Reversal by tolazoline hydrochloride of xylazine hydrochloride-ketamine hydrochloride immobilizations in free-ranging desert mule deer.

We captured 10 free-ranging desert mule deer (Odocoileus hemionus crooki) (five males and five females) by net-gun from a helicopter and immobilized them with xylazine hydrochloride (HCl) (100 mg) and ketamine HCl (300 to 400 mg) injected intramuscularly. Arousal and ambulation times were 13.9 +/- 4.2 and 14.3 +/- 4.2 min in eight deer injected intravenously with tolazoline HCl (3.0 mg/kg). We observed a curvilinear relationship (R = 0.50, P less than 0.01) between rectal temperature and time after induction of anesthesia. Mean peak temperature (41.4 C) occurred at 23.7 +/- 3.2 min postinduction and was greater (P less than 0.01) than the mean temperature measured initially (40.8 C). Heart and respiratory rates (108 beats/min and 75 breaths/min) were elevated prior to immobilization. Mean heart rate increased (P less than 0.05) from 90 +/- 9 beats/min in anesthetized deer to 120 +/- 13 beats/min after tolazoline HCl injection. A 20% capture-related mortality rate suggests this combination of physical and chemical capture has serious limitations. Captive deer permitted to recover from xylazine HCl-ketamine HCl immobilization without a reversal agent were able to walk in 290 +/- 79 min.

Rectal temperatures of immobilized, snare-trapped black bears in Great Dismal Swamp.

Rectal temperature was determined for 84 black bears (Ursus americanus) during 99 handlings in Great Dismal Swamp, Virginia and North Carolina (USA). All bears had been trapped with cable snares and immobilized with a 2:1 ketamine hydrochloridexylazine hydrochloride mixture. Temperatures were significantly greater in males and varied significantly by season. Immobilized bears began panting at rectal temperatures greater than 42.0 C. One death occurred at 43.0 C. We recommended cooling measures on black bears at rectal temperatures of greater than or equal to 40.0 C.

Clinical investigations of medetomidine in dogs.

Experiments with 3 doses of medetomidine (20, 40 and 80 micrograms/kg, iv. and im., respectively) were carried out on 90 dogs of 16 breeds in the Small Animal Surgery of the University of Veterinary Science, Budapest. Changes in hematology as well as in AST, AP, BUN, creatinine were studied. Medetomidine administered iv deepened the sedation and lengthened tranquillization dose-dependently. After im administration the sedative effect was still dose-dependent, but the duration of its clinical effectiveness could not be lengthened significantly. The development of the sedation could however, be quickened. The iv administration increased the level of analgesia in proportion to dosage; the im application could change the level of pain-killing effect of the drug, but could not lengthen it. According to the laboratorical determinations, regardless of the dosage and the route of application, medetomidine did not affect the AST and AP enzyme activities, or the BUN and creatinine values.

Effects of medetomidine in dogs with mitral regurgitation.

Thirteen small breed dogs with heart murmurs due to mitral regurgitation of varying severity received medetomidine as a sedative drug for teeth cleaning procedures. The dose was 30 micrograms/kg as an intramuscular injection. The drug caused a considerable reduction of the body temperatures and the heart rates over the 6 hrs of monitoring. The respiratory rates increased over the first 30 min and later decreased below control values. Systolic arterial blood pressures did not change significantly. Arterial oxygen tensions were significantly lower at 30 min after drug administration, but the arteriovenous oxygen differences and the carbon dioxide tensions changed very little. On electrocardiograms, sinus bradycardia, marked sinus arrhythmia with sinus pauses, AV-blocks 1st. and rarely 2nd. degree, supraventricular premature contractions (4 dogs) and paroxysmal tachycardia (1 dog) were observed. Echocardiograms showed an insignificant reduction of the shortening fraction and an increase of the left ventricular enlargement ratio as well as the left atrial to aortic root ratio at 30 min after drug administration. All measured parameters had returned to normal values (pre-drug levels) at 24 hrs after sedation. One dog had delayed cardiovascular complications at 3 hrs after drug administration, (period of prolonged asystole), necessitating the use of the antidote MPV 1248, which successfully reversed the abnormality. Two dogs collapsed briefly, at 4 and 5 hrs respectively, after excitement and struggling against physical restraint. In conclusion, medetomidine will have a safe clinical use for sedation of dogs with murmurs from compensated mitral regurgitation as soon as the antidote MPV 1248 (atipamezole) is licensed for clinical use. This will allow the reversion of the cardiopulmonary effects before the time of expected complications.

Influence of F strain Mycoplasma gallisepticum infection on response of commercial layers to heat exposure.

Commercial layers were inoculated with F strain Mycoplasma gallisepticum (MG) and housed in either conventional chicken houses or the lower-stress environment of biological isolation units. At the end of 2 weeks, all treatment groups were placed in environmental chambers and subjected to 4 hr of heat stress (40 C with a dew point of 21 C). Rectal temperature, an indicator of response to high heat, was monitored. Rectal temperatures of F strain MG-inoculated hens housed in the conventional chicken house environment were significantly higher than those of uninoculated controls, whereas rectal temperatures of hens held in isolation units were comparable to those of their uninoculated controls.

Changes in circulating prostaglandin E and F2 alpha levels, cloacal temperature, and leukocyte counts in turkeys inoculated with Pasteurella multocida.

The inoculation of Pasteurella multocida (P-1059) intravenously into turkeys increased significantly the plasma prostaglandin (PG) F2 alpha levels to 157% of the control values and the plasma PGE levels to 171% of control values at 3 hr after treatment. At 12 hr, the cloacal temperature of the inoculated birds was significantly higher than that of the control. The leukocyte count of inoculated birds remained unchanged from that of the control. However, the differential leukocyte count shifted in favor of significant increases in heterophils and decreases in lymphocytes and monocytes at 6 and 12 hr after inoculation. This study provides evidence that increases in plasma levels of PGF2 alpha and PGE may be partly responsible for the clinicopathological manifestations of acute fowl cholera.