American journal of veterinary research
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Cardiovascular effects and pulmonary gas exchange were compared during conventional mechanical ventilation (CMV) and interrupted high-frequency, positive-pressure ventilation (IHFPPV) in 6 anesthetized ponies in dorsal recumbency. When the peak airway pressure (Paw) was held constant at control values attained during CMV (18 to 20 cm of H2O), and the ventilator frequency of IHFPPV was varied over the range, 2.5 to 12.5 Hz, significant (P less than 0.05) changes from control values were observed only in the ratio of dead-space volume to tidal volume (VD/VT) and in the respiratory minute volume (VE). The mean (+/- SEM) carbon dioxide excretion (VCO2) was 2.12 +/- 0.1 ml/kg/min during IHFPPV. ⋯ With increasing Paw, VD/VT decreased directly with increasing Paw from 98 to 69.3%. Gas exchange at a Paw of 15 cm of H2O during IHFPPV was equivalent to conditions at Paw of 20 cm of H2O during CMV. At a higher Paw during IHFPPV, improvements over control values were observed in gas exchange.
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The effect of ketamine administration on the ventricular arrhythmogenic dose of epinephrine (VADE) was studied in 4 halothane-anesthetized cats. Each cat was anesthetized 4 times, 1 week apart, with halothane (end-tidal concentration, 1.5%) and with halothane (end-tidal concentration, 1.5%) combined with ketamine infusion (50, 100, and 200 micrograms/kg of body weight/min). Epinephrine was infused in progressively increasing doses. ⋯ Plasma ketamine and norketamine concentrations after a 4-hour infusion and immediately after determination of the VADE were similar for any given ketamine infusion rate, indicating that steady-state plasma concentrations had been reached for each infusion rate. Blood pressure and heart rate were measured immediately before (base line) and immediately after infusion of the VADE. Ketamine infusion significantly (P less than 005) lowered base-line blood pressure, but not heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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Spinal evoked potentials (SpEP) were recorded on an electromyograph from electrodes placed percutaneously in the ligamentum flava at the lumbosacral junction and between the 10th and 11th thoracic vertebrae following tibial nerve stimulation in 31 anesthetized dogs with acute compressive spinal cord injuries. The neurologic status of each dog was determined by clinical examination before SpEP recordings, and the neurologic status was monitored for 2 months in dogs that had surgical or conservative treatment. Two months after spinal injury, the response to treatment (outcome) of each dog was evaluated and graded as favorable (ambulatory and urinary continent) or unfavorable (nonambulatory, urinary incontinent, or euthanatized with confirmation of myelomalacia). ⋯ Analysis of data from the T10-11 recordings indicated significant differences between the reference and spinal injury groups and between the favorable and unfavorable outcome groups within the spinal injury group. A CV/DPN index was less than 30 in dogs with unfavorable outcomes and greater than 30 in dogs with favorable outcomes. Stepwise discriminant analysis of data from the spinal injury group predicted outcome correctly in all dogs.
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Adrenocortical function in canine surgical patients given etomidate at 1 of 2 dosages (1.5 mg/kg of body weight or 3 mg/kg, IV) was evaluated and compared with that of dogs given thiopental (12 mg/kg, IV). The adrenocortical function was evaluated by use of adrenocorticotropic hormone (ACTH) stimulation tests and determination of plasma cortisol concentrations at 0 minute (base line) and 60 minutes after ACTH administration. At 24 hours before administration of either drug (ie, induction of anesthesia), each dog had an increase in plasma cortisol concentration when given ACTH. ⋯ Dogs given thiopental had base-line plasma cortisol concentrations greater than preinduction base-line values, but did not increase plasma cortisol in response to ACTH stimulation. Postinduction ACTH stimulation tests in dogs given etomidate at either dose indicated base-line and 60-minute plasma cortisol concentrations that were not different from preinduction base-line values. Therefore, adrenocortical function was suppressed 2 and 3 hours after the administration of etomidate in canine surgical patients.
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The arrhythmogenic dose of epinephrine (ADE) was determined in 6 pigs during steady-state anesthesia (1.5% halothane in O2) and steady-state anesthesia plus xylazine (1.1 mg X kg-1 X hr-1; IV infusion) and after either prazosin (alpha 1) or metoprolol (beta 1) adrenergic blockade during halothane-xylazine (H-X) anesthesia. A constant infusion (1, 2, 3, 5, and 10 micrograms X kg-1 X min-1) of freshly mixed epinephrine (100 micrograms X ml-1 in saline solution) was used to determine ADE. The ADE was defined as the total dose of epinephrine which produced 4 or more continuous or intermittent, premature, ventricular contractions within a 15-s period. ⋯ Xylazine administration did not significantly decrease ADE, although mean arterial pressure significantly increased. Prazosin administration significantly increased ADE and was associated with an increased heart rate and a decreased mean arterial pressure. We conclude that alpha 1-blockade with prazosin is more protective to epinephrine-induced arrhythmias in H-X-anesthetized pigs than is beta 1-blockade with metoprolol.