Abstract
Four experimental groups of equines were used in order to study morphological abnormalities and apoptosis in lamellar tissue. Group Cg (control) was composed of animals without any surgical procedure; group Ig (instrumented), animals that underwent enterotomy; group Tg (treated), animals that were subjected to intestinal obstruction and were treated with hydrocortisone; and group Ug (untreated), animals that were subjected to intestinal obstruction without treatment. The lamellar tissue was analyzed regarding the presence of tissue abnormalities and apoptosis. No morphological abnormalities were observed in animals of surgical groups, and no difference in apoptosis was observed between groups. It was concluded that intestinal obstruction allowed laminitis to develop, probably by systemic activation, and that the maneuvers performed in the enterotomy aggravated the process. Hydrocortisone did not aggravate the lesions of the lamellar tissue
Highlights
Laminitis occurs secondarily to other diseases, such as those of the gastrointestinal tract that follow a course involving sepsis (Dabareiner et al, 1998; Eades et al, 2002)
The morphological abnormalities that were observed using optical microscopy consisted of spherical nuclei of basal cells, thinning of the secondary epidermal lamina, undulation of the primary epidermal lamina, and irregular outline of the basal membrane, for staining with periodic acid-Shiff (PAS), among the animals in the Ig, to surgical procedures (Tg), and Ug groups (Figure 1)
The difference in the severity of the abnormalities observed between the obstructed groups (Tg and Ug) and control group (Cg) indicates that the damage caused by intestinal ischemia can give rise to a predisposition towards laminitis
Summary
Laminitis occurs secondarily to other diseases, such as those of the gastrointestinal tract that follow a course involving sepsis (Dabareiner et al, 1998; Eades et al, 2002). There is evidence that apoptosis is involved in lamellar lesions. The apoptosis occur due to activation of caspases in cell cytosol, causing cell death that differs from necrosis, without inducing an evident inflammatory response (Hathaway and Kuechle, 2002; Creagh et al, 2003). Since laminitis is associated with systemic inflammation, administration of anti-inflammatory agents can prevent it from appearing for reducing the systemic inflammatory response (Campbell et al, 2007). This approach is questionable when it is observed that laminitis has developed after glucocorticoids administration (Pollitt, 1999; Johnson et al, 2002)
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