The effect of IV administration of the alpha2-adrenoceptor agonist xylazine hydrochloride (0.5 mg/kg of body weight) was examined in ponies with recurrent obstructive pulmonary disease, commonly called heaves. Six ponies with the disease (principals) were studied during clinical remission and during an acute attack of airway obstruction precipitated by stabling and feeding of dusty hay. Six control ponies were also studied. In principal ponies with airway obstruction, xylazine administration significantly (P < 0.05) decreased pulmonary resistance and increased dynamic compliance, but did not affect PaO2 or PaCO2. The alpha 2-antagonist yohimbine blocked the pulmonary effects of xylazine. Administration of saline solution was without effect in both groups of ponies at all periods and xylazine did not have effect in controls or in principals in clinical remission.

The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 (Lg/kg/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate to the nearest 0.25 microgram/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 microgram/kg/min; xylazine, 1.21 +/- 0.46 microgram/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.

The effects of 3 commonly used dosages (0.3, 0.5, and 1.1 mg/kg of body weight, IV) of xylazine on ventilatory function were evaluated in 6 Thoroughbred geldings. Altered respiratory patterns developed with all doses of xylazine, and horses had apneic periods lasting 7 to 70 seconds at the 1.1 mg/kg dosage. Respiratory rate, minute volume, and partial pressure of oxygen in arterial blood (PaO2) decreased significantly (P < 0.001) with time after administration of xylazine, but significant differences were not detected among dosages. After an initial insignificant decrease at 1 minute after injection, tidal volume progressively increased and at 5 minutes after injection, tidal volume was significantly (P < 0.01) greater than values obtained before injection. Partial pressure of carbon dioxide in arterial blood (PaCO2) was insignificantly increased. After administration of xylazine at a dosage of 1.1 mg/kg, the mean maximal decrease in PaO2 was 28.2 +/- 8.7 mm of Hg and 22.2 +/- 4.9 mm of Hg, measured with and without a respiratory mask, respectively. Similarly, the mean maximal increase in PaCO2 was 4.5 +/- 2.3 mm of Hg and 4.2 +/- 2.4 mm of Hg, measured with and without the respiratory mask, respectively. Significant interaction between use of mask and time was not detected, although the changes in PaO2 were slightly attenuated when horses were not masked. The temporal effects of xylazine on ventilatory function in horses should be considered in selecting a sedative when ventilation is inadequate or when pulmonary function testing is to be performed.

Eighteen rats were anesthetized with xylazine/ketamine and placed in right lateral recumbency, and a small incision was made in the skin of the left hemithorax. A 21-gauge, 1-inch, short-beveled hypodermic needle, attached directly to a pressure transducer filled with degassed saline solution, was advanced through the incision into the left ventricle and then advanced through the septum into the right ventricle. High-fidelity tracings of right and left ventricular pressures and their derivatives were obtained through this approach in 13 rats. In 5 rats, measurements of right ventricular pressures were obtained by additional right ventricular puncture through the incision in the left hemithorax. Right and left ventricular pressures were recorded on single occasions in 18 rats, twice at 2-week intervals in 6 rats, and 3 times at 2-week intervals in 3 rats. Minimal hemopericardium was observed, but most rats had evidence of hemorrhage on the visceral pericardium. Left and right ventricular pressures can be measured rapidly, safely, and repeatedly in anesthetized rats by this method.