Abstract:
Objective To determine the effects of acepromazine and detomidine standing sedation on
haematological and biochemical variables in horses.
Study design A blinded randomised, comparative study.
Animal population Twelve Nooitgedachter horses and four Thoroughbred horses.
Methods Horses were enrolled into the study to receive one of two intravenous treatments (n
= 8 per treatment group): acepromazine maleate (ACE; 0.05 mg kg-1), or detomidine
hydrochloride (DET; 0.01 mg kg-1). One week later, eight of the horses were randomly assigned
to undergo a control treatment (CON; received no drug, but underwent the same procedures).
On the day of data collection, all horses underwent a routine physical examination and then
placed in stocks or a stable to rest for 30 minutes. Baseline blood samples and clinical variables
(sedation score, heart and respiratory rates, temperature) were obtained (time zero) and then
the horse received the treatment, followed by blood sampling and clinical parameter
measurements at 15-minute intervals until 60 minutes. Blood sampling at each time point
involved the collection of jugular blood (single venous puncture, alternating between left and
right jugular) into five vacuum storage tubes to measure: haematocrit, differentiated cell
counts, total serum protein, albumin, globulins, cortisol, ACTH, insulin, glucose, AST, ALT,
GGT, ALP, GLDH and CRP. Once the procedures were complete, the horses were observed
until recovered from the effects of the sedative drugs (no signs of sedation or ataxia) before
being allowed to continue with their daily routine. Quantitative data (clinical, hematological
and biochemical values) were compared among treatments using a two-way analysis of
variables. Significant findings were then compared using Dunnett’s method of post-hoc
analysis where the baseline data within each treatment group was used as the control variable.
Categorical data were compared among treatments using the Friedman Test (sedation scores).
Results The sedation scores were significantly higher, indicating sedation, in the horses that
received DET or ACE when compared to CON, indicating that there was drug effect (p < 0.01
for both drugs). The haematocrit decreased in DET and ACE over time (both p < 0.01) but not
in CON. The changes over time for the red blood cell count were similar to that of the
haematocrit (both p < 0.01). The white cell count decreased significantly over time after DET
and ACE compared to CON (both p = 0.03). The platelet counts were not different among
groups and over time. Most of the biochemistry analytes remained unchanged over time,
however, there were statistically and clinically relevant observations. The glucose
concentration raised from 30 minutes onwards within DET compared to ACE and CON which
remained constant over time (p < 0.01).
Conclusions and clinical relevance Acepromazine and detomidine induced standing sedation
caused changes in haematological and some biochemical variables in the horses. These changes
were detectable from 15 minutes of administration of the drugs and in some cases lasted the
hour of observation. The present study highlights the clinical relevance of obtaining venous
blood for analysis in equine patients prior to the administration of sedative drugs.