobin concentration and ceruloplasmin activity were comparable to or better than fibrinogen concentration or various oxidase leukocyte counts in detection of inflammation in a variety of disease conditions. We concluded that serum haptoglobin and ceruloplasmin oxidase assays could be used as adjuncts for diagnosis of the inflammation in dogs.

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine causes of hyperphosphatasemia (high serum alkaline phosphatase [ALP] activity) in apparently healthy Scottish Terriers.

Design—Prospective case-controlled study.

Animals—34 apparently healthy adult Scottish Terriers (17 with and 17 without hyperphosphatasemia).

Procedures—Serum activities for 3 isoforms (bone, liver, and corticosteroid) of ALP were measured. Concentrations of cortisol, progesterone, 17-hydroxyprogesterone, androstenedione, estradiol, and aldosterone were measured before and after cosyntropin administration (ie, ACTH; 5 μg/kg [2.27 μg/lb], IM). Liver biopsy specimens from 16 dogs (11 with and 5 without hyperphosphatasemia) were evaluated histologically.

Results—In dogs with hyperphosphatasemia, the corticosteroid ALP isoform comprised a significantly higher percentage of total ALP activity, compared with the percentage in dogs without hyperphosphatasemia (mean ± SE, 69 ± 5.0% and 17 ± 3.8%, respectively). In 6 dogs with hyperphosphatasemia, but none without, serum cortisol concentrations exceeded reference intervals after ACTH stimulation. Six dogs with and 15 without hyperphosphatasemia had increased concentrations of ≥ 1 noncortisol steroid hormone after ACTH stimulation. Serum ALP activity was correlated with cortisol and androstenedione concentrations (r = 0.337 and 0.496, respectively) measured after ACTH stimulation. All dogs with and most without hyperphosphatasemia had abnormal hepatocellular reticulation typical of vacuolar hepatopathy. Subjectively, hepatocellular reticulation was more severe and widespread in hyperphosphatasemic dogs, compared with that in nonhyperphosphatasemic dogs.

Conclusions and Clinical Relevance—Hyperphosphatasemia in apparently healthy Scottish Terriers was most likely attributable to hyperadrenocorticism on the basis of exaggerated serum biochemical responses to ACTH administration and histologic hepatic changes, but none of the dogs had clinical signs of hyperadrenocorticism.

Full access
in Journal of the American Veterinary Medical Association