Evaluation of recurrent laryngeal neuropathy in domestic and feral horse populations in Australia using histologic and immunohistochemical analysis: A pilot study.

BACKGROUND: Little is known about potential differences in the left recurrent laryngeal nerve (Lrln) and left cricoarytenoideus dorsalis (LCAD) muscle between domestic and feral horse populations. If a difference exists, feral horses may provide a useful control population for research related to recurrent laryngeal neuropathy (RLN) and increase our understanding of potential population pressures influencing the incidence RLN. OBJECTIVES: The objective of this study was to compare the Lrln and LCAD of domestic and feral horses using histological and immunohistochemical techniques (IHC). METHODS: Sixteen horses, domestic (n = 8) and feral (n = 8), without clinical or ancillary examinations that were processed at an abattoir had the Lrln and LCAD muscle harvested immediately following death. Carcass weights were recorded. Subjective and morphometric histologic assessment were performed on Lrln sections. The LCAD was assessed for myosin heavy chain (fibre type proportion, diameter and grouping using IHC. RESULTS: Fibre-type grouping consistent with RLN was seen in both groups. Regenerating fibre clusters were more common in domestic compared to feral horses (p = 0.04). No other histologic differences occurred between groups. Muscle fibre typing demonstrated a lower mean percentage of type IIX fibres in the feral group compared to the domestic group (p = 0.03). There was no difference in type I or IIA proportions or mean diameter of any fibre type between the groups. CONCLUSIONS: The domestic population showed evidence of nerve regeneration suggesting RLN in this group, yet this was not supported by the higher proportion of type IIX muscle fibres compared to the feral population. Further evaluation to clarify the significance and wider occurrence of the differences is indicated.

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.