Abstract: Crib-biting is a common oral stereotype. Because of perceived deleterious effects on the health and appearance of subjects the prevention of crib-biting is regularly attempted. The resourcefulness of horses in satisfying their motivation to perform this behaviour often frustrates owners' efforts at prevention. This paper reviews the efficacy and observable consequences of attempting to prevent crib-biting by a variety of methods. These include attempts to prevent the grasping of objects, to interfere with air-engulfing and to introduce punishment for grasping and neck-flexion. Other approaches include the use of surgery, acupuncture, pharmaceuticals, operant feeding and environmental enrichment. A remedy that is effective for every crib-biter remains elusive. We conclude that, rather than concentrating on remedial prevention, further research should be directed at establishing why horses crib-bite and how the emergence of crib-biting can be avoided.

Abstract: There is confusion in the veterinary literature concerning the definition of oral based stereotypies in the horse. This study reports the use of fluoroscopy and endoscopy during cribbiting/wind-sucking in afflicted horses. This permitted observations of movements of the pharyngeal and oesophageal tissues and of the air column within during the stereotypic behaviour. The findings reported show that the sequence of events during crib-biting/wind-sucking is not related to deglutition and that air is not swallowed to the stomach. Transient dilation of the upper oesophagus was recorded and the characteristic noise of wind-sucking coincided with the in-rush of air through the cricopharynx. The oesophageal distension was relieved when the air returned to the pharynx although small quantities passed caudally. It is proposed that the role of contraction of the strap muscles of the neck is to create a pressure gradient in the soft tissues surrounding the oesophagus which provokes movement of air from the pharynx into the oesophagus. The findings suggest that the definitions currently used in the sale of horses are in need of revision.

Abstract: OBJECTIVE: To compare nociceptive withdrawal reflexes (NWRs) evoked from the distal aspect of the left forelimb and hind limb in conscious standing horses and to investigate NWR recruitment for graded electrical stimulation intensities. ANIMALS: 20 adult horses. PROCEDURE: Surface electromyographic (EMG) activity evoked by transcutaneous electrical stimulation of the digital palmar (or plantar) nerve was recorded from the common digital extensor and cranial tibial muscles. Stimuli consisted of 25-millisecond train-of-5 constant current pulses. Current intensity was gradually increased until NWR threshold intensity was reached. The EMG signal was analyzed for quantification of the NWR. Behavioral responses accompanying the reflex were scored (scale, 0 to 5). The NWR recruitment curves were determined at 0.9, 1.1, 1.2, and 1.3 times the NWR threshold intensity. RESULTS: The NWR threshold was significantly higher for the hind limb (median value, 6.6 mA; range, 3 to 10 mA) than the forelimb (median, 3 mA; range, 1.7 to 5.5 mA). The NWR of the hind limb had a significantly longer latency (median, 122.8 milliseconds; range, 106 to 172 milliseconds), compared with the forelimb (median, 98 milliseconds; range, 86 to 137 milliseconds), and it was associated with significantly stronger behavioral reactions. Gradual increase of NWR amplitude was evident at increasing stimulation intensities and supported by the behavioral observations. CONCLUSIONS AND CLINICAL RELEVANCE: We documented NWRs evoked from the forelimb and hind limb and their recruitment with stimuli of increasing intensity in horses. These results provide a basis for use of NWRs in studies on nociceptive modulation in horses.

Abstract: Six ponies were used to investigate the effect of tolazoline antagonism of detomidine on physiological responses, behavior, epinephrine, norepinephrine, cortisol, glucose, and free fatty acids in awake ponies. Each pony had a catheter inserted into a jugular vein 1 hour before beginning the study. Awake ponies were administered detomidine (0.04 mg/kg intravenously [i.v.]) followed 20 minutes later by either tolazoline (4.0 mg/kg i.v.) or saline. Blood samples were drawn from the catheter 5 minutes before detomidine administration (baseline), 5 minutes after detomidine administration, 20 minutes before detomidine administration which was immediately before the administration of tolazoline or saline (time [T] = 0), and at 5, 30, and 60 minutes after injections of tolazoline or saline (T = 5, 30, and 60 minutes, respectively). Compared with heart rate at T = 0, tolazoline antagonism increased heart rate 45% at 5 minutes. There was no difference in heart rate between treatments at 30 minutes. Blood pressure remained stable after tolazoline, while it decreased over time after saline. Compared with concentrations at T = 0, tolazoline antagonism of detomidine in awake ponies resulted in a 55% increase in cortisol at 30 minutes and a 52% increase in glucose at 5 minutes. The change in free fatty acids was different for tolazoline and saline over time. Free fatty acids decreased after detomidine administration. Free fatty acids did not change after saline administration. After tolazoline administration, free fatty acids increased transiently. Tolazoline tended to decrease sedation and analgesia at 15 and 60 minutes postantagonism. Antagonism of detomidine-induced physiological and behavioral effects with tolazoline in awake ponies that were not experiencing pain appears to precipitate a stress response as measured by cortisol, glucose, and free fatty acids. If antagonism of an alpha-agonist is contemplated, the potential effect on hormones and metabolites should be considered.

Abstract: Studies were performed in the conscious pony instrumented with a Doppler flow probe and hydraulic occluder on the left anterior descending coronary artery (LAD), sonomicrometry crystals and intraventricular micromanometer in the left ventricle, and catheters in the left atrium and anterior interventricular vein. Two-minute LAD occlusions were performed every 30 min continuously or during working hours. Data on release of catabolites (potassium, hydrogen ions, and lactate) and norepinephrine from the initially dysfunctional region were obtained periodically during a regimen of 445 +/- 56 occlusions in six animals. Regional myocardial blood flow was measured (microsphere method) before and after an occlusion regimen in four animals. Marked release of catabolites and norepinephrine from the initially dysfunctional region was noted in association with early occlusions when myocardial segment function was severely reduced. With further occlusions, release of these substances decreased while segment function improved. Blood flow was markedly decreased in the initially dysfunctional region during an early occlusion but was at the control level during a later occlusion. Although the metabolic findings are consistent with protection due to “ischemic preconditioning” and no increase in collateral perfusion, the inverse relationship noted between catabolite release and segment function is best explained by flow-dependent mechanisms. These results, together with the myocardial blood flow data, serve to validate a previous assumption that protection against regional myocardial dysfunction under these conditions is due to increased collateral perfusion.