Efficacy of treatment of equine anhidrosis with acupuncture and Chinese herbs is low but higher in treated horses compared with placebo.

OBJECTIVE: To assess the therapeutic efficacy of acupuncture in combination with Chinese herbs for treatment of horses affected with anhidrosis. ANIMALS: 44 horses affected with anhidrosis for up to 3 years' duration were enrolled. Inclusion required both compatible clinical signs and results of a quantitative intradermal terbutaline sweat test. METHODS: Study horses were randomly allocated into 2 groups. Group 1 (n = 19) was treated with daily Chinese herbs and 4 weekly acupuncture sessions. Group 2 (n = 25) was given daily hay powder as a placebo and 4 weekly sham acupuncture sessions. Horses were tested by quantitative intradermal terbutaline sweat test within 2 days after treatment completion and again 4 weeks following treatment. RESULTS: Terbutaline-induced sweat responses (mg) were not different between groups within 2 days and 4 weeks after treatment. Two days after treatment, ratios of sweat responses (compared to baseline) were higher (P < .05) in the treatment group compared to the placebo group at terbutaline concentrations of 1.0, 100, and 1,000 µg/mL. The number of horses responding to treatment was higher in the treatment group (5/19 [26%]), compared to horses in the placebo group (1/25 [4%]) for 1 of 5 terbutaline concentrations 2 days (10 µg/mL) or 4 weeks (0.1 µg/mL) after treatment. CLINICAL RELEVANCE: Ratios of sweat responses were higher in treatment horses 2 days after treatment, compared to baseline, but not 4 weeks later. The efficacy of a traditional Chinese veterinary medicine protocol for anhidrosis treatment with acupuncture and Chinese herbs was low but higher in treated horses compared with placebo.

Effect of prolonged administration of clenbuterol on airway reactivity and sweating in horses with inflammatory airway disease.

OBJECTIVE: To determine whether prolonged administration of clenbuterol results in tachyphylaxis, specifically regarding its bronchoprotective properties and effect on sweating in horses. ANIMALS: 8 Thoroughbreds with inflammatory airway disease. PROCEDURES: In a crossover design, horses received clenbuterol (0.8 µg/kg, p.o., q 12 h) or placebo for 21 days, with a washout period of ≥ 30 days between the 2 treatments. Airway reactivity was evaluated by use of flowmetric plethysmography and histamine broncho-provocation before (day 0; baseline) and every 7 days after the start of treatment. Sweat function was evaluated via response to epinephrine administered ID before and every 10 days after the start of treatment. RESULTS: The concentration of histamine required to increase total airway obstruction by 35% (PC35) was significantly reduced during treatment with clenbuterol (mean change, 11.5 mg/mL), compared with during administration of the placebo (mean change, -1.56 mg/mL), with a peak effect at 14 days. Tachyphylaxis was evident by day 21, with 7 of 8 horses having a PC35 below the baseline value (mean change, -0.48 mg/mL), which returned to baseline values during the washout period. No effect of clenbuterol was seen in sweat response to epinephrine administration. CONCLUSIONS AND CLINICAL RELEVANCE: Clenbuterol initially reduced airway sensitivity to inhaled histamine, but tachyphylaxis that resulted in increased airway reactivity was evident by day 21. Although no effects on sweating were detected, the technique may not have been sensitive enough to identify subtle changes. Prolonged administration of clenbuterol likely results in a clinically important reduction in its bronchodilatory effects.

An epidemiologic study of anhidrosis in horses in Florida.

OBJECTIVE-To estimate prevalence of and identify factors associated with anhidrosis in horses in Florida. Design-Cross-sectional study and case-control study. ANIMALS-4,620 horses on 500 farms. PROCEDURES-A questionnaire was structured and mailed to farm owners or managers to obtain information related to diagnosis of anhidrosis in horses and exposure factors associated with this condition. The frequency of investigated farm- and animal-level factors was compared between farms and horses affected and not affected with anhidrosis, respectively. RESULTS-The prevalence of anhidrosis was 11% at the farm level and 2% at the animal level. The odds of anhidrosis were 2.13 and 4.40 times as high in farms located in central and southern Florida, respectively, compared with odds for farms in northern Florida. The odds of anhidrosis were 5.26 and 15.40 times as high in show and riding instruction operations, respectively, compared with odds for ranch operations. At the animal level, breed (Thoroughbreds and warmblood horses), foaling place (western or midwestern region of the United States), and family history of anhidrosis were significantly associated with anhidrosis. CONCLUSIONS AND CLINICAL RELEVANCE-This study provides new information on the prevalence of and factors for anhidrosis in horses in Florida. Horses with a family history of anhidrosis should be examined by a veterinarian for diagnosis of this condition before they are exposed to exercise in a hot and humid climate.

Thyroid function in anhidrotic horses.

BACKGROUND: This study was performed to determine whether anhidrotic horses have altered thyroid function compared with horses that sweat normally. HYPOTHESIS: Anhidrotic horses have normal thyroid function. ANIMALS: Ten client-owned horses with clinical signs of anhidrosis were paired with 10 horses living in the same environment that had normal sweat production. METHODS: Horses were diagnosed as having normal sweat production or being anhidrotic based on responses to intradermal injections of terbutaline and physiologic responses to lunging exercise. Control horses were selected from the same environment and matched as closely as possible to anhidrotic horses in terms of age, sex, breed, and athletic condition. Thyrotropin-releasing hormone (TRH) stimulation tests were performed in both horses at the same time, once in the summer or fall, and once again in winter. RESULTS: Anhidrotic horses produced less sweat in response to intradermal injections of terbutaline and exercise than did control horses. They also had greater increases in body temperature and respiratory rate in response to exercise. Resting concentrations of thyroid hormones and thyroid-stimulating hormone (TSH) were not different between anhidrotic and control horses. Thyroid hormone responses to TRH also were not different between the 2 groups of horses. However, anhidrotic horses had a significantly different TSH response to TRH compared with control horses, particularly in the winter. CONCLUSIONS AND CLINICAL IMPORTANCE: The biologic relevance of the altered TSH response to TRH in anhidrotic horses is uncertain, considering that TSH concentrations remained within previously reported normal ranges and thyroid hormone responses were not different between anhidrotic and control horses.

A preliminary study of the short circuit current (Isc) responses of sweat gland cells from normal and anhidrotic horses to purinergic and adrenergic agonists.

The causal factors of equine anhidrosis have not yet been elucidated but defective electrolyte transport mechanisms in the gland are likely to be involved. To investigate this possibility, experiments were performed on cultured equine sweat gland epithelia from five free-sweating UK horses (3 intact males, 2 mares, aged 2-4 years) and from three free-sweating Singapore horses (1 intact male, 2 mares, aged 3-5 years) and three anhidrotic (Singapore) horses (1 intact male, 1 gelding, 1 mare, aged 3-6 years). Cultured cells from each animal were grown on permeable supports and loaded into Ussing chambers to quantify transepithelial resistance and agonist-induced electrolyte transport by the short circuit current (Isc) technique. Transepithelial resistances across the layers of cultured cells were not significantly different between cells from UK and Singapore free-sweating horses, but were significantly reduced in anhidrotic animals. Purinergic agonists added to the apical and basolateral aspects of the cultured cells caused similar increases in Isc between the two populations of unaffected cells, but Isc increases were significantly reduced in anhidrotic animals. Beta-adrenergic agonist stimulation of the anhidrotic cell layers failed to elicit any change in Isc. These pilot results not only confirm earlier conclusions from anatomical findings that failure in the secretory process occurs in anhidrosis but also indicate that both of the known ion transport mechanisms are involved. The trigger for these failures warrants further investigation.

Equine sweating and anhidrosis Part 2: anhidrosis.

The condition of anhidrosis is described in this review, and the latest theories on the causal factors are explored. The evidence supports the hypothesis that anhidrosis is an inappropriate response to prolonged climatic stress (generally combined heat and high humidity), which can be evoked in a small (approximately 10 +/- 5%) proportion of the equine population. It is caused by gradual failure of the glandular secretory cell processes, initiated by desensitization and subsequent down-regulation of the cell receptors as a result of continued adrenaline-driven hyperactivity. It progresses through secretory failure and culminates in gradual, probably irreversible, glandular dedifferentiation and ultimate degeneration. There is a need for considerably more research on the secretory and transcriptional processes to document the changes arising within the glandular secretory mechanism as a prelude to development of a corrective treatment.

Equine sweating and anhidrosis Part 1--equine sweating.

Sweating has a variety of functions in mammals including pheromone action, excretion of waste products and maintenance of the skin surface ecosystem. In a small number of mammalian species, which includes humans and the Equidae, it also has an important role in thermoregulation. This review is focused specifically on the thermoregulatory role of sweat in Equidae and the causes of sweating failure (anhidrosis). The first part describes the glandular appearance, sweat composition, and output rates; and considers the latest theories on the glandular control and secretory mechanisms. It is concluded that the glands are not directly innervated but are controlled by the interplay of neural, humoral and paracrine factors. The secretory mechanism is not as simple as previously thought and is mediated by the dynamic interaction of activating pathways, including autocrine control not only of the secretory process but probably also of secretory cell reproduction, growth, and death.

A preliminary passive surveillance of clinical diseases of cart pulling camels in Faisalabad metropolis (Pakistan).

We identified clinical disorders of all 200 city-dwelling cart pulling male camels attending the Veterinary Teaching Hospital, University of Agriculture, Faisalabad, Pakistan during a 7-year period (1993-1999). Data were collected prospectively on a predesigned form and collated. Diagnoses of different diseases/disorders were based on clinical examination supplemented with relevant laboratory tests. A total of 463 entries of 34 different clinical diseases/disorders were recorded. Sarcoptic mange (35% of 200 camels) followed by anhidrosis (23%) and trypanosomosis (19%) were the three most frequently encountered disorders. The body system most often involved was the integument (31%) followed by gastrointestinal (21%), locomotory (12%), thermoregulatory (6%), blood (6%), urogenital (6%), lymphatic (3%), nervous (3%), respiratory (3%) and ocular (3%).

Immunolocalization of aquaporin-5 expression in sweat gland cells from normal and anhidrotic horses.

Western blot analysis showed that sweat gland cells from freely sweating horses expressed the water channel aquaporin-5 (AQP-5). Immunohistochemistry revealed a strong AQP-5-like activity reaction at the apical membrane of the glandular secretory cells, which was absent from the surrounding myoepithelium and all other skin structures. In anhidrotic horses, AQP-5 was also found at the apical membrane of the luminal sweat gland cells, but the level of expression reduced with the length of time that the animal had displayed anhidrosis. The level of AQP-5 expression was substantially reduced in animals with long-term anhidrosis, hence implicating water channel impairment as a possible factor in the development of this disorder.

Equine anhidrosis.

The molecular basis of the pathophysiology of anhidrosis is still not well understood. Therefore, treatments are more often based on clinical impressions than on scientific fact. Treatment options for this condition will improve only when more is known about the molecular events that cause anhidrosis, especially as they relate to beta2-receptor dysfunction and stimulus-secretion coupling in the sweat glands of affected horses. Although this additional information is being attained, sound environmental management will continue to be a very important aspect of the treatment of horses affected with anhidrosis.

Sweating and skin temperature responses of normal and anhidrotic horses to intravenous adrenaline.

Anhidrosis has been recognised for over half a century, but despite some excellent epidemiological studies, there has been little progress in understanding the aetiology of the condition. Using a modified ventilated capsule, we obtained dynamic, quantitative data on sweating responses in anhidrotic horses and normal sweating controls from the same environment. Ten horses with current seasonal anhidrosis and 10 matched normal sweating controls were selected. Each horse was given two 10 min infusions of 1 and 2 micrograms/kg/min adrenaline, separated by at least 6 h. Sweating responses and skin temperatures on the neck and gluteal region were measured. Plasma and sweat for analysis of total protein and electrolytes and plasma for analysis of adrenaline were collected. Anhidrotic horses produced significantly less sweat, had lower initial and peak sweat rates and a greater neck:gluteal ratio for sweat production. Plasma adrenaline at rest or at the time of peak sweating rate was not different between groups. In nearly three-quarters of the anhidrotic horses, the shape of the sweat rate against time curve was different compared to controls. Volume of sweat produced was significantly correlated with skin temperature on the neck of controls and anhidrotic horses and on the gluteal region of controls, but not anhidrotic horses. Plasma total protein and electrolyte concentrations were not different between groups. There were significant differences in sweat electrolyte concentrations between controls and anhidrotic horses. These differences were reduced when sweat electrolytes were expressed per g of total protein, and no differences existed when expressed as g/m2. This study has provided insight into the response of anhidrotic horses to beta 2 adrenergic stimulation and may be a useful technique to investigate this condition.

Use of a semi-quantitative sweat test in thoroughbred horses.

A practical test for evaluating the sweating response to various concentrations of the specific beta 2 agonist, salbutamol sulphate, is described. The results of performing this test on horses (n = 54) considered to be "free sweaters", horses (n = 6) that showed signs of heat stress following exercise, and horses with complete anhidrosis (n = 2) are presented. The results indicate that intradermal injections of 0.1 ml of salbutamol sulphate at dilutions of 10(-7) or less are suitable stimuli to elicit a visually detectable local sweating in horses with a normal sweating response. Horses that only sweated at the sites where salbutamol solutions with dilutions of between 10(-4) and 10(-6) were injected, probably had a reduced sweating response and could be considered to be suffering from partial anhidrosis. Horses with severe anhidrosis of long duration did not sweat, even in response to salbutamol solutions with dilutions of 2 x 10(-3).

Effects of season and lower ambient temperature on the structure of the sweat glands in anhidrotic horses.

Histological studies of the sweat glands of anhidrotic horses in the Hong Kong summer and under conditions of reduced thermal stress, both natural and controlled, were undertaken to determine if glandular regeneration occurs. Clinical data were collected for comparison with the histological results in each instance. Horses were assigned to one of three categories on the basis of the resulting change in the number of thin glandular profiles in a cooler environment. Group 1, which was classed as normal, had a low initial value, which was maintained. Group 2, typical of mild and moderately affected animals, had a high initial value, which fell markedly after as little as six weeks in the cool environment. Animals in Group 3, classed as severely affected, had a high initial value which remained high even after prolonged exposure to the cool environment. Light microscopical examination of the sweat glands in the heat, and after six weeks in a cool environment, provided a means of predicting the degree of anhidrotic severity and the potential for recovery in a cool climate. This was superior to clinical observation, although a diagnostic test based on glandular function is still required.

Clinical, clinicopathologic, and epidemiologic features of anhidrosis in central Florida Thoroughbred horses.

A group of 834 Thoroughbred horses was surveyed on four central Florida farms for clinical and epidemiologic features of anhidrosis. In addition, comparative analysis was made of serum thyroxine, serum electrolytes, and fractional urinary electrolyte excretion ratios. An overall disease prevalence of 6.12% was observed. Training horses and nonpregnant broodmares had a predilection for the disease. Adolescent horses were infrequently affected. There was no correlation with sex or color. Comparative clinical signs, related to thermoregulatory compromise, included tachypnea and hyperthermia. Long-term effect included focal and generalized alopecia, decreased appetite, and impaired performance. Previously reported hypothyroidism and hypochloremia were not demonstrated; however, fractional urinary chloride excretion ratios indicated a significant relative conservation of chloride.

Ultrastructural variations in the sweat glands of anhidrotic horses.

The ultrastructure of sweat glands from the skin of free sweating horses was compared with that of glands from anhidrotic cases. Evidence of atrophied and abnormal sweat glands in the anhidrotic horses indicates that the condition involves progressive failure of the glandular mechanism of sweat production.

Equine anhidrosis: a review of pathophysiologic mechanisms.

Anhidrosis is loss of the ability to sweat. The problem is seen in horses kept in a hot humid climate, and it may cause severe impairment of thermoregulation in the equine athlete. British Thoroughbreds imported to her tropical colonies are the earliest recorded cases, and since then the syndrome has come to be described as one of Thoroughbreds, usually performance athletes, undergoing acclimatization to heat and humidity. A recent epidemiologic study of cases in Florida has shown, however, that many different breeds, and long time inhabitants of a hot climate, may be affected. Equine sweat glands are of the apocrine type, and sweating is stimulated by direct local release of epinephrine from adrenergic nerve endings and by circulating epinephrine. Lack of sweating could be due to a number of possible flaws in a sequence from central nervous stimulation through sweat stimulation and secretion to delivery of sweat to the skin surface. The most likely possibilities are inadequate sweat gland response due to habituation of receptors to a high circulating level of epinephrine and occlusion of the sweat ducts by keratin plugs. Hormonal or metabolic imbalance may play a role both in the onset and secondary signs associated with anhidrosis.