Susan W. Eberhart

Effect of tracheal mucus and tracheal cytology on racing performance in Thoroughbred racehorses

REASON FOR PERFORMING STUDY Accumulations of mucus within the trachea are often found during endoscopic examinations of the airways of poorly performing racehorses, but the clinical importance of this finding is unknown. OBJECTIVES To determine the effect of tracheal mucus, pharyngeal lymphoid hyperplasia (PLH) and cytological indices of tracheal aspirate on racing performance in Thoroughbred horses assessed by race place and whether the horse was raced. METHODS Endoscopic examination of the nasopharynx, larynx and trachea was performed, and a tracheal aspirate obtained monthly at Thistledown racetrack from April to December, 2002 and 2003. Horses received a score of 0-4 for the degree of PLH and 0-4 for the amount of mucus visible in the trachea. The tracheal aspirate was assessed for turbidity, and total and differential cell counts. Generalised estimating equations models were used as repeated measures models for each risk factor and the level of association assessed through the risk factors P value in the model. RESULTS Moderate to severe tracheal mucus (2-4) was a risk factor for poor racing performance. There was no association between degree of PLH, cell counts or turbidity of tracheal wash fluid and racing performance. However, horses that raced had higher total neutrophil counts in tracheal wash aspirates than horses that did not race. CONCLUSIONS Grades 2-4 tracheal mucus should be considered a potential cause of poor racing performance in Thoroughbred horses. CLINICAL RELEVANCE Because moderate to severe tracheal mucus accumulation, and not increased tracheal neutrophils, was a risk factor for poor racing performance, functionally significant airway inflammation may best be confirmed by the presence of mucus rather than increased number of neutrophils in the trachea.

Thermographic study of in vivo modulation of vascular responses to phenylephrine and endothelin-1 by dexamethasone in the horse.

REASONS FOR PERFORMING STUDY In vitro, glucocorticoids potentiate vasoconstriction of equine digital vessels to catecholamines and this has been implicated as a mechanism of glucocorticoid-induced laminitis. This observation has never been confirmed in vivo. OBJECTIVES To study the effects of glucocorticoid therapy on vasoconstrictor responsiveness in the horse in vivo. METHODS In a blinded, randomised cross-over experiment, 9 horses were treated with either dexamethasone (0.1 mg/kg bwt i.v. q. 24 h) or saline i.v. for 6 days. The changes in local average skin temperature before (baseline) and after intradermal injections of the alpha1-adrenoceptor agonist phenylephrine (PHE; 10(-4), 10(-5), 10(-6), 10(-7) and 10(-8) mol/l), endothelin-1 (ET-1; 10(-5), 10(-6), 10(-7), 10(-8) and 10(-9) mol/l) or ET-1 plus a blocker (BQ-123 10(-6) mol/l; RES-701 10(-6) mol/l; and L-NAME 10(-4) mol/l) were investigated with a thermograph. RESULTS Dexamethasone (DEX) decreased baseline skin temperatures, suggesting reduced blood flow as a consequence of an increase in vasomotor tone. This was accompanied by potentiation of the response to PHE as demonstrated by a left shift in the dose-response curve and a decrease in the EC50. Dexamethasone did not potentiate ET-1, but the interplay with the lower baseline temperature resulted in a significantly lower skin temperature for this vasoconstrictor after DEX. The different ET-1 blockers had no effect on ET-1 modulated skin temperatures. CONCLUSIONS Dexamethasone decreases skin perfusion. This is accompanied by a potentiated alpha1-adrenoceptor agonist response and a greater response to ET-1. POTENTIAL RELEVANCE Glucocorticoid therapy probably decreases perfusion of the equine hoof. During disease states that already are characterised by hypoperfusion and/or increased levels of circulating catecholamines, glucocorticoid therapy could, according to the vascular model of laminitis, tilt the balance in favour of laminitis.

Response to nasopharyngeal oxygen administration in horses with lung disease

REASONS FOR PERFORMING STUDY Guidelines for administration of oxygen to standing horses are unavailable because previous investigations of the efficacy of oxygen administration to increase arterial oxygenation in standing horses have produced equivocal results. OBJECTIVE To determine the effect of nasal oxygen supplementation on inspired and arterial blood gas tensions in control horses and those with moderate to severe recurrent airway obstruction (RAO). METHODS Normal horses (n = 6) and horses during an attack of RAO induced by stabling (n = 6) were studied. Oxygen was administered through either one or 2 cannulae, passed via the nares into the nasopharynx to the level of the medial canthus of each eye. Intratracheal inspired oxygen and carbon dioxide concentration and arterial blood gas tensions were measured at baseline and during delivery of 5, 10, 15, 20 and 30 l/min oxygen. RESULTS Nasal cannulae and all but the highest oxygen flow rates were well tolerated. Fractional inspired oxygen concentration (F(I)O2) increased with flow but was significantly lower at all flow rates in horses with RAO compared with controls. Arterial oxygen tension (PaO2) was significantly increased (P < 0.001) by all flow rates, but was always lower in RAO-affected animals. At 30 l/min, PaO2 increased to 319 +/- 31 mmHg in control horses and 264 +/- 69 mmHg in horses with RAO. Additionally, a large arterial to end-tidal gradient for CO2 in RAO-affected horses was observed, indicating increased alveolar deadspace ventilation in these animals. CONCLUSIONS The use of nasal cannulae to deliver oxygen effectively increases both F(I)O2 and PaO2 in horses with moderate to severe RAO. Oxygen flow rates up to 20 l/min are well tolerated, but flow rates of 30 l/min produce occasional coughing or gagging. POTENTIAL RELEVANCE Oxygen therapy delivered by means of an intranasal cannula is a highly effective means of increasing arterial oxygen tension in horses with respiratory disease. Generally, flows of 10-20 l/min should be effective. If higher flows (20-30 l/min) are necessary, they should be delivered by means of 2 cannulae.

Rehydration fluid temperature affects voluntary drinking in horses dehydrated by furosemide administration and endurance exercise

To determine whether temperature of rehydration fluid influences voluntary rehydration by horses, six 2-3-year-old horses were dehydrated (4-5% body weight loss) by a combination of furosemide administration and 30 km of treadmill exercise. For the initial 5 min following exercise, horses were offered a 0.9% NaCl solution at 10, 20, or 30 degrees C. Subsequently, after washing and cooling out, voluntary intake of water at 10, 20, or 30 degrees C from 20 to 60 min after exercise was measured. Fluid intake (FI) during the first 5 min of recovery was 9.8+/-2.5,12.3+/-2.1 and 9.7+/-2.0L (p>0.05) for saline at 10, 20, and 30 degrees C, respectively. Although not a significant finding, horses offered 0.9% NaCl at 20 degrees C tended to take fewer (p=0.07), longer drinks than when saline at either 10 or 30 degrees C was offered. Between 20 and 60 min of recovery, intake of water at 20 degrees C (7.7+/-0.8L) and 30 degrees C (6.6+/-1.2L) was greater (p<0.05) than that at 10 degrees C (4.9+/-0.5L). Thus, total FI was 14.7+/-2.5,19.9+/-2.5, and 16.3+/-2.4L for rehydration fluids at 10, 20, and 30 degrees C, respectively (p<0.05, value for 20 degrees C water greater than that for 10 degrees C water). Although the amount of metabolic heat transferred to the initial saline drink was correlated with the decrease in core temperature during the initial 5 min of recovery, heat transfer to ingested fluid was most likely responsible for the dissipation of, at most, 5% of the heat generated during endurance exercise. In conclusion, following exercise these dehydrated-normothermic horses voluntary drank the greatest amount of fluid at near ambient (20 degrees C) temperature. Although not determined in this study, greater satiation of thirst by oropharyngeal cooling may have contributed to lesser intake of colder (10 degrees C) fluid.

Trimetoquinol: bronchodilator effects in horses with heaves following aerosolised and oral administration

REASON FOR PERFORMING STUDY The bronchodilator effects of trimetoquinol (TMQ) have been studied when administered i.v. or intratracheally, but not in an aerosolised form. OBJECTIVES To define the relationship between the therapeutic and adverse responses (therapeutic index) of TMQ when administered as an aerosol or by the oral route. METHODS Increasing doses of TMQ were administered to horses with heaves as an aerosol and by the oral route. Dose ranged 100-1000 microg/horse for aerosolised TMQ and from 6-60 microg/kg bwt for the oral route. Airway and cardiac effects were assessed by measurement of maximal change in pleural pressure (deltaPplmax) and heart rate (HR), respectively. Side effects of sweating, agitation and muscle trembling were scored subjectively. Duration of action of aerosolised (1000 pg/horse) and oral (6-60 microg/kg bwt) TMQ was evaluated over 6 h. RESULTS Aerosol administration of TMQ caused dose-dependent bronchodilation but did not change HR or cause other observable side effects. When 1000 microg/horse was administered via aerosol, TMQ produced a 2-phase bronchodilation; an immediate effect lasting up to 30 min and a second phase between 2 and 4 h. Oral TMQ was therapeutically ineffective. CONCLUSION Aerosol administration of TMQ is a safe and effective method of producing bronchodilation in horses.

Effect of varying initial drink volume on rehydration of horses

Body mass (BM), water intake (WI), and plasma osmolality (P(osm)) and electrolyte concentrations were measured in six 2-year-old Arabian horses provided either 4 l, 8 l, or an unlimited amount of water (UW) for drinking during the initial 5 min of recovery from 45-km of treadmill exercise. After weighing, horses were placed in a stall and further WI between 20 and 60 min of recovery was measured. During exercise, horses lost 3.3+/-0.3%, 3.2+/-0.1%, and 3.3+/-0.2% (P>.05) of BM and P(osm) increased by 7.2+/-0.5, 7.9+/-0.8, and 7.7+/-0.5 mOsm/kg (P>.05) for 4 l, 8 l, and UW, respectively. WI during the first 5 min of recovery was 4.0+/-0.0, 8.0+/-0.0, and 9.0+/-1.3 l and was accompanied by 2.4+/-0.4, 5.8+/-0.9, and 6.1+/-0.7 mOsm/kg decreases (P<.05) in P(osm) for 4 l, 8 l, and UW, respectively. Between 20 and 60 min of recovery, WI was 6.2+/-1.5, 1.2+/-0.6, and 1.0+/-0.7 l (P<.05) for 4 l, 8 l, and UW, respectively. Thus, total WI was 10.2+/-1.5, 9.2+/-0.6, and 10.0+/-1.1 l (P>.05) for 4 l, 8 l, and UW, respectively. After 60 min of recovery, persisting BM loss was 1.3+/-0.5%, 1.1+/-0.2%, and 1.0+/-0.2% (P>.05) for 4 l, 8 l, and UW, respectively and P(osm) had returned to pre-exercise values for all treatments. In conclusion, limiting the volume of water initially provided to horses dehydrated by endurance exercise had no significant effect on total WI during the initial 60 min of recovery; however, persisting BM loss was observed with all treatments. Further, following exercise-induced dehydration, the primary stimulus of thirst was an increase in plasma tonicity rather than hypovolemia.

Effect of oral administration of electrolyte pastes on rehydration of horses

OBJECTIVE To determine whether the composition of electrolyte pastes formulated for oral administration influences voluntary water intake (WI) by horses recovering from furosemide-induced dehydration. ANIMALS 6 horses. PROCEDURES Voluntary WI, body weight, and blood and urine constituents were measured before and after induction of dehydration by furosemide administration and overnight withholding of water; these same variables also were measured during a 36-hour rehydration period. Each horse was evaluated 4 times with random application of 4 treatments (electrolyte pastes) that provided 0.5 g of KCl/kg of body weight, 0.5 g of NaCl/kg, 0.25 g of NaCl and 0.25 g of KCl/kg, or no electrolytes (control treatment). Electrolyte pastes were administered 3 times (4, 8, and 12 hours after start of the rehydration period). RESULTS Administration of all electrolyte pastes resulted in significantly greater voluntarily WI, compared with the control treatment, and was accompanied by significantly greater recovery of body weight when NaCl was a component of the paste. Administration of NaCl and NaCl-KCl pastes tended to produce a state of transient hyperhydration; however, electrolyte administration also resulted in significantly greater urine production and electrolyte excretion during the final 24 hours of the rehydration period. Adverse effects of oral administration of hypertonic electrolyte pastes were not observed. CONCLUSIONS AND CLINICAL RELEVANCE Oral administration of electrolyte pastes to dehydrated horses increases voluntary WI and improves rehydration during the rehydration period. Rehydration is more rapid and complete when NaCl is a component of the electrolyte paste.