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  • Author or Editor: Annette P. N. Kutter x
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Abstract

Objective—To determine the effect of inhalation of isoflurane at end-tidal concentrations greater than, equal to, and less than the minimum anesthetic concentration (MAC) on bispectral index (BIS) in chickens.

Animals—10 chickens.

Procedures—For each chicken, the individual MAC of isoflurane was determined by use of the toe-pinch method. After a 1-week interval, chickens were anesthetized with isoflurane at concentrations 1.75, 1.50, 1.25, 1.00, and 0.75 times their individual MAC (administered from higher to lower concentrations). At each MAC multiple, a toe pinch was performed and BIS was assessed and correlated with heart rate, blood pressure, and an awareness score (derived by use of a visual analogue scale).

Results—Among the chickens, mean ± SD MAC of isoflurane was 1.15 ± 0.20%. Burst suppression was detected at every MAC multiple. The BIS and awareness score were correlated directly with each other and changed inversely with increasing isoflurane concentration. Median (range) BIS values during anesthesia at 1.75, 1.50, 1.25, 1.00, and 0.75 MAC of isoflurane were 25 (15 to 35), 35 (25 to 45), 35 (20 to 50), 40 (25 to 55), and 50 (35 to 65), respectively. Median BIS value at extubation was 70 ± 9. Values of BIS correlated with blood pressure, but not with heart rate. Blood pressure changed with end-tidal isoflurane concentrations, whereas heart rate did not.

Conclusions and Clinical Relevance—Assessment of BIS can be used to monitor the electrical activity of the brain and the degree of unconsciousness in chickens during isoflurane anesthesia.

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether inhaled nitric oxide (NO) prevents pulmonary hypertension and improves oxygenation after IV administration of a bolus of dexmedetomidine in anesthetized sheep.

Animals—6 healthy adult sheep.

Procedure—In a crossover study, sevoflurane-anesthetized sheep received dexmedetomidine (2 µg/kg, IV) without NO (DEX treatment) or with inhaled NO (DEX-NO treatment). Cardiopulmonary variables, including respiratory mechanics, were measured before and for 120 minutes after bolus injection of dexmedetomidine.

Results—Dexmedetomidine induced a transient decrease in heart rate and cardiac output. A short-lived increase in mean arterial pressure (MAP) and systemic vascular resistance (SVR) was followed by a significant decrease in MAP and SVR for 90 minutes. Mean pulmonary arterial pressure (MPAP) and pulmonary vascular resistance increased transiently after dexmedetomidine injection. The PaO2 was significantly decreased 3 minutes after injection and reached a minimum of (mean ± SEM) 13.3 ± 7.8 kPa 10 minutes after injection. The decrease in PaO2 was accompanied by a sudden and prolonged decrease in dynamic compliance and a significant increase in airway resistance, shunt fraction, and alveolar dead space. Peak changes in MPAP did not differ between the 2 treatments. For the DEX-NO treatment, PaO2 was significantly lower and the shunt fraction significantly higher than for the DEX treatment.

Conclusions and Clinical Relevance—Inhalation of NO did not prevent increases in pulmonary arterial pressures induced by IV administration of dexmedetomidine. Preemptive inhalation of NO intensified oxygenation impairment, probably through increases in intrapulmonary shunting. (Am J Vet Res 2005;66:1496–1502)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To compare anesthesia recovery quality after racemic (R-/S-) or S-ketamine infusions during isoflurane anesthesia in horses.

Animals—10 horses undergoing arthroscopy.

Procedures—After administration of xylazine for sedation, horses (n = 5/group) received R-/S-ketamine (2.2 mg/kg) or S-ketamine (1.1 mg/kg), IV, for anesthesia induction. Anesthesia was maintained with isoflurane in oxygen and R-/S-ketamine (1 mg/kg/h) or S-ketamine (0.5 mg/kg/h). Heart rate, invasive mean arterial pressure, and end-tidal isoflurane concentration were recorded before and during surgical stimulation. Arterial blood gases were evaluated every 30 minutes. Arterial ketamine and norketamine enantiomer plasma concentrations were quantified at 60 and 120 minutes. After surgery, horses were kept in a padded recovery box, sedated with xylazine, and video-recorded for evaluation of recovery quality by use of a visual analogue scale (VAS) and a numeric rating scale.

Results—Horses in the S-ketamine group had better numeric rating scale and VAS values than those in the R-/S-ketamine group. In the R-/S-ketamine group, duration of infusion was positively correlated with VAS value. Both groups had significant increases in heart rate and mean arterial pressure during surgical stimulation; values in the R-/S-ketamine group were significantly higher than those of the S-ketamine group. Horses in the R-/S-ketamine group required slightly higher end-tidal isoflurane concentration to maintain a surgical plane of anesthesia. Moderate respiratory acidosis and reduced oxygenation were evident. The R-norketamine concentrations were significantly lower than S-norketamine concentrations in the R-/S-ketamine group.

Conclusions and Clinical Relevance—Compared with R-/S-ketamine, anesthesia recovery was better with S-ketamine infusions in horses.

Full access
in American Journal of Veterinary Research