D. Parmentier

A preliminary study on the effects of atropine sulphate on bradycardia and heart blocks during romifidine sedation in the horse.

Romifidine (STH 2130-Cl or Sedivet) is an ά2-agonistic imino-imidazol sedative for intravenous use in horses recently developed by Boehringer Ingelheim, Vetmedica GmbH. An exploratory study was done in nine warm-blood horses, randomly divided into three groups, which received different dosages of romifidine (0.04, 0.08 and 0.12 mg/kg of body weight (BWT) intravenously (i.v.)) with at least one weeks interval between tests.Romifidine induced a marked bradycardia accompanied by second degree atrioventricular (AV) block and some sinus blocks at all tested dosages. A placebo (NaCl 0.9% i.v.) given 5 min before and after romifidine did not affect the cardiac disturbances induced by romifidine.A low dose of atropine sulphate (0.005 mg/kg of BWT i.v.) given 5 min before romidifine counteracted the bradycardia and caused a normal to increased heart rhythm at all romifidine dosages. A higher dose of atropine sulphate (0.01 mg/kg of BWT i.v.) administered 5 min before sedation induced a tachycardia (average 70 beats/min) at all romifidine dosages and completely prevented the bradycardia and the heart blocks. The positive chronotrope effects of atropine sulphate were attenuated by increasing doses of romifidine.The effects of atropine sulphate (low or high doses) given 5 min after romifidine only appeared after 5 min. Both dosages counteracted the bradycardia and suppressed the heart blocks.No atropine-dependent side effects were observed in non-fasted horses. The degree of the romifidine induced sedation was not affected by the use of atropine sulphate given before or after romifidine.

Haemodynamic changes during sedation in ponies.

The cardiovascular changes induced by several sedatives were investigated in five ponies with a subcutaneously transposed carotid artery by means of cardiac output determinations (thermodilution technique), systemic and pulmonary artery pressure measurements (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume).The cardiovascular depression (decrease in systemic blood pressure and cardiac output) was long lasting (>90 min) after administration of propionylpromazine (0.08 mg/kg intravenous (i.v.)) together with promethazine (0.08 mg/kg i.v.). The phenothiazine-induced sedation was not optimal.α2-Agonists (xylazine (0.60 mg/kg i.v.) and detomidine (20 μg/kg i.v.)) induced initial but transient cardiovascular effects with an increase in systemic blood pressure and a decrease in cardiac output for about 15 min. Second degree atrioventricular blocks and bradycardia were seen during this period. The cardiovascular depression was more pronounced during detomidine sedation.Atropine (0.01 mg/kg i.v.) induced a tachycardia with a decrease in stroke volume but did not alter the cardiac output or other cardiovascular parameters. It prevented the occurrence of the bradycardia and heart blocks normally induced by xylazine or detomidine. Atropine potentiated the initial hypertension induced by the α2-agonists sedatives (especially detomidine). The decrease in cardiac output induced by xylazine, and to a lesser extent by detomidine, was partially counteracted when atropine was given in advance.The atropine-xylazine combination seemed the best premedication protocol before general anaesthesia as it only resulted in minor and transient cardiovascular changes.