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Introduction Anhidrosis is a serious condition of horses characterized by decreased or absent ability to produce sweat in response to increased body temperature. 1 This condition is reported primarily in hot and humid climates, although it

Open access
in Journal of the American Veterinary Medical Association

treatment with β 2 -adrenoceptor agonists results in tolerance or tachyphylaxis (desensitization) to the effects of the drug. 8 This can be a positive attribute in that adverse effects (eg, sweating, tachycardia, and agitation) attributable to

Full access
in American Journal of Veterinary Research

Abstract

Objective

To quantify total fluid loss in sweat of Thoroughbreds during > 3 hours of low-intensity exercise in controlled conditions and to calculate and compare estimated ion losses in sweat, according to 3 methods.

Animals

6 exercise-trained Thoroughbreds.

Procedure

Fluid and ion losses in sweat were measured in 6 horses exercising at 40% of the speed that elicited maximum oxygen consumption for 45 km. Horses were given a 15-minute rest period at the end of three 15-km exercise phases. Horses completed 2 exercise trials. Ion losses in sweat were calculated, using measurements of local sweating rate and sweat ion composition (SWT), change in net exchangeable cation content (CAT), and change in extracellular ion content (PLAS) derived from plasma total solids and ion concentrations.

Results

Measurement of SWT revealed a mean (± SEM) fluid loss in sweat during 45 km of exercise of 27.5 ± 1.6 L. Total ion loss in sweat was approximately 241 g or 7.8 mol with higher sodium losses in the second and third phases of exercise compared with the first phase. Losses of sodium and potassium calculated by SWT or CAT were not significantly different from each other, whereas losses of these ions as determined by PLAS were significantly lower.

Conclusions and Clinical Relevance

Calculation of ion losses from a mean whole body sweating rate extrapolated from either local sweating rate and sweat ion composition or from change in net exchangeable cation content provide similar results, whereas ion losses determined by changes in extracellular ion content derived from plasma total solids and ion concentration results in underestimation of actual losses. (Am J Vet Res 1999;60:1248–1254)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To compare dew-point hygrometry, direct sweat collection, and measurement of body water loss as methods for determination of sweating rate (SR) in exercising horses.

Animals

6 exercise-trained Thoroughbreds.

Procedure

SR was measured in 6 horses exercising at 40% of the speed that elicited maximum oxygen consumption for 45 km, with a 15-minute rest at the end of each 15-km phase. Each horse completed 2 exercise trials. Dew-point hygrometry, as a method of local SR determination, was validated in vitro by measurement of rate of evaporative water loss. During exercise, local SR was determined every 10 minutes by the following 2 methods: (1) dew-point hygrometry on the neck and lateral area of the thorax, and (2) on the basis of the volume of sweat collected from a sealed plastic pouch attached to the lateral area of the thorax. Mean whole body SR was calculated from total body water loss incurred during exercise.

Results

Evaporation rate measured by use of dewpoint hygrometry was significantly correlated (r 2 = 0.92) with the actual rate of evaporative water loss. There was a similar pattern of change in SR measured by dew-point hygrometry on the neck and lateral area of the thorax during exercise, with a significantly higher SR on the neck. The SR measured on the thorax by direct sweat collection and by dew-point hygrometry were of similar magnitude. Mean whole body SR calculated from total body water loss was not significantly different from mean whole body SR estimated from direct sweat collection or dew-point hygrometry measurements on the thorax.

Conclusions

Dew-point hygrometry and direct sweat collection are useful methods for determination of local SR in horses during prolonged, steady-state exercise in moderate ambient conditions. Both methods of local SR determination provide an accurate estimate of whole body SR. (Am J Vet Res 1997;58:175–181)

Free access
in American Journal of Veterinary Research

detected in reserve cells (ie, proliferative undifferentiated sebocytes) at the periphery of sebaceous glands. Cannabinoid receptor type 1 immunoreactivity was also detected in the cytoplasm of secretory and ductal cells of sweat glands. In the dermis

Full access
in American Journal of Veterinary Research

Personnel at an equine boarding facility with 74 resident horses noticed that one of the mares was sweating profusely and was not able to ambulate normally. The Equine Ambulatory Service at the Texas A&M University Veterinary Teaching Hospital was

Full access
in Journal of the American Veterinary Medical Association

compulsive circling in a counterclockwise direction while in the stall. When tied up, the horse threw itself forcefully against the walls of the stable and had episodes of profuse sweating. Flunixin meglumine (1.1 mg/kg, IV), acepromazine (0.05 mg/kg [0

Full access
in Journal of the American Veterinary Medical Association

signs of additional drug effects at the same time points (eg, sweating or behavioral changes other than sedation), and these signs were recorded if present. Blood samples were obtained at the same time points for measurement of plasma trazodone

Full access
in American Journal of Veterinary Research

Abstract

Objective

To examine effects of atipamezole on detomidine midsacral subarachnoidally-induced analgesia, cardiovascular and respiratory activity, head ptosis, and position of pelvic limbs in healthy mares.

Animals

10 healthy mares.

Procedure

Using a randomized, blinded, crossover study design, mares received detomidine (0.03 mg/kg of body weight, diluted in 3 ml of CSF) midsacral subarachnoidally, followed by atipamezole (0.1 mg/kg [test]) or sterile saline (0.9% NaCl) solution (control), IV 61 minutes later and saline solution (3 ml, midsacral subarachnoidally) on a separate occasion, at least 2 weeks later. Analgesia was determined by lack of sensory perception to electrical stimulation at the perineal dermatome and no response to needle-prick stimulation extending from the coccygeal to T15 dermatomes. Arterial acid-base (pH, standard bicarbonate, and base excess values), gas tensions (PO2 , PCO2 ), PCV, total solids concentration, heart and respiratory rates, rectal temperature, and arterial blood pressure were determined, and mares were observed for sweating and urination. Mean scores of perineal analgesia, head ptosis, position of pelvic limbs, and cardiovascular and respiratory data were compared for the 3-hour test period.

Results

Subarachnoidally administered detomidine induced perineal analgesia (mean ± SD onset, 9.0 ± 4.6 minutes; duration, 130 ± 26 minutes), marked head ptosis, moderate changes in pelvic limb position, cardiovascular and respiratory depression, sweating in analgesic zones, and diuresis. Intravenously administered atipamezole significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, pelvic limb position, sweating and diuresis; partially antagonized detomidine-induced bradycardia; and did not effect detomidine-induced bradypnea.

Conclusions and Clinical Relevance

Most effects of midsacral subarachnoidally administered detomidine, except bradycardia and bradypnea, were reversed by atipamezole (0.1 mg/kg, IV), indicating that most of the actions of detomidine were mediated via activation of α2-adrenergic receptors. (Am J Vet Res 1998;59:468–477)

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine effects of IV administered yohimbine on perineal analgesia, cardiovascular and respiratory activity, and head and pelvic limb position in healthy mares following epidural administration of detomidine hydrochloride solution.

Animals

8 healthy mares.

Procedure

Each mare received detomidine hydrochloride (0.06 mg/kg of body weight), administered in the caudal epidural space, followed 61 minutes later by yohimbine (0.05 mg/kg; test) or sterile saline (0.9% NaCl) solution (control), administered IV, in a randomized, crossover study design with ≥ 2 weeks between treatments. Analgesia was determined by lack of sensory perception to electrical stimulation of perineal dermatomes and needle-prick stimulation of coccygeal to 15th thoracic dermatomes. Arterial pH, Paco2, Pao2, heart and respiratory rates, rectal temperature, arterial blood pressure, and cardiac output were determined, and mares were observed for sweating and urination. Mean scores obtained for test and control groups were compared.

Results

Intravenously administered yohimbine significantly reduced mean scores of detomidine-induced perineal analgesia, head ptosis, changes in pelvic limb position, and sweating and diuresis; antagonized detomidine-induced decreases in heart rate and cardiac output; but did not affect detomidine-induced decrease in respiratory rate.

Conclusions and Clinical Relevance

Most effects of epidurally administered detomidine, except bradypnea, were antagonized by yohimbine, suggesting that detomidine may influence respiratory rate by mechanisms other than stimulation of α2-adrenoceptors, or that yohimbine induces respiratory depressant effects. Yohimbine may be an effective α2-adrenoceptor antagonist for all but respiratory depression following epidural administration of detomidine to mares. (Am J Vet Res 1999;60:1262–1270)

Free access
in American Journal of Veterinary Research