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Biomedical subjects

L E Davis

Publications and source records attributed to L E Davis.

At least 145 records · Page 8Linked to original sources
PubMed1986

Pharmacokinetics of procainamide hydrochloride in dogs.

Pharmacokinetics of procainamide hydrochloride were studied in 2 groups of dogs. In a group of 6 dogs, procainamide was administered IV at a small dose of 8 mg/kg (group 1), and blood samples were obtained for 3.5 hours. In another group of 6 dogs, procainamide was administered IV and orally at an average dose of 25.5 mg/kg (group 2) in a crossover manner. Blood samples were obtained for 48 hours. In 2 dogs (previously used in part II), N-acetylprocainamide (NAPA) was administered IV at a dose of 10 mg/kg. Plasma samples were assayed for procainamide by fluorescence polarization immunoassay, and NAPA samples were assayed by high-performance liquid chromatography. In group 1, the elimination of procainamide was described by a 1-compartment, open pharmacokinetic model. The elimination half-life was 2.43 hours, the apparent volume of distribution was 1.44 L/kg, and the systemic clearance was 0.412 L/kg/hr. In group 2, 2 of the 6 dogs were described by a 1-compartment model, and 4 of the 6 dogs were described with a 2-compartment pharmacokinetic model. The elimination half-life for the IV dosage was 2.85 hours, the apparent volume of distribution was 2.13 L/kg, and the systemic clearance was 0.519 L/kg/hr. For the orally administered dose, the bioavailability was 85%, and the absorption half-life was 0.5 hours. There was no evidence of acetylation of procainamide to NAPA or deacetylation of NAPA to procainamide. The estimated elimination half-life of NAPA was 4.7 hours.

Acecainide↗
PubMed1986

Endotoxin-induced bovine mastitis: arachidonic acid metabolites in milk and plasma and effect of flunixin meglumine.

Arachidonic acid metabolites (AAM) were measured in milk and plasma during the course of acute endotoxin-induced mastitis in 12 lactating cows. Mastitis was induced by intramammary challenge exposure with 10 micrograms of Escherichia coli (026:B6) endotoxin. Endotoxin was injected into the teat cistern via the teat canal of a single randomly selected rear quarter of each cow. Concentrations of prostaglandin (PG) F2 alpha and thromboxane (Tx) B2 in fat-free unextracted milk and of 15-keto-13,14-dihydro-PGF2 alpha in plasma were measured by radioimmunoassay. Total production of AAM in milk was determined by measuring quarter milk production. The AAM were compared in 6 cows administered flunixin meglumine (1.1 mg/kg of body weight) and in 6 cows administered saline solution. Concentrations of TxB2 in milk were significantly (P less than 0.001) increased during the early course of acute mastitis in endotoxin-treated quarters of cows not administered flunixin meglumine. Peak concentrations of TxB2 in milk occurred at 8 hours after endotoxin inoculation. Flunixin meglumine treatment produced significant (P less than 0.05) reductions in milk TxB2 and plasma 15-keto-13,14-dihydro-PGF2 alpha concentrations. Concentrations of PGF2 alpha in milk and total PGF2 alpha and TxB2 production per quarter per milking were not significantly influenced by endotoxin challenge or by flunixin meglumine treatment.

Animals↗
PubMed1986

Efficacy of flunixin meglumine for the treatment of endotoxin-induced bovine mastitis.

The clinical effect of flunixin meglumine administration was determined in cows with acute mastitis induced by intramammary administration of endotoxin. In 12 lactating cows, 10 micrograms of Escherichia coli 026:B6 endotoxin were administered via a teat cannula into the teat cistern of single randomly selected rear quarters. Cows were challenge exposed as pairs. One cow in each pair was administered parenteral flunixin meglumine (6 cows) and 1 cow per pair was administered saline solution (6 cows). Multiple doses (7) of 1.1 mg of flunixin meglumine/kg of body weight or saline solution were administered at 8-hour intervals beginning 2 hours after endotoxin. Cow and quarter clinical signs as well as milk somatic cell concentrations, bovine serum albumin, electrical conductivity, and milk production were determined before and for 14 days after endotoxin inoculation. Intramammary endotoxin produced signs characteristic of acute coliform mastitis. Quarter and systemic abnormalities occurred and milk production was reduced by approximately 50% at 12 hours after endotoxin. Flunixin meglumine therapy significantly (P less than or equal to 0.05) reduced rectal temperatures and quarter signs of inflammation and improved clinically graded depression when compared with these signs in saline solution-treated controls. Milk production and laboratory indicators of inflammation in milk were not significantly (P greater than 0.05) different for flunixin meglumine vs saline solution controls. The clinical response observed was consistent with the antipyretic, analgesic, and anti-inflammatory properties of flunixin meglumine.

Animals↗
PubMed1986

Endotoxin-induced bovine mastitis: immunoglobulins, phagocytosis, and effect of flunixin meglumine.

Milk whey immunoglobulins (Ig) and phagocytosis of staphylococci by milk polymorphonuclear neutrophilic leukocytes (PMN) were measured in 12 cows (allotted to 6 pairs) during acute bovine mastitis induced by intramammary inoculation of endotoxin. Six of these cows (or 1 in each pair) were treated with flunixin meglumine and were compared with the others (given only saline solution). The endotoxin inoculation comprised 10 micrograms of Escherichia coli O26:B6 lipopolysaccharide injected into one of the rear quarters (mammae). Flunixin meglumine was administered parenterally at a dosage of 1.1 mg/kg every 8 hours (total of 7 doses) beginning at 2 hours after endotoxin was injected. Milk samples were obtained, and whey samples were prepared from each quarter of each cow 3 times before inoculation and at 2, 4, 8, 12, 24, 48, 72, 96, 120, 144, 168, and 336 hours after endotoxin was inoculated. Significant increases (P less than 0.05) in milk whey IgG1, IgG2, IgM, and IgA concentrations were observed in whey samples from endotoxin-inoculated quarters. Greatest relative increase was seen for IgG2. Increased whey Ig concentrations were not observed in quarters which were not inoculated with endotoxin. Concentrations of whey IgG1 and IgM in endotoxin-inoculated quarters were significantly (P less than 0.05) decreased in flunixin meglumine-treated cows, compared with those in saline solution-treated cows. Significant increases in phagocytosis of staphylococci by milk PMN were observed in whey samples from endotoxin-inoculated quarters. Significant differences in PMN phagocytosis were not found in whey samples from cows given flunixin meglumine when compared with whey samples from cows given saline solution.

Analysis of Variance↗
PubMed1986

Plasma cortisol and norepinephrine concentrations in castrated male pigs maintained in pairs in outdoor pens and in a confinement finishing house: assessment of stress.

A catheter-backpack system was developed for repeated blood collection in pigs. Castrated male pigs (n = 12) were maintained in pairs in outdoor pens and later in a slotted-floor confinement finishing house. Blood collection required no restraint and appeared to be stress free. Serum cortisol concentration was unchanged by mode of maintenance. However, diurnal variation of cortisol was more pronounced when pigs were housed. A significant decrease (P less than 0.05) in serum norepinephrine concentration occurred during the housing period.

Animals↗
PubMed1985

Influenza B virus model of Reye's syndrome in mice: the effect of aspirin.

Aspirin is a possible cofactor with influenza B virus in Reye's syndrome. In an attempt to determine whether single or multiple doses of acetylsalicylic acid (ASA) alter mortality in an influenza B virus mouse model of Reye's syndrome, either ASA (300 to 667 mg/kg) or saline was given intraperitoneally to 3-week-old Balb/c mice. Two hours later, one median lethal dose (LD50) of influenza B/Lee virus was given intravenously. Mortality was not significantly increased by the single ASA dose. Blood ASA levels rose as high as 68 mg/dl. The average ASA blood levels in mice 12 hours after receiving the virus plus 667 mg/kg ASA was 22.6 mg/dl, which was significantly higher than the 3.4 mg/dl for mice who received saline plus ASA. No significant increase in mortality occurred in mice given 67 mg/kg ASA twice daily for 7 days and one LD50 dose of virus on day 4. We conclude that a single dose of ASA at up to half the median lethal dose or multiple doses of ASA do not significantly increase mortality in this influenza virus model of Reye's syndrome. However, influenza B virus infection appears to interfere with ASA metabolism.

Animals↗
PubMed1985

Neuropathology of ornithine carbamyl transferase deficiency.

Neuropathologic findings in two cases of ornithine carbamyl transferase (OCT) deficiency are presented. In one, a boy 3 days old, the only abnormality related to the enzyme defect was metabolic gliosis which was unusual in distribution being present mainly in the brain stem. In the other case, a girl who died at the age of 2 3/12 years, the brain showed metabolic gliosis in typical location, widespread ulegyria, and moderate atrophy of the internal granular layer in the cerebellum accompanied by development of expansions of Purkinje cell dendrites. Case 2 demonstrates how rapidly changes previously demonstrated in the cerebral cortex after a few months of illness can proceed to massive hemispheric destruction. By now ulegyria has been observed in several disorders of the urea cycle.

Brain↗
PubMed1985

Drugs and the liver.

The authors discuss the liver's influence on drug disposition in the body and the influence of drugs on the liver. Drug-induced hepatotoxicity with regard to mechanisms and causative agents is discussed, as well as administration of drugs to patients with existing liver disease.

Animals↗
PubMed1985

Preparation and characterization of antibodies with specificity for the amino-terminal tetrapeptide sequence of the platelet-derived connective tissue activating peptide-III.

Antisera selectively reactive with the N-terminal tetrapeptide sequence of the platelet-derived connective tissue activating peptide-III mitogen were prepared and characterized. Solid phase synthesized Z-Asn-Leu-Ala-Lys(Z)-OH tetrapeptide representing the N-terminus of the mitogen was used as an immunogen after carbodiimide mediated coupling to methylated bovine serum albumin carrier and subsequent removal of Z groups. Anti-tetrapeptide sera demonstrated cross-reactivity to the mitogen but not beta-thromboglobulin, fibroblast growth factor, or epidermal growth factor, and a limited cross-reactivity to parathyroid hormone. The studies indicate that the N-terminal sequence of the mitogen is accessible for binding with antibody and the antitetrapeptide sera provide a reagent for the selective measurement of biologically active mitogen in the presence of structurally similar beta-thrombo-globulin. In addition, computer analysis of amino acid sequences revealed that few proteins contain the Asn-Leu-Ala-Lys sequence and of those that do, many are retroviral proteins or transforming polyproteins.

Amino Acid Sequence↗
PubMed1984

Cisplatin neuropathy. Clinical, electrophysiologic, morphologic, and toxicologic studies.

Ten of 11 patients with ovarian cancer receiving cisplatin developed a distal sensory neuropathy, manifested early by decreased vibratory sensibility in toes and depressed ankle jerks and later by uncomfortable paresthesias. Eleven patients receiving cisplatin, 50 mg/m2 monthly (mean total, 580 mg/m2) were studied prospectively with monthly neurologic examinations and conduction velocity determinations of median, peroneal, and sural nerves. Early signs were decreased vibratory sensibility in toes (mean dose, 417 +/- 132 mg/m2 [SD]) and loss of ankle jerks (mean dose, 455 +/- 86 mg/m2). With continued therapy, four developed paresthesias. Strength was unaffected. Sural nerve responses abruptly disappeared in six of peripheral nerves from four patients showed axonal degeneration and secondary myelin breakdown. Platinum concentrations in three patients were similar in tumor (3.3 micrograms/g), sural nerves (3.5 micrograms/g), and spinal ganglia (3.8 micrograms/g), but lower in brain (0.17 microgram/g). This may explain the cisplatin toxicity of peripheral nerves with relative sparing of the central nervous system.

Adult↗
PubMed1984

Inner ear anomalies in Waardenburg's syndrome associated with Hirschsprung's disease.

Congenital inner ear anomalies are reported in temporal bones of a 22-month-old boy with Waardenburg's syndrome and Hirschsprung's disease. Although no changes in the central auditory pathway were identified, peripheral lesions of the cochlear and vestibular membranous labyrinth were observed. Bilateral atrophy of the organ of Corti and stria, and a sparsity of spiral ganglion cells were observed in the cochlea. Degeneration of the vestibular end organs, including a loss of Scarpa's ganglion cells, was also seen. This is the first report of temporal bone histopathology associated with Waardenburg's syndrome and Hirschsprung's disease. The pathoembryology of these inner ear anomalies associated with aganglionosis of the colon supports the hypothesis that Waardenburg's syndrome and Hirschsprung's disease are hereditary defects of neural crest cells.

Abnormalities, Multiple↗
PubMed1984

Halothane-sparing effect of xylazine in dogs and subsequent reversal with tolazoline.

Halothane MAC (the minimum alveolar concentration of halothane to produce anaesthesia in 50% of the animals tested) was determined to be 0.92 +/- 0.16 volumes % in eight English Pointer dogs. Alterations in halothane MAC induced by an intravenous bolus of xylazine (1.1 mg/kg) and then tolazoline (5 mg/kg) was determined in each dog following control (halothane MAC) measurement. Following xylazine administration, MAC significantly decreased to 0.57 +/- 0.023%. Immediately following determination of the xylazine-halothane MAC value in each dog, tolazoline was administered and the halothane requirement (MAC) was again assessed. Halothane MAC significantly increased to 1.24 +/- 0.036%. Tolazoline administration induced immediate arousal in the xylazine-halothane anaesthetized dogs requiring a rapid increase in halothane concentration to maintain anaesthesia. Thus, the administration of tolazoline, an alpha adrenergic antagonist, following xylazine administration significantly increased the anaesthetic requirement (MAC) of halothane. Xylazine, an alpha 2 adrenergic agonist, decreased halothane anaesthetic requirement (MAC) in the eight dogs studied. These results are consistent with the hypotheses that stimulation of central alpha 2 receptors is the mechanism by which xylazine produces sedation and that inhibition of CNS excitatory neurotransmitter release decreases halothane anaesthetic requirement.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗