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  • Author or Editor: Susan D. Semrad x
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Summary

Saline (0.9% NaCl) solution, flunixin meglumine (1.1 mg/kg), prednisolone sodium succinate (1.1 mg/ kg), U74389F (1.5 mg/kg), and dimethyl sulfoxide (0.5 g/kg) were each administered FV to 5 neonatal calves 15 minutes after the start of a 3-hour infusion of Escherichia coli lipopolysaccharide (lps; 2 µg/kg/hr). Four additional calves were given a 3-hour IV infusion of saline solution alone. Only flunixin significantly suppressed eicosanoid production and mitigated clinical signs associated with endotoxemia. Prednisolone provided partial protection against lps-induced hypotension and lacticemia. Pronounced hypoglycemia and lacticemia were observed in U74389F-treated calves; LPS-induced hypotension and hypoglycemia were marked in dimethyl sulfoxide-treated calves.

Free access
in American Journal of Veterinary Research
in Journal of the American Veterinary Medical Association
Author:

Summary

Saline (0.9% NaCl) solution or 1 of 3 nonsteroidal anti-inflammatory drugs (nsaid) was administered iv to 5 neonatal calves 15 minutes after the start of a 3-hour iv infusion of Escherichia coli lipopolysaccharide (lps; 2 µg/kg/h). Four additional calves were given a 3-hour iv infusion of saline solution alone. Clinical attitude, mean arterial blood pressure, pcv, wbc, and plasma lactate, glucose, and eicosanoid concentrations (thromboxane B2, 6-keto-PGF) were monitored for 12 hours.

Flunixin meglumine (1.1 mg/kg of body weight, iv), ketoprofen (2.2 mg/kg, iv), and ketorolac tromethamine (1.1 mg/kg, iv) each ameliorated the clinical signs of endotoxemia and lps-induced lacticemia, but failed to significantly alter the degree of leukopenia or hypoglycemia associated with infusion of lps. Although the 3 nsaid prevented eicosanoid production, they provided only partial protection against lps-induced hypotension. Each nsaid modified the response to lps, but none was clearly superior to the others in modulating the clinical signs or physiologic alterations induced by infusion of lps in neonatal calves.

Free access
in American Journal of Veterinary Research

Summary

Twenty newborn Holstein calves were allotted at random to 4 groups: group A received 0.9% sterile saline solution; group B received phenylbutazone (5 mg/kg of body weight, iv) and 0.9% sterile saline solution; group C received progressively increasing doses of endotoxin (0.1 to 15 μg/kg); and group D received phenylbutazone and endotoxin similarly as did calves of groups B and C, respectively. Phenylbutazone was given once daily and saline solution or endotoxin were given every 8 hours for 5 days. Clinical variables—pcv, plasma total protein and fibrinogen concentrations, platelet count, prothrombin time, activated partial thromboplastin time, and fibrin degradation products concentration were measured at 24-hour intervals. Necropsy was performed on each calf.

Phenylbutazone suppressed the clinical response to endotoxin challenge until large doses (7.5 to 15 μg/kg) were administered. Calves of groups C and D remained stable until they abruptly developed severe dyspnea necessitating euthanasia. Thrombocytopenia and leukopenia developed after the initial endotoxin dose. Prothrombin time was prolonged and pcv suddenly decreased at 96 hours. Necropsy revealed consistent lesions in the vascular endothelium and lungs. Phenylbutazone administration did not enhance or ameliorate endotoxin-induced hemostatic alterations or pathologic lesions.

Free access
in American Journal of Veterinary Research

Summary

The clinical efficacy of the lazaroid, tirilazad mesylate, a new therapeutic agent for prophylaxis and treatment of endotoxemia, was evaluated in 24 neonatal Holstein calves. Endotoxemia was induced by iv infusion of commercial Escherichia coli lipopolysaccharide (3.25 µg/kg of body weight) over 3 hours. Group-1 calves were given endotoxin alone; group-2 calves were given an infusion of 0.9% sterile saline solution, then were treated with tirilazad mesylate (1.5 mg/kg) 1 hour after the infusion was started. Group-3 calves were treated with tirilazad mesylate 1 hour after the start of the endotoxin infusion, and group-4 calves were given tirilazad mesylate 1 hour before the start of the endotoxin infusion.

Clinical signs of endotoxemia were mitigated by tirilazad mesylate. In addition, tirilazad mesylate protected calves from endotoxin-induced hyperglycemia; treatment after endotoxin infusion decreased the severity of hypoglycemia and prevented lactic acidosis. Treatment with tirilazad mesylate after initiation of endotoxin infusion was as protective as was pretreatment.

Free access
in American Journal of Veterinary Research

Summary

The cellular response induced in the host animal by endotoxin contributes greatly to the morbidity and mortality of gram-negative infections in bovine neonates. We characterized the temporal sequence, magnitude, and duration of mediator release during endotoxemia and evaluated the effect of endotoxin dose and method of administration. Thromboxane B2 (TxB2), and 6-keto prostaglandin F (PGF) concentrations and tumor necrosis factor (tnf), and interleukin-1β (il-1β) activities were measured in 34 newborn calves given Escherichia coli endotoxin at dosage of 0 (saline solution), 0.2, 2.0, or 20 μg/kg of body weight, either by iv administered bolus or infusion over 50 minutes. In all groups and at each lipopolysaccharide dosage, mediators peaked in this sequence: TxB2 and tnf, followed by PGF, then il-1β. Neither dose nor method of administration affected the sequence of mediator release. The magnitude of eicosanoid reponse to endotoxin was dose-dependent. During induced endotoxemia, duration and/or magnitude of mediator response reflected the dose of endotoxin administered, indicating that the outcome of endotoxemia, in neonatal calves, may be related to the amount of circulating endotoxin.

Free access
in American Journal of Veterinary Research
in Journal of the American Veterinary Medical Association