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Biomedical subjects

D D Morris

Publications and source records attributed to D D Morris.

At least 73 records · Page 4Linked to original sources
PubMed1987

Endotoxin-induced production of thromboxane and prostacyclin by equine peritoneal macrophages.

Equine peritoneal macrophages were isolated and cultured in vitro to assess their ability to produce thromboxane (TxA2) and prostacyclin (PGI2) in response to endotoxin. Peritoneal macrophages (2.5 x 10(6)/ml) were incubated in tissue culture media, containing 1) no additive (nonstimulated control), 2) endotoxin (0.5 to 100 ng/ml) or 3) the calcium ionophore, A23187 (0.95 microM) for two and six h. Concentrations of the stable metabolites of TxA2 and PGI2 thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), in the incubation media were determined by radioimmunoassay. The concentrations of both metabolites increased from two to six h incubation. Endotoxin increased the production of TxA2 and PGI2 over the nonstimulated control values at both two and six h and endotoxin-induced concentrations of 6-keto-PGF1 alpha were higher at six than at two h. The response of macrophages to A23187 was similar to endotoxin. Mean eicosanoid concentrations did not differ among the range of endotoxin concentrations at either time; however there was significant curvilinear regression between endotoxin concentration and TxB2 at both times, and between endotoxin and 6-keto-PGF1 alpha at two h. The results indicate that equine macrophages may be a significant source of TxA2 and PGI2 during endotoxemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Esophageal dysfunction in a weanling thoroughbred.

A 6-month-old Thoroughbred colt was examined because of persistent dysphagia noted since birth. Moderately severe regurgitation occurred when the colt ate semi-solid food or drank. Complete esophageal impaction developed when the colt ate solid material. Endoscopic examination revealed ulceration, dilatation and lack of peristalsis in the area of the previous impaction. Barium esophagram demonstrated the dilatation in the area of the previous impaction. Esophageal manometry revealed prolonged simultaneous contractions throughout the esophagus suggesting the presence of a motor abnormality. The colt was maintained on a slurry of complete pelleted feed, but the esophageal dysfunction persisted until euthanasia at 17 months of age. Gross post mortem and histologic examinations showed no abnormalities in the muscularis mucosa, myenteric plexus, vagus nerve, or brain stem. The history, signs, and manometric findings suggested esophageal dysfunction in this colt. Motor disorders of the esophagus should be considered in horses with persistent dysphagia or recurrent episodes of choke and esophageal manometry can help characterize these disorders.

Animals↗
PubMed1987

Esophageal manometry in horses, cows, and sheep during deglutition.

Esophageal pressure events during deglutition were evaluated in healthy adult animals (6 horses, 6 cattle, and 5 sheep), using a 3-side hole catheter assembly perfused with water by use of a hydraulic-capillary infusion system. The peak postdeglutition pressure, contraction time, and contraction length were determined for the cranial and caudal esophageal sphincter regions and for each functionally different region within the body of the esophagus. The percentage of deglutitions in which relaxation developed at the sphincter regions and the propagation speed (velocity at which pressure waves traversed the esophagus) for the regions within the body of the esophagus also were determined. Mean (+/- SEM) resting pressures within the cranial and caudal esophageal sphincter regions in the horse were 84.8 +/- 4.39 and 12.7 +/- 0.61 mm of Hg, respectively, with postdeglutition peaks of 208.0 +/- 4.78 and 100.0 +/- 1.06 mm of Hg, respectively. Peak postdeglutition pressure was 92.3 +/- 1.59 mm of Hg in the cranial two thirds of the esophageal body and 100.9 +/- 1.31 mm of Hg in the caudal third. Mean resting pressure of the cranial esophageal sphincter region in the cow was 82.0 +/- 7.81 mm of Hg, whereas that of the caudal esophageal sphincter region was 20.5 +/- 0.36 mm of Hg. The peak postdeglutition pressures for the cranial esophageal sphincter region, proximal portion of the esophageal body, caudal portion of the esophageal body, and caudal esophageal sphincter region in the bovine esophagus were 238.1 +/- 2.93, 105.4 +/- 1.97, 114.5 +/- 1.49, and 112.0 +/- 1.20 mm of Hg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Plasma antithrombin-III values in healthy horses: effect of sex and/or breed.

Plasma antithrombin-III (AT-III) values were determined in 74 healthy horses by an automated spectrophotometric assay. The mean plasma AT-III value was 218% +/- 18% of normal human plasma. Plasma AT-III values did not differ significantly (P less than 0.05) among Thoroughbred, Standardbred, Quarter Horse, and other breeds or among mares, geldings, or stallions.

Animals↗
PubMed1987

Evaluation of granulocyte transfusion in healthy neonatal pony foals.

Granulocyte transfusions (GT), 0.98 X 10(9) neutrophils/kg of body weight, were performed on 7 healthy pony foals between 2 and 7 days old. The mean neutrophil count of the foals was significantly (P less than 0.05) greater than base line (4,830 +/- 1,260/microliter) 1 hour after GT (8,870 +/- 3,350/microliter) and was similar to base line by 15 to 18 hours after GT (6,550 +/- 2,310/microliter). Leukocyte concentrates (LC) used for GT were harvested from clinically normal adult horses by continuous-flow centrifugation leukapheresis (CL), 3 to 6 hours after hydrocortisone sodium succinate was administered to increase the blood neutrophil count. The mean neutrophil count of the LC used for GT was 68,050 +/- 13,990/microliter, and the mean LC volume was 377.4 +/- 79.2 ml (14.82 +/- 3.54 ml/kg). The mean time required to collect the LC used for GT was 232.1 +/- 73.4 minutes. Neutrophils from LC had significantly reduced in vitro stimulated migration to zymosan-activated serum, when compared with peripheral blood neutrophils of the donors (P less than 0.05). Neutrophil phagocytosis and bactericidal capacity were not significantly changed in LC. Mean neutrophil migration indices were not significantly different in foals after GT. Mild depression and transient diarrhea was noticed in 1 foal 30 minutes after the start of the GT. The donor of LC for this foal and 1 other donor experienced depression, piloerection, and muscle tremors during CL, indicating that complement had been activated. Problems were eliminated by the use of new disposable plastic materials for blood processing in each CL procedure.

Animals↗
PubMed1986

Role of leukocytes in response to acute myocardial ischemia and reflow in dogs.

Recent evidence indicates that leukocytes (LEU) are large, stiff, viscous cells that naturally adhere to vascular endothelium. Their broad role in the early myocardial microvascular response to acute ischemia was suggested by 1) the role of leukocyte capillary plugging in the no-reflow phenomenon, 2) resistance increases in skeletal muscle with LEU infusions, and 3) salvage of ischemic myocardium by anti-LEU agents. We perfused the coronary circulation under matched, controlled conditions with whole blood or granulocyte-depleted whole blood. During 1 h of ischemia (left anterior descending occlusion) circumflex perfusion pressure was servocontrolled to a constant value. In whole blood-perfused hearts, flow measured by the radiolabeled microsphere method decreased in endocardium from 0.12 +/- 0.05 at 5 min of ischemia to 0.09 +/- 0.04 ml X min-1 X g-1 at 60 min of ischemia and in epicardium from 0.27 +/- 0.17 to 0.21 +/- 0.16 ml X min-1 X g-1, both P less than 0.05. In granulocyte-depleted blood-perfused hearts, flow increased over the same period from 0.18 +/- 0.15 to 0.29 +/- 0.18 ml X min-1 X g-1 in endocardium (P less than 0.05) and did not change significantly in epicardium (0.36 +/- 0.22 to 0.41 +/- 0.24 ml X min-1 X g-1). The LEU-depleted blood perfusate contained less than 33 granulocytes/microliter, whereas control perfusate contained 4,265/microliter. Reperfusion at normal pressures with carbon suspension allowed for histologic evaluation of the no-reflow phenomenon. With whole blood perfusion the no-reflow phenomenon in the endocardium was present with 27% of capillaries occluded, compared with nearly complete reperfusion in LEU-depleted animals (1% of capillaries occluded, P less than 0.05). Furthermore, LEU depletion prevented the increases in tissue water content seen in control hearts and decreased the incidence of ventricular arrhythmias. These studies demonstrate the significant participation of granulocytes in the unfavorable responses of flow, edema formation, and arrhythmias to the 1st h of myocardial ischemia and further document their role in the no-reflow phenomenon.

Acute Disease↗
PubMed1986

Endotoxemia in horses: protection provided by antiserum to core lipopolysaccharide.

An equine antiserum to core lipopolysaccharide was produced by inoculation of 6 horses with a boiled cell bacterin made from the J-5 mutant of Escherichia coli O111:B4. The antiserum immunoglobulin G titer to J-5 mutant E coli, as determined by enzyme-linked immunosorbent assay, was 1:15,006. Pooled serum prepared before inoculation (preimmune serum) had a J-5 immunoglobulin G titer of 1:350. The J-5 antiserum was tested for its protective efficacy in sublethal endotoxemia in 14 horses. Four horses served as nontreated controls and were given nothing before endotoxin challenge exposure (10 micrograms/kg of body weight, IV). Pooled preimmune serum (3 ml/kg, IV) was administered to 5 horses and J-5 antiserum (3 ml/kg, IV) was administered to 5 other horses 2 to 15 hours before endotoxin challenge exposure. During the 24 hours postendotoxin challenge exposure, endotoxemia was accompanied by significant (P less than 0.05) time-related changes in temperature, heart rate, pulse character, respiratory rate and character, capillary refill time, mucous membrane color, fecal composition, attitude, PCV, total plasma protein, WBC count, platelet count, plasma fibrinogen, prothrombin time, activated partial thromboplastin time, fibrinolytic degradation products, plasma glucose, and plasma lactate in all horses. There were no apparent treatment vs time interactions (P greater than 0.05). Two horses (1 control and 1 given J-5 antiserum) died suddenly from unknown causes immediately after endotoxin challenge exposure. Seemingly, equine antiserum to core lipopolysaccharide did not provide protection from the adverse effects of experimental endotoxemia produced by bolus IV infusion of 10 micrograms of endotoxin/kg.

Animals↗
PubMed1986

Endotoxin-induced changes in the hemostatic system in neonatal calves: the effect of antiserum to a mutant Escherichia coli (J-5).

Changes in the hemostatic system were studied in 22 neonatal calves given a small dosage of Escherichia coli endotoxin (0.5 microgram/kg) by slow (5-hour) IV infusion. The effect of pretreatment with an antiserum to mutant of E coli O111:B4 (J-5) was evaluated. The platelet count, plasma fibrinogen concentration, prothrombin time, and activated partial thromboplastin time changed significantly from base line during and after endotoxin infusions in all calves. The mean platelet count was significantly decreased from 1 through 24 hours after endotoxin infusion was started. Mean plasma fibrinogen was decreased 2 through 12 hours after endotoxin infusion was started. The mean prothrombin time and activated partial thromboplastin time were significantly greater than base line at 3 to 6 hours and 3 to 12 hours, respectively, after endotoxin infusion was started. Serum concentration of fibrinolytic degradation products remained less than 10 micrograms/ml. Bovine J-5 antiserum did not prevent the endotoxin-induced changes in the hemostatic system of these neonatal calves.

Animals↗
PubMed1986

Endotoxin-induced changes in plasma concentrations of thromboxane and prostacyclin in neonatal calves given antiserum to a mutant Escherichia coli (J-5).

Plasma concentrations of the stable hydrolysis products of thromboxane (Tx) A2, TxB2, and prostacyclin (6-keto-prostaglandin F1 alpha; PGF1 alpha) were evaluated in 22 neonatal calves given endotoxin (0.5 microgram/kg) by slow IV infusion over a 5-hour period. The effect of pretreatment with bovine antiserum to a mutant of Escherichia coli O111:B4 (J-5) on plasma concentrations of these eicosanoids was determined. Plasma concentrations of TxB2 and 6-keto-PGF1 alpha were increased in response to endotoxin infusion. The mean plasma concentrations of TxB2 peaked 1 hour after endotoxin infusion began and was significantly increased from base line through 8 hours. Mean plasma 6-keto-PGF1 alpha concentration increased more slowly and was increased from base line only at 2 hours after endotoxin infusion began. Administration of bovine J-5 antiserum had no significant effect on endotoxin-induced thromboxane and prostacyclin production.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Endotoxemia in neonatal calves given antiserum to a mutant Escherichia coli (J-5).

Endotoxemia was characterized in neonatal calves given a small amount of colostrum and smooth Escherichia coli endotoxin by small-dosage (0.5 microgram/kg of body weight), slow (5-hour) IV infusion to mimic natural conditions. Responses were compared among 22 calves freely allotted to groups treated with saline solution (group I), preimmunization plasma (PP, group II), or antiserum to the rough mutant of E coli O111:B4 (J-5, group III) before endotoxin was infused. Bovine J-5 antiserum was produced by immunization of 4 cattle with J-5 boiled cell bacterin. The antiserum titers of immunoglobulin (Ig) M, IgG1, and IgG2 to the J-5 boiled cells, as determined by enzyme-linked immunosorbent assay, were 240, 7,680, and 960, respectively. The PP had enzyme-linked immunosorbent assay titers to J-5 of 240, 480, and 60 of IgM, IgG1, and IgG2, respectively. Endotoxemia in the 3 groups was characterized by significant (P less than 0.05) time-related changes in rectal temperature, heart rate, respiratory rate, capillary refill time, oral mucous membranes, nose moistness, scleral injection, attitude, PCV, total plasma protein concentration, WBC count and differential, plasma glucose, and lactate concentrations. The only significant treatment effects on clinical or laboratory values were higher mean total plasma protein concentrations in groups II and III 10 to 30 hours after endotoxin infusion was started than that in group I and increasing mean most-severe attitude abnormality score in groups I, III, and II (P less than 0.05). The administration of bovine J-5 antiserum to neonatal calves resulted in significantly higher serum IgG1 and IgG2 titers to J-5 boiled cells (P less than 0.05), and cross-reactive IgG2 to the challenge endotoxin (P less than 0.01) than did treatment with PP or saline solution; however, this antiserum did not mitigate the effects of sublethal endotoxemia. There was a significant negative correlation between IgG2 to J-5 at base line and the mean attitude abnormality score at 4.5 hours after infusion was started (P less than 0.05).

Animals↗
PubMed1985

Pleural effusion secondary to metastasis of an ovarian adenocarcinoma in a horse.

An 11-year-old Quarter Horse mare was presented with ventral edema and pleural effusion, secondary to a disseminated ovarian adenocarcinoma. Bilateral thoracocentesis yielded 30 L of thin, blood-tinged fluid, which was a modified transudate. Cytologic examination of the fluid revealed large atypical cells, suggestive of carcinomatous neoplasia. Similar cells were found in the peritoneal fluid. The mare was euthanatized. Necropsy revealed a 35-cm diameter mass in the cranial mediastinum, ventral to the trachea. The left ovary was 25 cm in diameter and most of the parenchyma was replaced by red or brown friable tissue, containing numerous 1-to 3-mm cysts. Papillary adenocarcinoma of the ovary was diagnosed, based on the appearance and arrangement of tumor cells in the ovary, sublumbar and tracheobronchial lymph nodes, and mediastinal mass. Ovarian neoplasia should be considered in the differential diagnosis of pleural effusion in the horse.

Adenocarcinoma, Papillary↗
PubMed1985

Bovine viral diarrhea in a newborn calf.

Bovine viral diarrhea virus was believed to be the cause of ill-thrift since birth, resulting in death of a Holstein calf. Bovine viral diarrhea virus was isolated from Peyer's patches and mesenteric lymph nodes, but serum neutralizing antibodies were not detected. The lymphoid depletion and myeloid suppression seen in this case may be a factor in the immune system dysfunction described for bovine viral diarrhea. Typical ulcerative lesions within the alimentary tract were not observed.

Animals↗
PubMed1985

Effects of phenylbutazone and anabolic steroids on adrenal and thyroid gland function tests in healthy horses.

Adrenal and/or thyroid gland function tests were evaluated in horses at various times during short-term therapy with phenylbutazone, stanozolol, and boldenone undecylenate. There were no significant treatment or time effects on mean basal plasma cortisol concentrations in horses during treatment with the following: phenylbutazone, given twice daily (4 to 5 mg/kg, IV) for 5 days; stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was no significant effect of phenylbutazone treatment on the changes in plasma cortisol concentration during the combined dexamethasone-suppression adrenocorticotropic hormone (ACTH)-stimulation test. Plasma cortisol concentration was significantly decreased from base line at 3 hours after dexamethasone administration and was significantly increased from base line at 2 hours after ACTH in all horses (P less than 0.05). Likewise, the stimulation of basal plasma cortisol concentrations at 2 hours after administration of ACTH (P less than 0.05) was not affected by treatment with stanozolol or boldenone undecylenate. There were no significant treatment effects on mean basal plasma concentrations of thyroxine (T4) or triiodothyronine (T3) among horses during the following treatments: stanozolol, given twice weekly (0.55 mg/kg, IM) for 12 days; boldenone undecylenate, given twice weekly (1.1 mg/kg, IM) for 12 days; or nothing. There was a significant time effect on overall mean basal plasma T4 and T3 concentrations (P less than 0.05): plasma T4 was lower on day 8 than on days 1, 10, and 12; plasma T3 was higher on day 8 than on days 4 and 12.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Function Tests↗
PubMed1985

Comparison of rectal mucosal cultures and fecal cultures in detecting Salmonella infection in horses and cattle.

Bacteriologic cultures of 65 rectal mucosal samples and 335 fecal samples from 53 horses and 5 cattle shedding Salmonella were performed. Salmonella spp were isolated from 34 (52%) rectal mucosal samples, 21 (32%) concurrent fecal samples, and 150 (45%) total fecal samples. The use of rectal mucosal samples when compared with concurrently obtained fecal samples significantly (P less than 0.025) improved the ability to isolate Salmonella spp. Concurrent bacteriologic culture of rectal mucosal samples and fecal samples resulted in 39 (60%) isolations. Compared with a series of fecal samples, Salmonella was isolated significantly more often when rectal mucosa and feces were cultured concurrently. Salmonella was isolated from rectal mucosal samples when it was not isolated from feces.

Animals↗
PubMed1985

Passive transfer failure in horses: incidence and causative factors on a breeding farm.

A prospective study was performed to determine the incidence and associated maternal and managemental factors of failure of passive transfer (FPT) in foals on a breeding farm. The zinc sulfate turbidity test (ZSTT) and latex agglutination test (LAT) were compared for accuracy in estimating serum immunoglobulin (Ig)G of foals, as determined by single radial immunodiffusion (SRID). Complete past and present foaling histories of 136 Standardbred mares were obtained. All foalings were witnessed by farm attendants, and colostral samples were collected from mares within 2 hours after parturition. Foals that did not rise and nurse were supplemented with colostrum from the dam, using a bottle or nasogastric tube. Serum samples were prepared from foals and mares between 24 and 36 hours after parturition, and from some mares 45 to 90 days before parturition. Serum IgG concentrations of mares and foals and colostral whey were determined, using SRID. Serum IgG also was estimated in foals, using ZSTT and a commercially available LAT. Four of the 136 foals (2.9%) had FPT (serum IgG less than or equal to 400 mg/dl). Serum IgG concentrations in foals significantly correlated with colostral IgG (P less than 0.001). A significantly larger proportion of foals with FPT were bottle-fed their colostrum (P less than 0.01). Month of parturition, mare age, parity, number of barren seasons, incidence of assisted births or retained placenta, or prepartum serum IgG concentrations did not significantly affect colostral IgG concentrations or serum IgG concentrations in foals. As serum IgG concentrations in foals decreased and as colostral IgG concentrations decreased, the proportion of mares that prelactated significantly (P less than 0.01) increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Eosinophilic myeloproliferative disorder in a horse.

An eosinophilic myeloproliferative disorder resulted in edema and hemorrhagic diathesis in a 10-month-old Standardbred colt. Laboratory abnormalities included severe thrombocytopenia, anemia, mild hypoproteinemia, and marked eosinophilia. Circulating eosinophils were immature or atypical with variation in granule size, disproportionate nuclear to cytoplasmic maturation, and abnormal nuclear size and shape. Bone marrow aspirate had mainly atypical eosinophil precursors, few erythroid precursors, and no megakaryocytes. A blood transfusion and dexamethasone therapy resulted in some improvement; however, the horse was euthanatized due to poor prognosis. Postmortem examination showed gastrointestinal parasitism; histologically the spleen was infiltrated by atypical eosinophils and there were sites of eosinophilopoiesis. The disease was broadly similar to idiopathic hypereosinophilic syndrome in people, but typical cardiac and neurologic involvement of hypereosinophilic syndrome were absent. Progressive myelophthesis and marked eosinophil atypia suggested malignancy.

Animals↗