Abstract: The use of reaction time has a great tradition in the field of human information processing research. In animal research the use of reaction time test paradigms is mainly limited to two research fields: the role of the striatum in movement initiation; and aging. It was discussed that reaction time responding can be regarded as “single behavior”, this term was used to indicate that only one behavioral category is measured, allowing a better analysis of brain-behavior relationships. Reaction time studies investigating the role of the striatum in motor functions revealed that the initiation of a behavioral response is dependent on the interaction of different neurotransmitters (viz. dopamine, glutamate, GABA). Studies in which lesions were made in different brain structures suggested that motor initiation is dependent on defined brain structures (e.g. medialldorsal striatum, prefrontal cortex). It was concluded that the use of reaction time measures can indeed be a powerful tool in studying brain-behavior relationships. However, there are some methodological constraints with respect to the assessment of reaction time in rats, as was tried to exemplify by the experiments described in the present paper. On the one hand one should try to control for behavioral characteristics of rats that may affect the validity of the parameter reaction time. On the other hand, the mean value of reaction time should be in the range of what has been reported in man. Although these criteria were not always met in several studies, it was concluded that reaction time can be validly assessed in rats. Finally, it was discussed that the use of reaction time may go beyond studies that investigate the role of the basal ganglia in motor output. Since response latency is a direct measure of information processing this parameter may provide insight into basic elements of cognition. Based on the significance of reaction times in human studies the use of this dependent variable in rats may provide a fruitful approach in studying brain-behavior relationships in cognitive functions.

Abstract: This study investigated the effect of lidocaine i.v. on halothane minimum alveolar concentration (MAC) in ponies. Six ponies were anaesthetised with thiopentone and succinylcholine, intubated and anaesthesia maintained with halothane. Ventilation was controlled and blood pressure maintained within clinically acceptable limits. Following a 2 h equilibration period, baseline halothane MAC was determined. The ponies were then given a loading dose of lidocaine (2.5 or 5 mg/kg bwt) or saline over 5 min, followed by a constant infusion of lidocaine (50 or 100 microg/kg/min, or saline, respectively). The halothane MAC was redetermined after a 60 min infusion of lidocaine or saline. The baseline halothane MAC for the control group was mean +/- s.d. 0.94 +/- 0.03%, and no significant decrease occurred following saline infusion. Lidocaine decreased halothane MAC in a dose-dependent fashion (r = 0.86; P < 0.0003). The results indicate that i.v. lidocaine may have a role in equine anaesthesia.

Abstract: Calcium gluconate was administered to conscious horses at 3 different rates (0.1, 0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dtmax). Mean arterial pressure and right atrial pressure were unchanged; heart rate decreased markedly during calcium administration. Ionized calcium concentration remained between 54% and 57% of total calcium concentration throughout the study. We conclude that calcium gluconate can safely be administered to conscious horses at 0.1 to 0.4 mg/kg/min and that administration will result in improved cardiac function.

Abstract: REASONS FOR PERFORMING STUDY: The ability to shorten the duration of sedation would potentially improve safety and utility of detomidine. OBJECTIVES: To determine the effects of tolazoline and atipamezole after detomidine sedation. HYPOTHESIS: Administration of tolazoline or atipamezole would not affect detomidine sedation. METHODS: In a randomised, placebo-controlled, double-blind, descriptive study, detomidine (0.02 mg/kg bwt i.v.) was administered to 6 mature horses on 4 separate occasions. Twenty-five mins later, each horse received one of 4 treatments: Group 1 saline (0.9% i.v.) as a placebo control; Group 2 atipamezole (0.05 mg/kg bwt i.v.); Group 3 atipamezole (0.1 mg/kg bwt i.v.); and Group 4 tolazoline (4.0 mg/kg bwt i.v.). Sedation, muscle relaxation and ataxia were scored by 3 independent observers at 9 time points. Horses were led through an obstacle course at 7 time points. Course completion time was recorded and the ability of the horse to traverse the course was scored by 3 independent observers. Horses were videotaped before, during and after each trip through the obstacle course. RESULTS: Atipamezole and tolazoline administration incompletely antagonised the effects of detomidine, but the time course to recovery was shortened. CONCLUSIONS AND POTENTIAL RELEVANCE: Single bolus administration of atipamezole or tolazoline produced partial reversal of detomidine sedation and may be useful for minimising detomidine sedation.