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D J Weiss

Publications and source records attributed to D J Weiss.

At least 19 recordsLinked to original sources
PubMed1992

Neutrophil-induced immunoglobulin binding to erythrocytes involves proteolytic and oxidative injury.

Neutrophil-induced alterations in feline erythrocytes were studied to better understand the pathogenesis of erythrocyte destruction associated with inflammatory diseases. As in previous studies, addition of superoxide dismutase/catalase to a coculture of erythrocytes and activated neutrophils attenuated neutrophil-induced immunoglobulin G (IgG) binding. However, incubation of erythrocytes with hydrogen peroxide or neutrophil-derived anuclear cytoplasts (neutroplasts) failed to induce IgG binding. Addition of phenylmethylsulfonyl fluoride, a serine protease inhibitor, to the erythrocyte-neutrophil coculture attenuated IgG binding. These observations suggest that neutrophil-derived serine protease activity is involved in IgG binding to erythrocytes. Further, incubation of erythrocytes with serine proteases, but not metalloproteases or sulfhydryl proteases, induced immunoglobulin binding. Freeze-fracture replicas of the erythrocyte membrane failed to demonstrate clustering of band 3 protein, suggesting that spatial rearrangement of band 3 protein was not the cause of the IgG binding. Neutrophil-induced IgG binding due to the combined action of proteases and oxidants may explain the accelerated destruction of erythrocytes in inflammatory diseases.

Animals↗
PubMed1992

Effects of Pasteurella haemolytica A1 leukotoxin on bovine neutrophils: degranulation and generation of oxygen-derived free radicals.

To further define the role of Pasteurella haemolytica A1 leukotoxin in the pathogenesis of bovine pneumonic pasteurellosis, its in vitro effects on bovine neutrophils were investigated. Leukotoxin-containing culture supernatant, from P. haemolytica, stimulated a neutrophil respiratory burst as measured by the generation of oxygen-derived free radicals O2- and H2O2. This effect was immediate because preincubation of neutrophils with the culture supernatant for 5 min or longer substantially suppressed this respiratory burst. This suppression was due to cytolysis of the neutrophils. Prolonged incubation of neutrophils with the same culture supernatant caused further cytolysis and degranulation. Heat-inactivated P. haemolytica culture supernatant that had lost its cytotoxic properties failed to stimulate respiratory burst by neutrophils. Furthermore, the respiratory burst, cytolysis and degranulation were abrogated only by leukotoxin-neutralizing monoclonal and polyclonal antibodies, but not by antibodies against the lipopolysaccharide. These studies show that the leukotoxin component in the culture supernatant was responsible for the generation of oxygen-derived free radicals and proteolytic enzymes from neutrophils which may participate in direct lung injury.

Animals↗
PubMed1992

Assessment of the hematopoietic system in ruminants.

The hemic system is examined to evaluate clinical signs referable to the hemic system, establish a data base, or monitor the course of disease processes. Clinical signs of hemic disorders include pale mucous membranes, icterus, hemorrhage, hemoglobinuria, and tachycardia. Compared to other species, ruminants have small red blood cells, respond to anemia by releasing stippled red blood cells, commonly become neutropenic during acute bacterial sepsis, and fail to develop marked neutrophilia or left shift in response to inflammation.

Animals↗
PubMed1992

Effects of pentoxifylline on equine neutrophil function and flow properties.

Pentoxifylline has been reported to improve peripheral vascular circulation by altering the flow properties of blood. To determine if the hemorrheological effects of pentoxifylline were mediated by alterations in neutrophil function and/or flow properties, we evaluated the drug's effects on equine neutrophils in vitro. Pentoxifylline, at a concentration of 1 x 10(-1) M, but not at concentrations of 1 x 10(-6) M to 1 x 10(-2) M, markedly suppressed neutrophil superoxide production, zymosan phagocytosis and adherence to nylon wool. Pentoxifylline failed to improve neutrophil filterability through 3 mu polycarbonate filters at any concentration tested. We conclude that equine neutrophil function and flow properties are unlikely to be affected by pentoxifylline concentrations achievable in vivo.

Animals↗
PubMed1992

Hematological alterations in kittens induced by 6 and 12% dietary propylene glycol.

Soft-moist cat foods containing 6-13% propylene glycol (PG) induce Heinz body formation and decreased red blood cell (RBC) lifespan in adult cats in a dose dependent manner. Since kittens eat relatively more food/kg of body weight and must expand their blood volume in addition to replacing senescent RBC, the hematologic dyscrasia associated with consumption of PG-containing diets may be exaggerated. To test this hypothesis 21 kittens were divided into 3 groups of 7 each and fed diets containing, 0,6 or 12% PG for 13 w. A dose-related increase in Heinz bodies occurred in the 6 and 12% PG groups within 2 w and persisted throughout the study. Although only slight changes occurred in hematocrit, hemoglobin and red blood cell (RBC) count, punctate reticulocytes increased significantly in the 6 and 12% PG groups indicating accelerated erythropoiesis. Mean RBC survival was decreased in the 6 and 12% groups by 44% and 63% respectively when compared to the control group. The increase in reticulocyte count and reduction in RBC lifespan was greater than observed in adult cats. The greater effect in kittens may be due to greater PG intake and not to an inate susceptibility of kitten RBC to PG.

Animal Feed↗
PubMed1992

Furosemide-induced electrolyte depletion associated with echinocytosis in horses.

Echinocytes have been incriminated in the pathogenesis of exertional diseases in horses. To evaluate the hypothesis that echinocytes are dehydrated erythrocytes, we decreased blood sodium and potassium concentrations in 4 horses by administering furosemide (1.0 mg/kg of body weight, q 12 h) for 2 days and we monitored CBC, serum and erythrocyte sodium and potassium concentrations, and echinocyte numbers. Serum sodium concentration decreased progressively over the 48 hours of furosemide administration, then returned to near baseline concentration at 168 hours. A statistically significant decrease (P < 0.05) in serum potassium concentration was observed at 24, 48, and 72 hours after initial furosemide administration, and remained less than the baseline value at the end of the study. Mean erythrocyte potassium concentration decreased rapidly and remained low at the end of the study. Minimal changes were observed in erythrocyte sodium concentration during the first 72 hours after furosemide administration, but the value was significantly (P < 0.05) increased at 168 hours. Type-I and type-II echinocyte numbers increased by 4 hours after furosemide administration and persisted throughout the study. Type-III echinocytes were not seen in baseline samples, but numbers increased only modestly after furosemide administration. Administration of epinephrine to well-hydrated horses increased echinocyte numbers only minimally, indicating that splenic contraction was not the likely cause for the furosemide-associated increase. To determine whether the decrease in erythrocyte potassium concentration and increase in sodium concentration was caused by furosemide acting directly on the erythrocyte membrane, we quantified erythrocyte potassium and sodium concentrations before and after incubation with furosemide in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of furosemide and pentoxifylline on blood flow properties in horses.

The effects of furosemide and pentoxifylline on blood flow properties in horses were investigated. Hematologic and rheologic changes were examined in 4 horses before and 3 minutes after administration of epinephrine (1 mg, IV). The next day, hemorheologic changes were determined before and 3 hours after administration of furosemide (1 mg/kg of body weight, IM), and after administration of epinephrine at the sampling at 3 hours. Hematologic and rheologic changes were evaluated weekly in 3 horses given pentoxifylline (8.5 mg/kg, q 12 h, PO) for 28 days. In addition, hemorheologic responses to epinephrine were determined on days 0, 14, and 28 of pentoxifylline treatment. Neutrophil filtration studies were also performed 2 hours after IV administration of pentoxifylline (8.5 mg/kg). Postepinephrine values for PCV, RBC and WBC counts, and blood viscosity were greater than preepinephrine values. Erythrocyte sedimentation rates decreased after epinephrine, whereas RBC filterability did not change. Treatment with furosemide was associated with increases in mean RBC hemoglobin concentration and blood viscosity. Filterability of RBC did not change. Treatment with pentoxifyllie resulted in an increase in RBC filterability and erythrocyte sedimentation rate and a decrease in PCV; however, mean values for hematocrit and RBC count did not change. Treatment with pentoxifylline did not result in a change in resting blood viscosity, but markedly reduced the postepinephrine increase in blood viscosity. Neither IV nor orally administered pentoxifylline had an effect on neutrophil filtration. It was concluded that pentoxifylline has beneficial effects on RBC filterability and postepinephrine changes in blood viscosity, which may contribute to improvements of microcirculatory blood flow. In addition, furosemide may exacerbate exercise-associated hyperviscosity in horses.

Animals↗
PubMed1992

Evaluation of hemorheologic variables as implications for exercise-induced pulmonary hemorrhage in racing thoroughbreds.

Hematologic and rheologic changes were examined in 49 Thoroughbreds before and after competitive racing. Mean postrace values for RBC count, hemoglobin concentration, and PCV increased by 58 to 61%, whereas blood viscosity increased 2 to 3 times. Postrace echinocyte numbers were 162% greater than prerace values. Smaller, but statistically significant, changes were found for mean corpuscular hemoglobin concentration, red cell distribution width, plasma total protein concentration, total WBC count, neutrophil count, and lymphocyte count. Variables measured did not predict whether a horse was a bleeder not treated with furosemide, a bleeder treated with furosemide, or a nonbleeder.

Animals↗
PubMed1992

Hematologic alterations in adult cats fed 6 or 12% propylene glycol.

Cat foods containing propylene glycol (PG) induce Heinz body formation in feline erythrocytes. To further study the hematologic importance of dietary PG, 21 adult cats were allotted to 3 groups of 7 each and fed diets containing 0, 6, or 12% PG on a dry-weight basis. Cats fed PG had a dose-related increase in Heinz bodies within 2 weeks, and the increase persisted throughout the study. Although only slight changes occurred in PCV, hemoglobin concentration, and RBC count, punctate reticulocytes were significantly increased in the group fed 12% PG. Mean RBC survival was decreased in the groups fed 6 or 12% PG by 30 and 55%, respectively, compared with the control group. These data indicate that PG-containing diets cause a dose-dependent erythrocyte destruction, even when fed at concentrations as low as 6%.

Animal Feed↗
PubMed1991

White cells.

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Animals↗
PubMed1991

Morphological and morphometrical analysis of the acute response of the bovine alveolar wall to Pasteurella haemolytica A1-derived endotoxin and leucotoxin.

Endotoxin or leucotoxin derived from Pasteurella haemolytica biotype A serotype 1 or saline was deposited by fibreoptic bronchoscopy into the caudal segment of the right anterior lung lobe of calves, and the lesions were characterized by light and transmission electron microscopy. Morphometric techniques were used to determine if changes in the arithmetic mean thickness of the alveolar wall occurred. Group 1 calves (n = 2) were inoculated with 6 ml saline, groups 2 calves (n = 3) received 6 ml of a partially purified leucotoxin preparation, group 3 calves (n = 3) received 96 micrograms of endotoxin in 6 ml of saline and group 4 calves (n = 3) received 2.5 mg of endotoxin in 6 ml of saline. Calves were killed 4 h after inoculation. Lesions in groups 2, 3 and 4 were similar and we found that (a) endotoxin alone is capable of initiating an inflammatory response in the bovine lung, (b) leucotoxin causes cytotoxic changes in alveolar macrophages but not in parenchymal cells of the lung, (c) neutrophil sequestration and platelet aggregation occur in alveolar capillaries in association with pulmonary intravascular macrophages, (d) neutrophils and fibrin were found in the alveolus in close association with alveolar macrophages, (e) disruption of the alveolar epithelial layer occurred in association with neutrophils and (f) there were no significant increases in the arithmetic mean thickness of the alveolar wall.

Animals↗
PubMed1991

Alterations in pulmonary morphology and peripheral coagulation profiles caused by intratracheal inoculation of live and ultraviolet light-killed Pasteurella haemolytica A1 in calves.

Eighteen male Holstein calves were divided into groups of three and inoculated intratracheally with 5 x 10(9) logarithmic phase or ultraviolet light-killed Pasteurella haemolytica biotype A serotype 1. Serial coagulation profiles were done on one calf from each group during the first 24 hours after inoculation. One calf from each group was necropsied at 4, 12, and 24 hours after inoculation and lesions were characterized with light and transmission electron microscopy. We found that 1) the pulmonary intravascular macrophage may have an important role in the early intravascular inflammatory events; 2) there was morphologic evidence for local initiation of the coagulation cascade in the lung early in the disease process but it was not a consumptive process; and 3) killed-bacteria were capable of causing fibrin exudation, platelet aggregation and alveolar epithelial damage similar to live bacteria, but the degenerative changes in neutrophils, endothelial cells and intravascular fibrin formation that occur with live bacteria were not seen.

Animals↗
PubMed1991

Changes in blood and bronchoalveolar lavage fluid components in calves with experimentally induced pneumonic pasteurellosis.

Pneumonic pasteurellosis was experimentally induced in calves by inoculation of 5 x 10(8) Pasteurella haemolytica organisms into the right diaphragmatic lung lobe. Blood and bronchoalveolar lavage fluid samples were obtained prior to inoculation and at postinoculation hour (PIH) 2, 4, and 6. Calves developed acute lung injury, characteristic of pneumonic pasteurellosis. Lesions were found only in the right diaphragmatic lobe. By PIH 4, significant (P less than 0.01) increases were detected in lavage fluid total cell count, neutrophil count, total protein and albumin concentrations, and alkaline phosphatase (ALP) and lactic dehydrogenase (LD) activities. Myeloperoxidase and elastase activities did not increase. Neutrophil depletion ameliorated the lung lesions and prevented the increase in lavage fluid cell count, total protein, and albumin concentrations and ALP and LD activities. Treatment with the iron chelator, deferoxamine mesylatehydroxyethyl starch, attenuated the increase in total protein and albumin concentrations and ALP and LD activities at PID 4, but not PIH 6. Treatment with a neutrophil function inhibitor, pentoxifylline, prevented the increase in lavage fluid neutrophil numbers, but accentuated the increase in total protein and albumin concentrations, and ALP, LD, myeloperoxidase, and elastase activities.

Animals↗
PubMed1990

Effects of propylene glycol-containing diets on acetaminophen-induced methemoglobinemia in cats.

Soft-moist cat foods contain 7 to 13% propylene glycol (PG) on a dry-weight basis. These diets induce Heinz body formation in feline RBC. In this study, we evaluated cats on a control diet and on a commercial diet containing 8.3% PG. All cats on the PG diet developed an increase in the number of circulating Heinz bodies. We then administered acetaminophen to cats on each diet to determine whether RBC from cats on PG diets were more susceptible to oxidant stress. Methemoglobin concentrations were significantly greater in cats in PG diets after acetaminophen administration. These data indicate that RBC from cats fed PG diets are more susceptible to oxidative stress.

Acetaminophen↗
PubMed1990

Drug-associated aplastic anemia in dogs: eight cases (1984-1988).

Records of 8 dogs with drug-associated aplastic anemia were reviewed. Drugs suspected as being causative included estradiol cyclopentylpropionate (3 dogs), phenylbutazone (2 dogs), meclofenamic acid (1 dog), trimethoprim-sulfadiazine and fenbendazole (1 dog), and quinidine (1 dog). Five of the dogs died or were euthanatized. One dog with estrogen-associated aplasia recovered after prolonged treatment. The dogs with trimethoprim-sulfadiazine and quinidine-associated marrow aplasia recovered promptly after treatment was discontinued.

Anemia, Aplastic↗
PubMed1990

Activated neutrophils induce erythrocyte immunoglobulin binding and membrane protein degradation.

Neutrophil-induced alterations in feline erythrocytes were investigated to elucidate the pathogenesis of the erythrocyte destruction associated with inflammatory disease. Incubation of erythrocytes with zymosan-activated neutrophils, at target:effector concentrations of 50:1, resulted in immunoglobulin binding to the erythrocyte membrane and degradation of membrane proteins. Vitamin E and superoxide dismutase/catalase attenuated the immunoglobulin binding. Proteolysis was not prevented by addition of antioxidants or protease inhibitors to the erythrocyte:neutrophil coculture and was not reproduced with chemical oxidation or calcium loading of erythrocytes.

Animals↗
PubMed1990

Immunohistochemical localization of Pasteurella haemolytica A1-derived endotoxin, leukotoxin, and capsular polysaccharide in experimental bovine Pasteurella pneumonia.

Six, 5- to 10-week-old male Holstein calves were inoculated intratracheally with 5 x 10(9) logarithmic growth phase Pasteurella haemolytica biotype A serotype 1 (A1). Immunohistochemical techniques in conjunction with the use of monoclonal antibodies directed against P. haemolytica A1-derived lipopolysaccharide (LPS), capsular polysaccharide, and a polyclonal rabbit anti-leukotoxin antibody were used to localize their respective antigens in tissue sections of pneumonic lung at the light and electron microscopic levels. We found the following: 1) LPS, capsular polysaccharide, and leukotoxin were released into the inflammatory exudate; 2) LPS was found within the cytoplasm of neutrophils (located in the alveolus and alveolar wall), alveolar macrophages, endothelial cells, pulmonary intravascular macrophages, and on epithelial cell surfaces; 3) capsular polysaccharide was found in the alveolus and alveolar macrophages but not in cells of the alveolar wall; and 4) leukotoxin was associated with cell membranes of degenerating inflammatory cells located in the alveolus. This is the first study that demonstrates the presence of leukotoxin in the pulmonary inflammatory lesions caused by P. haemolytica A1 and implicates endotoxin as an important factor in the genesis of the pulmonary lesions.

Animals↗