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Characterization of the use of antiemetic agents in dogs with parvoviral enteritis treated at a veterinary teaching hospital: 77 cases (1997-2000).

OBJECTIVE: To characterize the use of antiemetic agents in dogs with canine parvovirus (CPV)-associated enteritis in a veterinary teaching hospital. DESIGN: Retrospective case series. ANIMALS: 77 dogs with CPV-associated enteritis. PROCEDURE: Medical records of 560 dogs with confirmed CPV-associated enteritis that were admitted to a veterinary teaching hospital were reviewed. Exclusion criteria included vaccination against CPV infection within the preceding 2 weeks, hospitalization for < 24 hours or removal from the hospital against advice, or an incomplete record. Signalment, duration of hospitalization, and daily antiemetic administrations were assessed; WBC counts and clinical findings were used to classify dogs as having systemic inflammatory response syndrome (SIRS). RESULTS: 77 dogs were included in the study; 55 (71%) received antiemetics (53 received metoclopramide at least once). Seventy-one dogs survived, and 6 dogs died (all 6 received antiemetics). Compared with dogs that did not receive antiemetics, duration of hospitalization was significantly longer for antiemetic-treated dogs. Daily values of rectal temperature and heart and respiratory rates did not predict administration of antiemetics or duration of hospitalization; however, compared with survivors, SIRS developed more frequently among nonsurvivors. Assessment of emetic events recorded hourly for 17 dogs indicated that antiemetic treatment did not control emesis. CONCLUSIONS AND CLINICAL RELEVANCE: Many dogs with CPV-associated enteritis had persistent vomiting despite antiemetic administration. The apparent difference in duration of hospitalization between antiemetic-treated dogs and other dogs may reflect a difference in disease severity between groups, although antiemetic-associated adverse events (e.g., signs of depression, hypotension, and immune modulation) may prolong hospitalization.

Animals↗

Frequency of urinary tract infection among dogs with pruritic disorders receiving long-term glucocorticoid treatment.

OBJECTIVE: To determine frequency of urinary tract infection (UTI) among dogs with pruritic disorders that were or were not receiving long-term glucocorticoid treatment. DESIGN: Observational study. ANIMALS: 127 dogs receiving glucocorticoids for > 6 months and 94 dogs not receiving glucocorticoids. PROCEDURE: Bacterial culture of urine samples was performed in dogs receiving long-term glucocorticoid treatment, and information was collected on drug administered, dosage, frequency of administration, duration of glucocorticoid treatment, and clinical signs of UTI. For dogs not receiving glucocorticoids, a single urine sample was submitted for bacterial culture. RESULTS: Multiple (2 to 6) urine samples were submitted for 70 of the 127 (55%) dogs receiving glucocorticoids; thus, 240 urine samples were analyzed. For 23 of the 127 (18.1%) dogs, results of bacterial culture were positive at least once, but none of the dogs had clinical signs of UTI. Pyuria and bacteriuria (present vs absent) were found to correctly predict results of bacterial culture for 89.9% and 95.8% of the samples, respectively. Type of glycocorticoid, dosage, frequency of administration, and duration of treatment were not associated with frequency of UTI. None of the urine samples from dogs not receiving glucocorticoids yielded bacterial growth. The frequency of UTI was significantly higher for dogs treated with glucocorticoids than for dogs that had not received glucocorticoids. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that dogs receiving long-term glucocorticoid treatment have an increased risk of developing a UTI. On this basis, we recommend that urine samples be submitted for bacterial culture at least yearly for such dogs.

Animals↗

Detection of portal and systemic bacteremia in dogs with severe induced hepatic disease and multiple portosystemic shunts.

OBJECTIVE: To determine existence of portal and systemic bacteremia in dogs with induced severe hepatic disease, compared with clinically normal dogs, before and after vena caval banding. ANIMALS: 6 control dogs and 10 dogs with induced severe hepatic disease and multiple portosystemic shunts (PSS). PROCEDURE: Dogs of the diseased group were given dimethylnitrosamine (2 mg/kg of body weight, PO) twice weekly until multiple PSS developed. Surgery was performed on dogs of both groups, and blood for baseline aerobic and anaerobic bacterial culture was collected from catheters placed in the portal and hepatic veins and caudal vena cava. All dogs underwent vena caval banding, and blood for aerobic and anaerobic bacterial culture was collected from the portal and hepatic venous catheters at 120, 240, and 360 minutes after banding. RESULTS: Compared with control dogs (16% gram-positive and 84% gram-negative bacteria), diseased dogs had significantly higher percentage of gram-positive bacteria (42% of positive culture results, P < or = 0.01) and significantly lower percentage of gram-negative bacteria (58% of positive culture results, P < or = 0.01) isolated. Pseudomonas aeruginosa was isolated most frequently from dogs of both groups; more than 1 organism was isolated from 5 dogs of each group. Antimicrobial susceptibility included that to aminoglycosides (particularly amikacin), fluorinated quinolones, and imipenem. CONCLUSION: Portal and systemic, predominantly gram-negative, bacteremia is present in catheterized, clinically normal dogs and dogs with dimethylnitrosamine-induced hepatic disease and multiple PSS.

Amikacin↗

Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995-1998).

OBJECTIVE: To determine relationships between plasma lactate concentration and gastric necrosis and between plasma lactate concentration and outcome for dogs with gastric dilatation-volvulus. DESIGN: Retrospective study. ANIMALS: 102 dogs. PROCEDURE: Information on signalment, history, plasma lactate concentration, medical and surgical treatment, cost of hospitalization, and outcome was retrieved from medical records. RESULTS: 69 of 70 (99%) dogs with plasma lactate concentration < 6.0 mmol/L survived, compared with 18 of 31 (58%) dogs with plasma lactate concentration > 6.0 mmol/L (1 dog euthanatized for economic reasons was not included). Gastric necrosis was identified in 38 (37%) dogs. Median plasma lactate concentration in dogs with gastric necrosis (6.6 mmol/L) was significantly higher than concentration in dogs without gastric necrosis (3.3 mmol/L). Specificity and sensitivity of using plasma lactate concentration (with a cutoff of 6.0 mmol/L) to predict which dogs had gastric necrosis were 88 and 61%, respectively. Sixty-two of 63 (98%) dogs without gastric necrosis survived, compared with 25 of 38 (66%) dogs with gastric necrosis. CONCLUSIONS AND CLINICAL RELEVANCE: Preoperative plasma lactate concentration was a good predictor of gastric necrosis and outcome for dogs with GDV. Preoperative measurement of plasma lactate concentration may assist in determining prognosis of dogs with GDV.

Animals↗

Percutaneous ultrasound-guided chemical parathyroid ablation for treatment of primary hyperparathyroidism in dogs.

OBJECTIVE: To evaluate the efficacy, feasibility, and safety of ultrasound-guided chemical ablation of parathyroid masses in dogs with primary hyperparathyroidism. DESIGN: Prospective clinical trial. ANIMALS: 8 dogs. PROCEDURE: In all dogs, a solitary parathyroid mass was evident ultrasonographically. Dogs were anesthetized with propofol, and a 27-gauge needle was directed into the parathyroid mass under ultrasound guidance. Ethanol (96%) was injected into the mass until there was evidence of diffusion of fluid throughout the mass. Serum total calcium, ionized calcium, phosphorus, and parathyroid hormone (PTH) concentrations were monitored daily for 5 to 7 days after the ablation procedure and again 1, 3, and 6 months after the procedure. Dogs were also monitored for adverse effects. Follow-up ultrasonography was performed 5 days and 1 month after the ablation procedure. RESULTS: One injection was required in 7 dogs, and 2 injections were required in 1. Serum total and ionized calcium concentrations were within reference ranges within 24 hours after treatment in 7 dogs and within 5 days in 1 dog. Serum PTH concentration decreased and serum phosphorus concentration increased within 24 hours after treatment in all 8 dogs. Transient hypocalcemia developed in 4 dogs during the first 5 days after treatment, but only 1 dog required treatment for hypocalcemic tetany. Hypercalcemia recurred in 1 dog 1 month after the procedure and surgical removal of the parathyroid mass was required. Other adverse effects were not reported. CONCLUSIONS AND CLINICAL RELEVANCE: Ultrasound-guided chemical ablation of parathyroid masses is a safe and effective alternative to surgery for dogs with primary hyperparathyroidism.

Adenoma↗

Effects of phenobarbital treatment on serum thyroxine and thyroid-stimulating hormone concentrations in epileptic dogs.

OBJECTIVE: To determine whether phenobarbital treatment of epileptic dogs alters serum thyroxine (T4) and thyroid-stimulating hormone (TSH) concentrations. DESIGN: Cross-sectional study. ANIMALS: 78 epileptic dogs receiving phenobarbital (group 1) and 48 untreated epileptic dogs (group 2). PROCEDURE: Serum biochemical analyses, including T4 and TSH concentrations, were performed for all dogs. Additional in vitro analyses were performed on serum from healthy dogs to determine whether phenobarbital in serum interferes with T4 assays or alters free T4 (fT4) concentrations. RESULTS: Mean serum T4 concentration was significantly lower, and mean serum TSH concentration significantly higher, in dogs in group 1, compared with those in group 2. Thirty-one (40%) dogs in group 1 had serum T4 concentrations less than the reference range, compared with 4 (8%) dogs in group 2. All dogs in group 2 with low serum T4 concentrations had recently had seizure activity. Five (7%) dogs in group 1, but none of the dogs in group 2, had serum TSH concentrations greater than the reference range. Associations were not detected between serum T4 concentration and TSH concentration, age, phenobarbital dosage, duration of treatment, serum phenobarbital concentration, or degree of seizure control. Signs of overt hypothyroidism were not evident in dogs with low T4 concentrations. Addition of phenobarbital in vitro to serum did not affect determination of T4 concentration and only minimally affected fT4 concentration. CONCLUSIONS AND CLINICAL RELEVANCE: Clinicians should be aware of the potential for phenobarbital treatment to decrease serum T4 and increase TSH concentrations and should use caution when interpreting results of thyroid tests in dogs receiving phenobarbital.

Alanine Transaminase↗

Diagnosis of disseminated intravascular coagulation in dogs admitted to an intensive care unit.

OBJECTIVE: To describe and evaluate hemostatic function in critically ill dogs with clinical signs of diseases that predispose to disseminated intravascular coagulation (DIC). DESIGN: Prospective case series. ANIMALS: 59 critically ill dogs (affected dogs) with clinical signs of diseases known to predispose to DIC and 52 clinically normal dogs (control dogs). PROCEDURE: Activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin clotting time (TCT), plasma fibrinogen concentration, serum concentration of fibrin and fibrinogen-related antigens (FRA), and plasma antithrombin III (AT III) activity were determined for all dogs. Results from affected dogs were compared with those of control dogs. In some affected dogs, postmortem tissue specimens were examined for evidence of microvascular thrombosis. A diagnosis of DIC was made by fulfilling at least 3 of the following criteria: 1) abnormal aPTT, PT, or TCT value, 2) low plasma fibrinogen concentration, 3) low plasma AT III activity, 4) high serum FRA concentration, or 5) low platelet count. To evaluate the severity of hemostatic dysfunction, 3 arbitrary categories (mild, moderate, and severe) were proposed. RESULTS: A diagnostic strategy based on moderate hemostatic dysfunction identified DIC in 16 of 59 (27.1%) affected dogs. The AT III activity was < 70% in 15 of 16 dogs with DIC. Microvascular thrombosis was observed in tissue specimens from 7 of 8 affected dogs. Serum FRA and plasma fibrinogen concentrations did not contribute in establishing a diagnosis of DIC. CONCLUSIONS AND CLINICAL RELEVANCE: A diagnosis of DIC can be made when hemostatic dysfunction is moderate in dogs with clinical signs of diseases associated with DIC.

Animals↗

Evaluation of risk factors for blastomycosis in dogs: 857 cases (1980-1990)

An epidemiologic study was conducted by use of the Veterinary Medical Data Base to investigate risk factors for blastomycosis in dogs. From January 1980 through June 1990, 971 cases of blastomycosis in dogs from 22 North American veterinary teaching hospitals were identified. Of these cases, 114 (11.7%) were excluded from the study because of incomplete information regarding age, body weight, sex, and neuter status. A control group of 417,079 dogs was selected that included all other dogs with medical conditions unrelated to blastomycosis for which records were submitted to the data base during the same period. The prevalence of blastomycosis in dogs was 205/100,000 admissions during the study period. When veterinary teaching hospitals were grouped on the basis of their general geographic location, dogs in the East South central, East North central, West South central, and South Atlantic regions had a significantly (P < 0.05) increased risk of acquiring blastomycosis, compared with that of dogs in the Mountain/Pacific region. When teaching hospitals from all geographic regions were considered, dogs had a significantly (P < 0.05) increased risk of acquiring blastomycosis in autumn, compared with that in spring. Sporting dogs and hounds, as defined by the American Kennel Club, were at increased risk for blastomycosis. At highest risk were Bluetick Coonhounds, Treeing-walker Coonhounds, Pointers, and Weimaraners, compared with mixed-breed dogs. Ages of dogs with blastomycosis tended to be normally distributed. Generally, the highest-risk group was composed of sexually intact male dogs, 2 to 4 years old, weighing 22.7 to 34.1 kg. This same pattern was observed for sporting dogs and hounds.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Comparison of mitotane treatment for adrenal tumor versus pituitary-dependent hyperadrenocorticism in dogs.

The purpose of this study was to determine the sensitivity of dogs with hyperadrenocorticism to treatment with the adrenocorticolytic agent mitotane. Specifically, we looked for differences in response to treatment using this drug in dogs with adrenocortical tumors (adrenal tumor hyperadrenocorticism, ATH) vs those with pituitary-dependent hyperadrenocorticism (PDH). For inclusion in this study, each dog must have had clinical signs, data base laboratory abnormalities, and endocrine screening test results consistent with the diagnosis of hyperadrenocorticism. Further, each dog had to have been treated for at least 6 months with mitotane and have histologic evidence for adrenocortical or pituitary neoplasia (all dogs were necropsied). Thirteen dogs with ATH (8 carcinomas, 5 adenomas) were identified. The ages and body weights of these 13 dogs were computer-matched to 13 dogs with PDH. All dogs were initially treated with approximately 50 mg of mitotane/kg/d of body weight. Reexaminations were performed after 7, 30, 90, and 180 days of treatment. Individual dosages varied widely after the initial 5 to 12 days of treatment. The mean (+/- SD) dose of mitotane (mg/kg/d) for the first 7 days of treatment was 47.5 +/- 9.4 for dogs with ATH vs 45.7 +/- 11.9 for dogs with PDH. The mean plasma cortisol concentrations 1 hour after ACTH administration at the 7-day recheck were significantly higher in dogs with ATH (502 +/- 386 nmol/L) than in dogs with PDH (88 +/- 94 nmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

Hypertrophic cardiomyopathy in the dog.

Clinical and necropsy findings in 10 dogs with a spontaneous primary hypertrophic cardiomyopathy are described. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Septal:free wall thickness ratios in the 10 dogs ranged from 1.1 to 1.5; 6 had ratios greater than or equal to 1.3. However, marked cardiac muscle cell disorganization in the ventricular septum, characteristic of patients with hypertrophic cardiomyopathy, was present in only 2 of the 10 dogs. Death occurred most commonly while the dogs were under anesthesia during the course of operative procedures (5 dogs) or suddenly and unexpectedly in animals without previous symptomatic manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. In addition, 2 of these 4 dogs with heart failure and 1 dog without previous symptoms (that died during a noncardiac operation) manifested complete heart block. It is conceivable that dogs with spontaneous hypertrophic cardiomyopathy may prove useful in the future investigations of the clinical, hemodynamic, and pathologic features of this disease in humans.

Animals↗

Clinical and metabolic findings in dogs with chronic renal failure fed two diets.

Exogenous creatinine clearance, urinary electrolyte excretions, calcium and phosphorus balance, serum cholesterol concentration, arterial blood pressure, and body weight were evaluated in dogs with chronic renal failure that were fed 2 commercial diets. Nine dogs ranging in age from 1 to 15 years were identified as having mild to moderate chronic renal failure (CRF, exogenous creatinine clearance = 0.5 to 2.13 ml/kg of body weight/min). These dogs and a group of 10 clinically normal controls were fed a diet containing 31% protein for 8 weeks at which time hematologic and biochemical evaluations and clearance studies were performed. All dogs then were fed a phosphorus-restricted diet containing 16% protein and then reevaluated after 8 weeks. The dogs in this study had hematologic and biochemical abnormalities typical of CRF. Urine absolute and fractional excretion of electrolytes was higher in dogs with CRF than in controls and was affected by diet. Serum cholesterol concentration was higher in dogs with CRF and increased in those dogs after feeding the low protein diet. Changes in dietary sodium intake did not affect arterial blood pressure. The phosphorus-restricted diet did not affect serum amino terminal parathyroid hormone concentration in either group. Control dogs lost body weight, whereas dogs with CRF gained weight when fed the low protein diet. We concluded that dogs with mild to moderately severe CRF have the same biochemical abnormalities and response to dietary restriction of protein and phosphorus as has been previously reported in dogs with experimentally induced CRF. Restriction of dietary sodium may not decrease arterial blood pressure in some dogs with CRF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗

Urine cortisol:creatinine ratio as a screening test for hyperadrenocorticism in dogs.

A urine cortisol:creatinine (c:c) ratio, determined from a free-catch morning sample, was evaluated in each of 83 dogs as a screening test for hyper-adrenocorticism. The dogs evaluated were allotted to 3 groups, including 20 healthy dogs, 40 dogs with confirmed hyperadrenocorticism (HAC), and 23 dogs with polyuria and polydipsia not attributable to HAC (polyuria/polydipsia group; PU/PD). Overlap in the urine c:c ratios (mean +/- SEM), comparing results from the healthy dogs (5.7 x 10(-6) +/- 0.9) with those from the HAC dogs (337.7 x 10(-6) +/- 72.0) was not found. However, 11 (64%) of the 18 values from the PU/PD dogs (42.6 x 10(-6) +/- 9.4) were above the lowest ratio in the HAC group and 50% of the HAC group had a urine c:c ratio below the highest value in the PU/PD group. When the mean urine c:c ratio (+/- 2 SD) for the group of healthy dogs was used as a reference range, 100% of the HAC dogs and 18 (77%) of 23 dogs in the PU/PD group had abnormal urine c:c ratios. The sensitivity of the urine c:c ratio to discriminate dogs with HAC was 100%. The specificity of the urine c:c ratio was 22% and its diagnostic accuracy was 76%. On the basis of our findings, a urine c:c ratio within the reference range provides strong evidence to rule out HAC. However, abnormal urine c:c ratios are obtained from dogs with clinical diseases other than HAC. Therefore, measurement of a urine c:c ratio should not be used as the sole screening test to confirm a diagnosis of HAC.

Adrenocortical Hyperfunction↗

Plasma free cortisol concentrations in dogs with hyperadrenocorticism.

Unbound or free cortisol constitutes a small fraction of total plasma cortisol, but is believed to represent the biologically active portion of this circulating glucocorticoid. We tested the hypothesis that the percentage free cortisol was altered in plasma from dogs with hyperadrenocorticism, which could account for a greater target tissue response to this circulating hormone. The percentage free cortisol in plasma samples from human beings, healthy dogs, and dogs with hyperadrenocorticism was estimated, using centrifugal ultrafiltration-dialysis. Total cortisol concentrations were determined by use of radioimmunoassay. Total cortisol concentrations appeared greater in plasma from human beings than in plasma from either group of dogs. However, the percentage free cortisol was lower in plasma from human beings, resulting in a calculated concentration of free cortisol that was quite similar between plasma from human beings and healthy dogs. Total plasma cortisol concentrations were greater (P less than 0.01) in samples from dogs with hyperadrenocorticism (190 +/- 113 nmol/L; mean +/- SD) than in healthy dogs (102 +/- 85 nmol/L), but the percentage free cortisol was not different between these 2 groups (dogs with hyperadrenocorticism, 16 +/- 9%; healthy dogs, 13 +/- 6%). However, plasma free cortisol concentrations (product of total and the percentage of free cortisol) were greater (P less than 0.01) in samples from dogs with hyperadrenocorticism (36 +/- 41 nmol/L) than in those from healthy dogs (16 +/- 9 nmol/L). Significant (P less than 0.001) positive linear relationships were found between total cortisol concentrations and percentage free cortisol in plasma samples from healthy dogs and dogs with hyperadrenocorticism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Thyroid hormones concentrations and ECG picture in the dog.

Disorders of the thyroid gland activity are the most commonly encountered disturbances of endocrine origin in the dog. Hypo- or hyperthyroidism may disturb the function of the cardiovascular system and cause arrhythmias. The aim of this study was to evaluate the influence of thyroid gland activity on electrocardiogram (ECG) picture in the dog by comparing ECG curves of healthy dogs, dogs with hypothyroidism and dogs with cardiac insufficiency caused by endocardiosis of the mitral valve. The study was performed on 38 dogs, patients of the Department of Internal and Parasitic Diseases with Clinic for Horses, Dogs and Cats in Wrocław. The animals were assigned to 3 groups: Group I--control group, 13 clinically healthy dogs; Group II--14 dogs with diagnosed cardiac insufficiency caused by endocardiosis of the mitral valve; Group III--11 dogs with hypothyroidism. Clinical examination of the animals was conducted according to the following pattern: anamnesis, general clinical examination, cardiological examination (ECG, USG of the heart) and laboratory analysis (triacylglycerydes, cholesterol, T3, T4, FT4). In this study, the significant influence of thyroid gland activity on ECG picture of the evaluated dogs was found. In the dogs with hypothyroidism a decrease in the sino-atrial node activity was observed, which led to decreased heart rate. In dogs with hypothyroidism, the innerheart conduction was reduced, which was demonstrated by prolongation of the P wave, QRS complex and the QT interval.

Animals↗

Effects of castration on chronic bacterial prostatitis in dogs.

An Escherichia coli bacterial prostatitis was experimentally induced in dogs to determine the effect of castration on chronic bacterial prostatitis. Two weeks after instillation of bacteria directly into the prostate gland, 17 of 22 adult mixed-breed male dogs had positive urine or prostatic fluid cultures or both. Seven of the 17 dogs were randomly chosen to be castrated, and 10 of the 17 served as sham-operated controls. At weekly intervals, urine was obtained from 17 dogs for aerobic microbiologic culturing. At each week, dogs with no bacterial growth in the cultured urine had prostatic fluid collected for aerobic microbiologic culture. Dogs with negative urine, prostatic fluid, and prostatic tissue needle biopsy culture results at week 7 were euthanatized. For remaining dogs, weekly cultures were continued until the dogs were euthanatized at week 12. None of the 7 castrated dogs and 6 of the 10 dogs subject to sham operation had prostatic infection at the time of necropsy. The castrated dogs had a mean infection duration of 4.2 weeks, which was statistically shorter than the 9.5-week mean duration of infection in the sham-operated controls. Cultures of prostatic tissue obtained immediately after euthanasia correlated 100% with urine and prostatic fluid cultures taken before euthanasia. All of the 6 dogs with positive prostatic cultures at termination had moderate to marked lymphoplasmacytic chronic prostatitis. The 11 dogs that were not infected at the end of the study had normal to moderate lymphoplasmacytic chronic prostatitis on histologic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Hematologic values and plasma and tissue folate concentrations in dogs given phenytoin on a long-term basis.

During earlier investigations of the hepatic effects in dogs of long-term administration of phenytoin alone or in combination with primidone, erythrocytic macrocytosis, neutropenia, neutrophilic hypersegmentation, and thrombocytopenia were observed. Such abnormalities were observed most often in dogs given phenytoin and resembled those known to be attributable to folate deficiency in human beings with epilepsy treated with phenytoin. To pursue the theory that these hematologic aberrations were caused by drug-induced folate deficiency, 12 dogs were given a diet specifically formulated to contain a minimally adequate concentration of folate. After 2 weeks, phenytoin was administered daily (400 mg, PO, q 8 h) to 8 of the 12 dogs for 54 weeks. A CBC, bone marrow aspiration biopsy, and measurement of plasma and RBC folate concentrations were done every 3 weeks. Bone marrow aspirates were examined by transmission electron microscopy after 24 and 36 weeks, and at the end of the treatment period. Hepatic folate concentration was also determined in all dogs before and after treatment. Excretion of formiminoglutamic acid, as a marker of folate deficiency, was measured in all dogs at the end of the study. All dogs remained healthy throughout the treatment phase. Consistent abnormalities were not observed in the blood or bone marrow of treated dogs. Plasma and RBC folate concentrations decreased in control and treated dogs as a result of dietary restriction (P less than or equal to 0.02), and remained stable until the end of the study. The RBC folate content decreased further in treated dogs (P less than or equal to 0.02), although the hepatic folate content was similar in control and treated dogs. Treated dogs did not excrete formiminoglutamic acid more rapidly than did control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Comparison of arrhythmogenic doses of epinephrine in heartworm-infected and noninfected dogs.

The arrhythmogenic dose of epinephrine (ADE) was determined in heartworm-infected and noninfected (control) dogs during thiamylal-induced and halothane-maintained anesthesia to assess the myocardial sensitization. The ADE in heartworm-infected dogs (2.42 +/- 0.26 micrograms/kg of body weight) was significantly lower than that for the controls (3.36 +/- 0.29 micrograms/kg). After 2 weeks, ADE was determined again in these dogs after atropine treatment. Atropine treatment lowered the ADE to 1.76 +/- 0.33 micrograms/kg and 1.77 +/- 0.19 micrograms/kg in heartworm-positive and -negative dogs, respectively. After 2 weeks more, the ADE was determined after administration of prazosin, an alpha 1-antagonist. Only 2 of 6 controls and 3 of 6 heartworm-positive dogs had arrhythmias after a threefold increase of ADE. The mean ADE in the dogs that responded to treatment were 7.4 micrograms/kg and 7.2 micrograms/kg for heartworm-positive and -negative dogs, respectively. The finding of this study indicated that ADE in heartworm-infected dogs were lower than those in the control dogs, which makes the heartworm-infected dogs more vulnerable to arrhythmia during anesthesia. Atropine did not protect the dogs of either group. However, prazosin protected the dogs of both groups by significantly increasing the threshold of the ADE. On the basis of our findings, to reduce the risk of arrhythmia, we suggest that routine screening of dogs for heartworm infection be done before anesthetics are used.

Anesthesia, Inhalation↗

Postnatal hematologic development in phosphofructokinase-deficient dogs.

Adult dogs with phosphofructokinase (PFK) deficiency have compensated hemolytic anemia, due to an absolute or functional deficiency of the muscle-type (M-type) subunit that normally accounts for a majority of total erythrocyte PFK activity in dogs. Potential effects of PFK deficiency on hematologic development were evaluated in dogs. Routine hematologic parameters were similar in normal and affected dogs when 1 day old, because all newborn dogs had erythrocyte PFK activities about three times that of normal adult dogs. Based on chromatographic separation of PFK isozymes and enzyme immunoprecipitation studies, the high PFK activity at birth was attributed to the predominance of the liver-type (L-type) subunit of PFK, which is negligible or absent in normal adult dog erythrocytes. Both total PFK activities and the amounts of L-type subunit present decreased dramatically during the first 6 to 8 weeks of life. The muscle-type subunit was negligible or absent at birth, but appeared and increased as the L-type decreased in normal dogs. These changes may result from the replacement of erythrocytes formed in the fetus with those formed after birth. A postnatal physiologic anemia developed to a similar degree in both affected and normal dogs because of decreases in both mean corpuscular volume and erythrocyte numbers. Reticulocyte counts were high in all dogs at birth and remained high in affected dogs, but decreased from 2 months of age onward in normal dogs. Erythrocyte 2,3-diphosphoglycerate (DPG) values were very low in all newborn pups and increased to values expected for adults in the respective groups by 2 to 4 weeks of age. A low 2,3-DPG concentration occurs in affected dogs because PFK deficiency inhibits glycolysis above the side shunt that forms 2,3-DPG.

Adenosine Triphosphate↗