Stingray injury to a horse in coastal waters off eastern Australia.
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Animals↗
Biomedical subjects
J B Carrick
Publications and source records attributed to J B Carrick.
Effect of intravenous infusion of omega-3 and omega-6 lipid emulsions on equine monocyte fatty acid composition and inflammatory mediator production in vitro.
The effect of intravenous administration of lipid emulsions enriched with omega-3 (n3) and omega-6 (n6) fatty acids on equine monocyte phospholipid fatty acid composition and the synthesis of inflammatory mediators in vitro was evaluated. In a randomized crossover design, horses were infused intravenously with 20% lipid emulsions containing n3 or n6 fatty acids. Monocytes were isolated from the horses before and 0 h, 8 h, 24 h, and 7 days after lipid infusion. Monocyte fatty acid analysis demonstrated incorporation of the parenteral n3 and n6 fatty acids in monocyte phospholipids immediately after infusion, with changes in the fatty acid composition persisting for up to 7 days after infusion. In vitro production of the inflammatory mediators thromboxane B2/thromboxane B3 (TXB(2/3)) and tumor necrosis factor-alpha (TNFalpha) by peripheral blood monocytes was diminished by n3 lipid infusion and was unchanged or increased by n6 lipid infusion. The results of this study demonstrate that short-term infusions of n3 and n6 fatty acid-enriched lipid emulsions alter the fatty acid composition of equine monocyte phospholipids and modify the inflammatory response of these cells in vitro. These results also support further investigation into the use of parenteral n3 fatty acids as part of the supportive therapy of patients with multiple organ dysfunction (MODS) or systemic inflammatory response syndrome (SIRS).
Animals↗
The effect of LPS on cytokine synthesis and lung neutrophil influx after hepatic ischemia/reperfusion injury in the rat.
OBJECTIVE: To determine if cytokine responses and lung injury induced by intravenous (i.v.) lipopolysaccharide (LPS) at 4 hr were enhanced in rats that had been previously subjected to 30 min of total liver ischemia (Pringle's maneuver) followed by 24 hr or 3 days of reperfusion. BACKGROUND: Many patients with liver trauma require occlusion of hepatic blood flow to control hemorrhage and facilitate repair. A significant number of these patients subsequently develop the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction (MOD) characterized by the release of cytokines and tissue neutrophil influx. Macrophages, including Kupffer cells, may be activated by ischemic injury and dysregulation of their response to LPS may contribute to the development of SIRS and acute respiratory distress syndrome. METHODS: Adult male Sprague-Dawley rats were randomly divided into six groups: three groups received total hepatic ischemia for 30 min and three groups had a sham procedure. Twenty-four hours or 3 days after hepatic ischemia/reperfusion injury, rats were treated with LPS (5 mg/kg) or saline and monitored for 4 hr. We collected serum, bronchoalveolar lavage (BAL) fluid, and lung tissue. RESULTS: Serum and BAL cytokine concentrations were significantly increased by i.v. LPS; however, hepatic ischemia/reperfusion injury 24 hr or 3 days before iv LPS ameliorated this cytokine response. The LPS-induced pulmonary neutrophil influx and histopathological changes were similar in sham and hepatic ischemia/reperfusion-injured groups. CONCLUSIONS: Hepatic ischemia/reperfusion injury significantly attenuated the serum and BAL cytokine concentrations, but did not change pulmonary neutrophil influx or histopathological alterations in response to i.v. LPS.
Animals↗
Increased phospholipid mass with decreased arachidonoyl molecular species is associated with decreased eicosanoid synthesis and increased tumor necrosis factor synthesis by thioglycollate-elicited rat peritoneal macrophages.
Because the activation state of macrophages may alter their response to endotoxin, we compared phospholipid arachidonic acid content, and synthesis of eicosanoids and tumor necrosis factor by resident and thioglycollate-elicited rat peritoneal macrophages. Thioglycollate elicitation increased macrophage phospholipid mass twofold, increased the relative percentages of 16:0-20:4 diacylglycerophosphocholine (PtdCho) and 18:0-20:4 diacylglycerophosphoethanolamine (PtdEtn), and decreased the relative percentages of 18:0-20:4 alkenylacylglycerophosphoethanolamine (PlsEtn) and 18:0-20:4 alkylacylglycerophosphocholine (PakCho) compared with resident peritoneal macrophages. Thioglycollate-elicited macrophages synthesized significantly less thromboxane B2, 6-keto-prostaglandin F1 alpha, and prostaglandin E2 and more tumor necrosis factor (TNF) activity in response to both endotoxin and A23187 than did resident macrophages. These results suggest that thioglycollate elicitation decreases specific arachidonic acid-containing molecular species in PlsEtn and PakCho, which may, in part, explain the decrease in eicosanoid and increase in TNF synthesis by thioglycollate-elicited macrophages. The differences between resident and thioglycollate-elicited macrophages in the synthesis of the eicosanoids and TNF activity was not altered by increasing either the concentration of either stimulus or the incubation time.
Animals↗
Arachidonic acid release in renal proximal tubule cell injuries and death.
Arachidonic acid release and the effect of phospholipase inhibitors on various types of cell injuries and death to rabbit renal proximal tubule suspensions were determined. Proximal tubules were exposed to the mitochondrial inhibitor antimycin A (0.1 microM), the protonophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone (1 microM FCCP), the oxidant tert-butyl hydroperoxide (0.5 mM TBHP), or the calcium ionophore ionomycin (5 microM) in the absence or presence of the putative phospholipase inhibitors dibucaine, mepacrine, chlorpromazine, or U-26384. The phospholipase inhibitors had no effect on the proximal tubule lactate dehydrogenase (LDH) release (a marker of cell death) produced by FCCP, antimycin A, or ionomycin after 1,2, or 2 hours of exposure, respectively. Only dibucaine and mepacrine decreased LDH release in TBHP-treated proximal tubules without decreasing TBHP-induced lipid peroxidation. Antimycin A and ionomycin did not release arachidonic acid from proximal tubules prelabeled with [1-14C] arachidonic acid. In contrast, TBHP released arachidonic acid from proximal tubules prior to the onset of cell death, and dibucaine and mepacrine decreased the TBHP-induced release. Thus, phospholipase inhibitors were cytoprotective in those injuries that produced arachidonic acid release. These results suggest that arachidonic acid release and phospholipase A2 activation play a contributing role in oxidant-induced renal proximal tubule cell injury and death but not in mitochondrial inhibitor- or calcium ionophore-induced proximal tubule cell injury and death.
Animals↗
Dietary source of omega-3 fatty acids affects endotoxin-induced peritoneal macrophage tumor necrosis factor and eicosanoid synthesis.
The effect of 8 weeks of feeding diets enriched with corn oil, linseed oil, or menhaden oil on endotoxin- and calcium ionophore (A23187)-induced tumor necrosis factor (TNF) and eicosanoid synthesis by rat peritoneal macrophages was determined. The fatty acid composition of macrophage phospholipids and TNF activity and eicosanoid synthesis in response to endotoxin and A23187 were determined. The ratio of omega-6/omega-3 fatty acids in macrophages from linseed oil or menhaden oil-fed rats decreased approximately 24- and 55-fold, respectively. Basal and endotoxin-induced synthesis of TNF was increased by ingestion of the menhaden oil diet but not by the linseed oil diet. Ingestion of the menhaden oil and linseed oil diets significantly reduced basal, endotoxin-, and A23187-induced synthesis of eicosanoids compared with the corn oil group. Ingestion of the menhaden oil diet resulted in a greater decrease in eicosanoid synthesis than the linseed oil diet.
Animals↗
Administration of a receptor antagonist for platelet-activating factor during equine endotoxaemia.
Platelet-activating factor (PAF) is an important mediator of endotoxaemia and various PAF receptor antagonists prevent many of the adverse effects of experimental endotoxaemia in laboratory animals. In this study a specific PAF receptor antagonist was used to investigate the role of PAF in equine endotoxaemia. At an interval of not greater than 10 days, 6 horses were each challenged with endotoxin and endotoxin with concurrent administration of SRI 63-441, a PAF receptor antagonist. The order of the treatments was randomised. Clinical signs, serum biochemical and coagulation profiles, and platelet aggregation in vitro were monitored in all horses for 24 h after treatment. Challenge with endotoxin increased maximal platelet aggregation induced by PAF. This response was blocked by administration of SRI 63-441 concurrently with endotoxin. No changes in percentage maximal platelet aggregation to ADP or collagen were noted after administration of endotoxin. The PAF receptor antagonist delayed the onset of fever, tachycardia, leucopenia and lactic acidaemia. Lack of more profound beneficial alterations of the horses' responses to endotoxin may have been due to the low dose of endotoxin administered in this model or to only partial effectiveness of SRI 63-441 in blocking the effects of endotoxin-induced PAF.
Animals↗
Hematuria and weight loss in a mare with pancreatic adenocarcinoma.
This clinical report describes an 11-yr-old Thoroughbred mare that presented with clinical signs of weight loss and hematuria. History and clinical findings suggested the mare had neoplasia of the urogenital system. Although ultrasound-guided biopsy of the perirenal mass did not yield abnormal cells, large irregular cells were isolated from the thoracic and peritoneal fluid. At necropsy, multiple firm nodules were disseminated throughout the peritoneal cavity. Histological examination of the nodules revealed cells that were consistent with a pancreatic exocrine adenocarcinoma. This is the first report of pancreatic adenocarcinoma causing dysfunction of the urogenital system.
Adenocarcinoma↗
Clinical and pathological effects of flunixin meglumine administration to neonatal foals.
The effects of daily intravenous administration of flunixin meglumine at dosages of 0.55, 1.1, 2.2 and 6.6 mg/kg for five days were examined in neonatal foals. Six two day old foals were used to evaluate the effect of each dosage. Foals were examined every day and blood samples collected on days 1, 3 and 6. All foals were euthanized after six days, necropsied and examined for lesions. The major clinical abnormality was diarrhea, but the incidence was not related to the dosage of flunixin meglumine administered. The foals receiving 6.6 mg/kg of flunixin meglumine had significantly more gastrointestinal ulceration and greater cecal pathology and cecal petechiation scores than those foals treated with saline. The foals in the 6.6 mg/kg treatment group had a greater loss of total protein during the study, but the difference was not significant. There were no statistically significant blood cellular or biochemical alterations associated with the administration of flunixin meglumine. There were no significant clinicopathological differences between healthy foals treated with the recommended dosage of flunixin meglumine and those treated with physiological saline.
Animals↗
Hemoperitoneum caused by rupture of a juvenile granulosa cell tumor in an equine neonate.
A neonatal foal was examined because of apparent abdominal pain and distention, anemia, and hemoperitoneum. Exploratory laparotomy was performed, and a large spherical mass, which had ruptured, was found in the area of the left ovary. Left salpingo-oophorectomy was performed. The mass was determined to be a juvenile granulosa cell tumor.
Animals↗
Chronic pyelonephritis in a brood mare.
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Animals↗
Failure of the administration of ACTH to affect the absorption of colostral immunoglobulin in neonatal foals.
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Adrenocorticotropic Hormone↗