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Summary

Twelve healthy dogs were used to determine the cardiorespiratory effects of iv administered ketamine (10 mg/kg of body weight) and midazolam (0.5 mg/kg). Half the dogs received a ketamine-midazolam combination (k-m) as a bolus over 30 seconds and the other half received the k-m as an infusion over 15 minutes. Induction of anesthesia by use of k-m was good in all dogs. Ketamine-midazolam combination as a bolus or infusion induced minimal cardiorespiratory effects, except for significant (P < 0.05) increases in mean heart rate and rate-pressure product. The increase in heart rate was greater in dogs of the infusion group. Mild and transient respiratory depression was observed in dogs of both groups immediately after administration of k-m, but was greater in dogs of the bolus group than in dogs of the infusion group. Duration of action of k-m for chemical restraint was short. Salivation and defecation were observed in a few dogs. Extreme muscular tone developed in 1 dog after k-m bolus administration.

Free access
in American Journal of Veterinary Research

Summary

Cardiovascular effects of iv administered ketamine (10 mg/kg) and midazolam (0.5 mg/kg) were determined in 12 healthy isoflurane-anesthetized (1.7% end-tidal concentration) dogs. Six dogs received a ketamine-midazolam combination (k-m) as a bolus over 30 seconds and 6 dogs received k-m as an infusion over 15 minutes. Ketamine-midazolam combination as a bolus and an infusion caused early significant (P < 0.05) reductions in mean systemic blood pressure, cardiac index, and stroke index, which returned to baseline values near the end of the study. Heart rate decreased significantly (P < 0.05) in dogs of the infusion group and returned to the baseline value near the end of the study. One dog died after k-m bolus administration. Mean maximal decreases from baseline for systemic blood pressure, cardiac index, and stroke index were significantly (P < 0.05) greater in dogs of the bolus group than in dogs of the infusion group; therefore, cardiovascular effects of k-m after infusion were less severe than those after bolus. Base excess and pHa decreased significantly (P < 0.05) in the infusion group, although similar changes occurred in both groups.

Four dogs were maintained with 1.7% end-tidal isoflurane to determine temporal effects of isoflurane; these dogs did not receive k-m. Increases in heart rate, cardiac index, stroke index, and left and right ventricular stroke work indexes were significant (P < 0.05) at various sample collection intervals, particularly during the later stages of the study.

Isoflurane anesthesia effectively blocked the cardiostimulatory properties of k-m. Ketamine-midazolam combination should be used cautiously during isoflurane anesthesia, and administration by slow infusion may be safer than by rapid bolus administration.

Free access
in American Journal of Veterinary Research

Summary

Cardiorespiratory effects of an iv administered bolus of ketamine (7.5 mg/kg of body weight) and midazolam (0.375 mg/kg) followed by iv infusion of ketamine (200 μg/kg/min) and midazolam (10 μg/kg/min) for 60 minutes was determined in 6 dogs. Ketamine-midazolam combination was administered to dogs on 3 occasions to determine effects of prior administration of iv administered saline solution (1 ml), butorphanol (0.2 mg/kg), or oxymorphone (0.1 mg/kg). The infusion rate of ketamine and midazolam was decreased by 25% for anesthetic maintenance after opioid administration.

There were no significant differences in cardiorespiratory variables after saline solution or butorphanol administration; however, oxymorphone caused significant (P < 0.05) increases in mean arterial blood pressure, systemic vascular resistance, and breathing rate. Bolus administration of ketamine-midazolam combination after saline solution caused significant (P < 0.05) increases in heart rate, mean arterial blood pressure, cardiac index, mean pulmonary blood pressure, venous admixture, and significant decreases in stroke index, pulmonary capillary wedge pressure, arterial and mixed venous oxygen tension, arterial oxygen content, and alveolar-arterial oxygen gradient. Opioid administration was associated with significantly (P < 0.05) lower values than was saline administration for heart rate, mean arterial blood pressure, and arterial and mixed venous pH and with higher values for stroke index, pulmonary capillary wedge pressure, and arterial and mixed venous carbon dioxide tension. Prior oxymorphone administration resulted in the highest (P < 0.05) values for mean pulmonary blood pressure, venous admixture, and arterial and mixed venous carbon dioxide tension, and the lowest values for arterial oxygen tension, and arterial and mixed venous pH. Each treatment provided otherwise uncomplicated anesthetic induction, maintenance, and recovery. Time to extubation, sternal recumbency, and walking with minimal ataxia was similar for each treatment.

Free access
in American Journal of Veterinary Research

Summary

The disposition of clorazepate, a benzodiazepine anticonvulsant, was determined in dogs after administration of a single oral dose of clorazepate (2 mg/kg of body weight) and after oral administration of clorazepate (2 mg/kg, q 12 h) concurrently with phenobarbital (5 mg/kg, q 12 h) for 44 consecutive days. Serum concentrations of nordiazepam, the active metabolite of clorazepate, were measured. After a single oral dose of clorazepate, maximal nordiazepam concentrations ranged from 569.6 to 1,387.9 ng/ml (mean, 880.2 ± 248.9 ng/ml) and were detected 16.8 to 131.4 minutes (mean, 85.2 ± 36 minutes) after dosing. After administration of phenobarbital for 44 consecutive days, maximal nordiazepam concentrations were significantly (P < 0.01) lower, ranging from 209.6 to 698.5 ng/ml (mean, 399.3 ± 155.6 ng/ml) at 68.4 to 145.8 minutes (mean, 93 ± 25.8 minutes) after dosing. Mean area under the curve (AUC) on day 1 (mean, 3.37 ± 0.598 ng·min/ml) was significantly (P < 0.001) greater than AUC on day 44 (1.66 ± 0.308 ng·min/ml). Oral clearance was significantly (P < 0.01) greater on day 44 (12.44 ± 2.55 ml/min/kg), compared with that on day 1 (6.16 ± 1.35 ml/min/kg). Values for area under the first moment curve, oral volume of distribution, mean residence time, and elimination half-life were not significantly altered by concurrent administration of phenobarbital.

Administration of phenobarbital altered the disposition of clorazepate such that the amount of nordiazepam in circulation during each dose interval was significantly reduced. Adequate control of seizures in epileptic dogs, therefore, may require higher dosages of clorazepate when it is coadministered with phenobarbital.

Free access
in American Journal of Veterinary Research

Summary

Cardiopulmonary consequences of iv administered glycopyrrolate (0.01 mg/kg of body weight), followed in 11 ± 2 minutes by butorphanol (0.2 mg/ kg) and xylazine (0.5 mg/kg), were evaluated in 6 dogs, with and without nasal administration of oxygen (100 ml/kg/min). Glycopyrrolate caused significant (P < 0.05) increases in heart rate and cardiac index and significant (P < 0.05) decreases in stroke index.

Subsequent administration of butorphanol and xylazine was associated with significant (P < 0.05) increases in systemic vascular resistance, mean arterial blood pressure, mean pulmonary artery pressure, central venous pressure, pulmonary capillary wedge pressure, PaCO2 , venous admixture, oxygen extraction ratio, and hemoglobin concentration. It caused significant (P < 0.05) decreases in cardiac index, stroke index, breathing rate, minute volume index, oxygen delivery, and oxygen consumption. Mean arterial blood pressure, pulmonary vascular resistance, tidal volume index, and minute volume index were significantly (P < 0.05) higher when dogs were breathing room air. The arterial and venous PO2 and PCO2 , and venous oxygen content were significantly (P < 0.05) higher, and the arterial and venous pH, and oxygen consumption were significantly (P < 0.05) lower when oxygen was administered. Pulsus alternans and S-T segment depression were observed in dogs of both groups. Ventricular premature contractions were observed in 1 dog breathing room air.

All dogs were intubated briefly 15 minutes after administration of butorphanol and xylazine. Time to first spontaneous movement was 45 minutes. All dogs remained in lateral recumbency without physical restraint for 60 minutes.

Free access
in American Journal of Veterinary Research

Summary

The accuracy of a pulse oximeter was evaluated over a wide range of arterial oxygen and carbon dioxide tensions, using 2 probes (finger probe and ear probe) and 2 monitoring sites (tongue and tail) in anesthetized dogs The arterial oxygen saturation of hemoglobin (SaO2) measured directly with a multiwavelength spectrophotometer was compared with saturation estimated by pulse oximetry (SpO2). Linear regression analysis of the pooled data from 399 simultaneous measurements of SpO2 and SaO2 indicated a highly significant correlation of SpO2 with SaO2 (r = 0.97; P ≤ 0.0001). Although the mean difference (± sd) between SpO2 and SaO2 for pooled data was small (- 0.06 ± 6.8%), SpO2 tended to underestimate high SaO2 values (≥ 70%) and to overestimate low SaO2 values (< 70%). When SaO2 values were ≥ 70%, the ear probe applied to the tail was less accurate (produced a significantly greater SpO2-SaO2 difference) than the ear probe on the tongue, or the finger probe at either site. When SaO2 values were ≤ 50%, the finger probe applied at the tail was more accurate (produced significantly smaller SpO2-SaO2 differences) than the ear probe at either site. When SaO2 values were ≤ 70%, high arterial carbon dioxide tension (≥ 60 mm of Hg) was associated with greater overestimation of SaO2.

Free access
in American Journal of Veterinary Research