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Biomedical subjects

C W Qualls

Publications and source records attributed to C W Qualls.

At least 55 records · Page 3Linked to original sources
PubMed1991

Xylazine-induced pulmonary edema in rats.

Inhibitors of cytochrome P450, such as SK&F 525-A, prolong the duration of xylazine-ketamine anesthesia and cause pulmonary edema (PE) and death in rats. To determine the cause of PE, Sprague-Dawley rats were given a single dose of xylazine (21 mg/kg, im) alone or in combination with ketamine (45 mg/kg, im) and/or SK&F 525-A (50 mg/kg, ip) and percentage lung to body weight (%LW/BW) ratios (as an indicator of PE) were compared. The results indicated that xylazine caused PE which was independent of ketamine and was enhanced by SK&F 525-A. Subsequently, it was determined that 42 mg/kg xylazine, im, is an optimal edemagenic dose. Xylazine (42 mg/kg, im) increased the %LW/BW ratio as compared to control. Pleural effusion (PLE) of various amounts was observed in 75% of the animals. The pleural fluid to serum protein ratio for xylazine was similar to that obtained for alpha-naphthylthiourea (5 mg/kg, ip). Extensive serous PLE and alveolar edema with hemorrhage were found at necropsy in xylazine-treated rats. Pretreatment with yohimbine (4.2 mg/kg), prazosin (20 mg/kg), tolazoline (20 mg/kg), yohimbine (4.2 mg/kg) plus prazosin (20 mg/kg), atropine (20 mg/kg), dimethyl sulfoxide (DMSO) (7.8 g/kg), allopurinol (50 mg/kg), superoxide dismutase (20,000 U/kg), catalase (20,000 U/kg), BW755C (50 mg/kg), ibuprofen (50 mg/kg), cystathionine (100 mg/kg) plus taurine (100 mg/kg) did not affect the %LW/BW ratio. PLE was increased by yohimbine, yohimbine plus prazosin, and allopurinol, reduced by DMSO, and not changed in other groups. The results indicate that xylazine caused increased-permeability PE characterized by rapid onset, cellular damage and protein-rich pleural fluid. PE may not be mediated by adverse cardiovascular effects of xylazine and oxygen radicals are possibly involved in its etiology.

Anesthetics↗
PubMed1991

Comparative biochemical and morphometric changes associated with induction of the hepatic mixed function oxidase system in the rat.

This study characterized the induction of the rat hepatic cytochrome P-450-dependent mixed function oxidase system by SK&F 86002 [6-(4'-fluorophenyl)-5-(4'-pyridyl)-2,3-dihydroimidazo-(2,1-b)thia zole], an inhibitor of both the cyclooxygenase and 5-lipoxygenase pathways of arachidonic acid metabolism. The induction characteristics of SK&F 86002 were compared to those of the classical inducer, phenobarbital, and morphological features of both SK&F 86002 and phenobarbital induced hepatocellular hypertrophy were quantitated. Rats were administered either SK&F 86002 (6, 18, or 60 mg/kg/day, po) or phenobarbital (8, 24, 80 mg/kg/day, ip) for 3 or 14 consecutive days. Liver to body weight ratio, total hepatic microsomal protein and cytochrome P-450 content, ethoxycoumarin-O-deethylase (ECOD) and leukotriene B4(LTB4) omega- and omega-1 hydroxylase were measured. Ultrastructural morphometry of the liver from control, and high dose SK&F 86002 (60 mg/kg/day) and phenobarbital (80 mg/kg/day) treated rats was completed. On day 3, phenobarbital increased liver to body weight ratio but only at the 80 mg/kg/day dosage; microsomal protein content was unchanged. ECOD activity increased in a dose-dependent fashion. LTB4 omega- and omega-1 hydroxylase activities were unaffected. Administration of SK&F 86002 for 3 days increased the liver to body weight ratio at both the 18 and 60 mg/kg/day dosage; microsomal protein content was unchanged. ECOD activity was significantly increased by the 60 mg/kg/day dosages of SK&F 86002. On day 14, phenobarbital increased the liver to body weight ratio and microsomal protein content but again only at the 80 mg/kg/day dosage. Cytochrome P-450 content was increased by all dosages.(ABSTRACT TRUNCATED AT 250 WORDS)

7-Alkoxycoumarin O-Dealkylase↗
PubMed1990

Lymphocytic-plasmacytic enteritis in two horses.

The primary hematologic abnormalities in 2 adult horses with chronic weight loss were hypoalbuminemia and hyperglobulinemia. One horse was anemic, had subclinical disseminated intravascular coagulation, and prolonged plasma sulfobromophthalein half-life. Small-intestinal dysfunction with malabsorption was indicated by abnormal D-xylose absorption test results. Clinicopathologic and pathologic findings were consistent with a diagnosis of malabsorption and protein-losing enteropathy, attributable to lymphocytic and plasmacytic infiltration of the intestine.

Animals↗
PubMed1990

Strongyloidiasis in cotton rats (Sigmodon hispidus) from central Oklahoma.

Thirty-one of 40 cotton rats (Sigmodon hispidus) collected from central Oklahoma were infected with Strongyloides sp. (78% prevalence). Larvae of Strongyloides sp. (rhabditiform or filariform) were not demonstrable in intestinal contents and scrapings. Female nematodes recovered from intestinal contents and scrapings had morphological similarities with Strongyloides sigmodontis. Cotton rats infected with Strongyloides sp. were indistinguishable clinically from non-infected hosts. Infected animals had no significant gross lesions, but the presence of Strongyloides sp. in the intestinal mucosa was associated with villus atrophy and mild to moderate infiltration of the lamina propria by lymphocytes, plasma cells and occasional eosinophils. Other organs or tissues examined were free from lesions induced by Strongyloides sp.

Animals↗
PubMed1989

Effects of phenobarbital and 3-methylcholanthrene on the hepatic cytochrome P-450 metabolism of various alkoxyresorufin ethers in the cotton rat (Sigmodon hispidus).

1. Microsomes isolated from phenobarbital and 3-methylcholanthrene induced cotton rats (Sigmodon hispidus) were tested for o-dealkylase activity with methoxy-, ethoxy-, pentoxy- and benzoxyresorufin ethers. 2. The activity of 3-methylcholanthrene induced microsomes was greater than controls. 3. Activity of phenobarbital induced microsomes was not different from controls. 4. There was a distinct difference between male and female animals. 5. The results obtained from cotton rats are markedly different from results obtained from Sprague-Dawley (S-D) rats.

Animals↗
PubMed1989

Effects of some hepatic microsomal enzyme inducers and inhibitors on xylazine-ketamine anesthesia.

Various inducers and inhibitors of hepatic microsomal enzymes were studied for their effects on xylazine-ketamine anesthesia. Pretreatment of Sprague-Dawley rats with chloramphenicol (100 mg/kg, ip), cimetidine (100 mg/kg, ip), ketoconazole (40 mg/kg, po), and SKF 525-A (25 mg/kg, ip) significantly (p less than 0.05) increased the duration of anesthesia in rats injected with ketamine (45 mg/kg, im) and xylazine (21 mg/kg, im). Pretreatment with phenobarbital (40 mg/kg, ip, once daily for 4 days) did not affect the duration of anesthesia significantly. The increase in duration of anesthesia in animals pretreated with SKF 525-A and ketoconazole was accompanied by secondary respiratory distress about 6 hr following recovery from anesthesia, often leading to death within 24 hr. Lesions consisting of extensive serous pleural effusion, alveolar edema rich in macrophages and extensive pulmonary hilar edema with hemorrhage were found at necropsy. These results indicate that inhibition of hepatic microsomal enzymes by commonly used therapeutic agents during xylazine-ketamine anesthesia to prolong the anesthetic effect, or as a result of concurrent pharmacotherapy, could have deleterious effects.

Animals↗
PubMed1987

Renal concentrating ability in dehydrated hyponatremic dogs.

Eleven hyponatremic dogs were unable to concentrate their urine during periods of severe dehydration and azotemia. When normonatremia was reestablished in eight of the dogs, their renal concentrating ability returned. Six dogs, including the 3 dogs in which normonatremia was not reestablished, died or were euthanatized; renal lesions were not found during postmortem examination. Two dogs had hypoadrenocorticism, which has been documented as a cause of hyponatremia and impaired renal concentrating ability. Two dogs had gastrointestinal disease, which has been documented as a cause of hyponatremia, but not of impairment of renal concentrating ability. All dogs without hypoadrenocorticism had clinical and clinicopathologic indications of blood loss, which has not been documented as a cause of hyponatremia or impairment of renal concentrating ability. Hyponatremia (less than 120 mEq/L) was induced by chronic blood removal in a dog maintained on a low-sodium diet. During the period of hyponatremia, the dog became azotemic, hypotensive, and severely dehydrated; renal concentrating ability was impaired. We conclude that hyponatremia may be caused by hemorrhage, but irrespective of the cause, hyponatremia impairs renal concentrating ability.

Adrenal Cortex Diseases↗
PubMed1986

Clostridium perfringens type C enterotoxemia in a newborn foal.

A 1-day old, full-term foal with a history of colic died 2 hours after admission. Necropsy revealed an extremely flaccid, fluid-filled intestinal tract. Histopathologically, the superficial intestinal mucosa was completely necrotic, with minimal inflammatory response. Numerous large, gram-positive rods covered the villi. Clostridium perfringens was isolated on bacteriologic culturing of the intestinal tract contents and was identified as type C by toxin neutralization tests.

Animals↗
PubMed1986

Hepatic enzyme changes in bovine hepatogenous photosensitivity caused by water-damaged alfalfa hay.

In the winter of 1983, practitioners reported extensive photosensitization in 7 herds of cattle. All herds had a history of having been fed water-damaged alfalfa hay. A cow from one herd was referred to the veterinary teaching hospital at Oklahoma State University. In this herd of approximately 40 adult Polled Herefords, all cattle had had some degree of clinical involvement over the past 4 to 6 weeks. Clinical signs included scaling and erythema of sparsely haired skin, muzzle, and teats, as well as icterus, anorexia, and weight loss. One cow died, and the remaining cattle recovered over an 8- to 10-week period after removal of the hay from the ration. In the referred cow, values for total and conjugated bilirubin, BUN, creatinine, sorbitol dehydrogenase, serum alkaline phosphatase, serum aspartate transaminase, and serum gamma-glutamyl transferase were higher than normal. In the herd of origin, extremely high serum gamma-glutamyl transferase values (180 to 1,400 IU/L) persisted (normal, 2 to 35 IU/L). Feeding the same alfalfa hay to 2 clinically normal cows reproduced the syndrome. The characteristic hepatic lesion was bile duct necrosis, with secondary bile duct hyperplasia.

Alkaline Phosphatase↗
PubMed1983

Babesiosis in the Greyhound.

Babesiosis was diagnosed in five 11- to 18-day old Greyhound pups. In 3 pups, Babesia canis organisms were identified by examination of a Wright's-Giemsa-stained smear of blood. In 2 pups, the diagnosis was established by examination of a splenic impression smear obtained at necropsy. Findings in the 3 clinical cases included depression, weakness, anorexia, pallor, anemia, and thrombocytopenia. Subcutaneous administration of diminazene aceturate resulted in rapid clinical recovery in these cases. In the 2 pups that were necropsied, variable numbers of erythrocytes containing Babesia organisms were observed in the microvasculature of tissues. Subinoculation of blood into an intact dog and a splenectomized dog resulted in parasitemia and B canis serum titers, as determined by indirect fluorescent antibody testing. A site visit to the kennel from which the pups had originated led to identification of numerous Rhipicephalus sanguineus in small buildings and pens. Of 107 dogs from this kennel that were tested, 63 had an indirect fluorescent antibody titer for B canis. A limited serologic survey of Greyhound kennels in West Virginia, Oklahoma, Texas, Mississippi, and Florida identified a large number of dogs with indirect fluorescent antibody titers for B canis.

Animals↗
PubMed1983

Four cases of pulmonary nodular eosinophilic granulomatosis in dogs.

Four cases of pulmonary nodular eosinophilic granulomatosis are described in dogs. All dogs were presented for chronic respiratory disease. Three dogs had radiographic and pathologic evidence of heartworm disease. One dog had lesions suggestive of past heartworm disease; but adult worms were not found at necropsy. Radiographically, single or multiple pulmonary densities up to 10 cm in diameter were seen. Hemograms on 3 dogs indicated a leukocytosis, neutrophilia, and eosinophilia. A microfilaremia was not detected in any of these dogs. Transtracheal washes yielded eosinophils, neutrophils, and macrophages. Three dogs were euthanatized. A 7 cm pulmonary nodule was excised surgically from the other dog. The pulmonary nodules were grossly yellow to gray in color, well-circumscribed, and solid. In one case, several nodules surrounded major branches of the pulmonary artery. Histologically, these nodules were composed of dense accumulations of epithelioid cells, macrophages, and eosinophils. There was no evidence of thrombosis due to Dirofilaria immitis. Possible pathogenetic mechanisms are discussed. Differentiation of pulmonary nodular eosinophilic granulomatosis from other types of pulmonary nodules in the dog can be accomplished by histologic examination.

Animals↗