Visual-evoked potentials (VEP) and electroretinograms (ERG) were recorded from 10 normal light-adapted adult dogs, using a 3 X 5 matrix of light-emitting diodes as a stimulator. Visual-evoked potentials were recorded from 4 scalp electrodes overlying cortical areas, whereas electroretinographic activity was recorded by 2 scalp electrodes placed near the eye and by a conjunctivally placed electrode. The waveform of the VEP consisted of 3 major positive waves (P1 through P3), with peak latencies in the 20- to 70-ms range. Waveform reproducibility was assessed by comparing peak latencies from VEP recorded on 2 separate days approximately 1 week apart. The peak latencies for P1 through P3 did not differ (P greater than or equal to 0 .05) between first and second recording sessions. To substantiate the postretinal origin of VEP, recordings were made before and after unilateral optic nerve transsections in 4 dogs. Electroretinograms were also measured before and after surgery to assess the integrity of the retina. Postsurgically, VEP were absent when the eye on the surgically treated side was stimulated. Stimulation of the contralateral eye induced VEP with the same waveform shape, but latencies were slightly prolonged (P less than or equal to 0.05) compared with presurgical recordings. The only effect of optic nerve transsection on the ipsilateral ERG was a prolongation (P less than or equal to 0.05) of the b-wave. However, when postsurgical ERG values were compared with those from the intact side after surgery, there were no differences.

We compared the ability of 3 alpha 2-adrenoreceptor antagonists, idazoxan (0.05 mg/kg), tolazoline (2 mg/kg), and yohimbine (0.2 mg/kg) to reverse xylazine (0.3 mg/kg)-induced respiratory changes and CNS depression in 6 ewes. Once weekly, each ewe was given a random IV treatment of xylazine, followed in 5 minutes by either an antagonist or 0.9% NaCl solution. Xylazine alone caused recumbency for 54.2 +/- 5.3 minutes (mean +/- SEM). Xylazine also increased respiratory rate and decreased PaCO2 for at least 45 minutes, but did not significantly change arterial pH or PaCO2. Idazoxan and tolazoline were equally effective in reversing the respiratory actions of xylazine; however, yohimbine was less effective in reducing the respiratory rate and was ineffective in antagonizing the decreased PaO2. Idazoxan and tolazoline decreased the duration of xylazine-induced recumbency to 6.3 +/- 0.6 and 9.5 +/- 2.3 minutes, respectively, whereas yohimbine did not significantly change this effect of xylazine. Thus, at the dosages studied, idazoxan and tolazoline appeared to be more effective than yohimbine in reversing the respiratory and CNS depressant actions of xylazine in sheep.