Jablonska, E. M., Ziolkowska, S. M., Gill, J., Szykula, R., & Faff, J. (1991). Changes in some haematological and metabolic indices in young horses during the first year of jump-training. Equine Vet J, 23(4), 309–311.
Abstract: Effects of an 18 min exercise test, on three separate occasions during a one year jump-training programme, was studied in seven horses. Determinations were carried out on venous blood for packed cell volume, haemoglobin, total protein, lactate and pyruvate, glucose, free fatty acids, insulin, glucagon, blood gases, bicarbonate, pH, aldolase, aspartate aminotransferase and alanine amino-transferase. Exercise caused a slight increase in lactate and pyruvate, total protein, aldolase, alanine aminotransferase, pO2, bicarbonate and pH. Glucose, free fatty acids and pCO2 levels decreased. Training caused no significant difference in these changes. However, during the year, increases in lactate and decreases in pH (resting levels) were observed.
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Tavernor, W. D., & Lees, P. (1968). A pharmacological investigation of the influence of suxamethonium on cardiac function in the horse. Experientia, 24(6), 582–583.
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Kraus-Hansen, A. E., Fackelman, G. E., Becker, C., Williams, R. M., & Pipers, F. S. (1992). Preliminary studies on the vascular anatomy of the equine superficial digital flexor tendon. Equine Vet J, 24(1), 46–51.
Abstract: The vascular and microvascular anatomy of normal equine superficial digital flexor tendons was studied by dissection of vinyl-perfused specimens and by microangiography on high detail film. The presence of an extensive intratendinous vascular latticework was confirmed, and a 'nutrient artery' described closely associated with the accessory ligament of the superficial digital flexor tendon (proximal check ligament). Circumferential stripping of the paratenon from the tendon to eliminate afferent vessels was performed bilaterally in three horses and unilaterally in a fourth, followed by a treadmill training regimen. No resulting intratendinous lesions could be documented on gross post mortem and histological examination at three, 10, or 35 days post operatively. There was mild paratendinous proliferation in all instances. In one horse, four intratendinous ligatures were placed within the medial and lateral borders of the contralateral tendon to isolate further from its blood supply a 10 cm segment. Gross lesions at 35 days post operatively included a marked paratendinous response involving the entire 10 cm segment, and a darkened, soft focus within the core of the tendon. Histopathology and electron microscopy demonstrated focal degeneration. It was concluded that the blood supply of the normal equine superficial digital flexor tendon is primarily intratendinous, rather than paratendinous as previously thought. The lesions in one horse similar to those in naturally occurring tendinitis supported a vascular aetiology of the disease, and set the groundwork for studies aimed at the development of a clinically relevant tendinitis model.
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Mellor, P. S. (1993). African horse sickness: transmission and epidemiology. Vet Res, 24(2), 199–212.
Abstract: African horse sickness (AHS) virus causes a non-contagious, infectious, arthropod-borne disease of equines and occasionally of dogs. The virus is widely distributed across sub-Saharan African where it is transmitted between susceptible vertebrate hosts by the vectors. These are usually considered to be species of Culicoides biting midges but mosquitoes and/or ticks may also be involved to a greater or lesser extent. Periodically the virus makes excursions beyond its sub-Saharan enzootic zones but until recently does not appear to have been able to maintain itself outside these areas for more than 2-3 consecutive years at most. This is probably due to a number of factors including the apparent absence of a long term vertebrate reservoir, the prevalence and seasonal incidence of the vectors and the efficiency of control measures (vaccination and vector abatement). The recent AHS epizootics in Iberia and N Africa spanning as they do, 5 or more yr, seem to have established a new pattern in AHS virus persistence. This is probably linked to the continuous presence of adult C imicola in the area. Culicoides imicola is basically an Afro-Asiatic insect and prefers warm climates. Therefore its continuous adult presence in parts of Iberia and N Africa may be due to some recent moderations of the climate in these areas.
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Munoz-Sanz, A. (2006). [Christopher Columbus flu. A hypothesis for an ecological catastrophe]. Enferm Infecc Microbiol Clin, 24(5), 326–334.
Abstract: When Christopher Columbus and his men embarked on the second Colombian expedition to the New World (1493), the crew suffered from fever, respiratory symptoms and malaise. It is generally accepted that the disease was influenza. Pigs, horses and hens acquired in Gomera (Canary Islands) traveled in the same ship. The pigs may well have been the origin of the flu and the intermediary hosts for genetic recombination of other viral subtypes. The Caribbean archipelago had a large population of birds, the natural reservoir of the avian influenza virus. In this ecological scenario there was a concurrence of several biological elements that had never before coexisted in the New World: pigs, horses, the influenza virus and humans. We propose that birds are likely to have played an important role in the epidemiology of the flu occurring on the second Colombian trip, which caused a fatal demographic catastrophe, with an estimated mortality of 90% among the natives.
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Jordan, J. (1970). [Modern views on the structure and function of the vomeronasal (Jacobson's) organ in mammals]. Otolaryngol Pol, 24(4), 457–462.
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Ishida, N., Hirano, T., & Mukoyama, H. (1994). Detection of aberrant alleles in the D-loop region of equine mitochondrial DNA by single-strand conformation polymorphism (SSCP) analysis. Anim Genet, 25(4), 287.
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Breen, M., Downs, P., Irvin, Z., & Bell, K. (1994). Intrageneric amplification of horse microsatellite markers with emphasis on the Przewalski's horse (E. przewalskii). Anim Genet, 25(6), 401–405.
Abstract: Primer sequences flanking 13 microsatellite loci isolated from the domestic horse (E. caballus) were successfully used to amplify homologous loci in the Przewalski's horse (E. przewalskii). The results demonstrate that the level of polymorphism at all 13 loci in the Przewalski's horse was comparable to that in the domestic horse and the overall exclusion probability in the Przewalski's horse was calculated to be 0.9994. The results suggest that it should be possible to use E. caballus-derived microsatellite markers to provide parentage verification and additional valuable information to the captive management of E. przewalskii. The ability to amplify corresponding loci in the remaining five species of the genus was also confirmed, illustrating the general application of markers isolated from the domestic horse to the evaluation of polymorphism in the other six species of the genus.
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Venter, G. J., Koekemoer, J. J. O., & Paweska, J. T. (2006). Investigations on outbreaks of African horse sickness in the surveillance zone in South Africa. Rev Sci Tech, 25(3), 1097–1109.
Abstract: Confirmed outbreaks of African horse sickness (AHS) occurred in the surveillance zone of the Western Cape in 1999 and 2004, both of which led to a two-year suspension on the export of horses. Light trap surveys in the outbreak areas showed that known vector competent Culicoides species, notably C. imicola, were abundant and present in numbers equal to those in the traditional AHS endemic areas. Isolations of AHS virus serotypes 1 and 7, equine encephalosis virus, and bluetongue virus from field-collected C. imicola in the surveillance zone demonstrated that this species was highly competent and could transmit viruses belonging to different serogroups of the Orbivirus genus. Molecular identification of recovered virus isolates indicated that at least two incursions of AHS into the surveillance zone had taken place in 2004. The designation of an AHS-free zone in the Western Cape remains controversial since it can be easily compromised, as evidenced by the two recent outbreaks. In light of the results reported in the present study, the policy of maintaining a large population of unvaccinated horses in the surveillance zone should be reconsidered, as it leaves them vulnerable to infection with AHS virus, which is the most pathogenic of all equine viruses.
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Carroll, G. L., Matthews, N. S., Hartsfield, S. M., Slater, M. R., Champney, T. H., & Erickson, S. W. (1997). The effect of detomidine and its antagonism with tolazoline on stress-related hormones, metabolites, physiologic responses, and behavior in awake ponies. Vet Surg, 26(1), 69–77.
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.
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