Morphologic and ultrastructural evaluation of effect of ischemia and dimethyl sulfoxide on equine jejunum

Warwick A. Arden From the Departments of Large Animal Clinical Sciences (Arden, Stick, Parks) and Pathology (Slocombe), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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 BVSc, MS
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Ronald F. Slocombe From the Departments of Large Animal Clinical Sciences (Arden, Stick, Parks) and Pathology (Slocombe), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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 BVSc, PhD
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John A. Stick From the Departments of Large Animal Clinical Sciences (Arden, Stick, Parks) and Pathology (Slocombe), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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Andrew H. Parks From the Departments of Large Animal Clinical Sciences (Arden, Stick, Parks) and Pathology (Slocombe), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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 Vet MB, MS

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SUMMARY

Morphologic changes in equine jejunal segments subjected to 1 hour of ischemia and 1 hour of reperfusion, and protective effects of systemic administration of dimethyl sulfoxide (dmso; 1 g/kg of body weight) were investigated in 18 ponies, using light microscopy and scanning and transmission electron microscopy. Ponies were allotted to 4 groups: group 1—control (n = 3); group 2—dmso (n = 3); group 3—ischemia (n = 6); and group 4—ischemia and dmso (n = 6). In each pony, 2 jejunal sections were evaluated. The first section was obtained prior to induction of ischemia, and the second was obtained 2 hours later after reperfusion. Mucosal lesions were graded from 0 (normal) to 5 (most severe).

Combined ischemia and reperfusion of 2 hours’ duration induced moderately severe mucosal injury to the equine jejunum (group 3; grade 1.5 to 2.5), characterized principally by disruption of enterocyte attachment from the basement membrane and lamina propria. Fluid accumulation disrupted enterocyte cell-to-cell adhesion toward cell bases, while apical tight junctions and desmosomal junctions toward the luminal surface remained intact. Intracytoplasmic organellar changes within enterocytes were not a prominent feature of the injury. The aforementioned processes were marked at the villus tip and progressed down the villus sides. These findings support the importance of mechanisms leading to early sub-epithelial fluid accumulation rather than that of direct severe enterocyte injury. Further, fluid accumulation does not appear to arise from intercellular migration from the luminal surface. In this model, a pathomechanical effect caused by vigorous villus retraction appears to exacerbate epithelial lifting toward the villus tip. Systemic administration of dmso (1 g/kg) prior to reperfusion failed to improve the appearance of the mucosa (group 4; grade 1.5 to 4.0), suggesting that it was ineffective in preventing this form of ischemia-reperfusion injury.

SUMMARY

Morphologic changes in equine jejunal segments subjected to 1 hour of ischemia and 1 hour of reperfusion, and protective effects of systemic administration of dimethyl sulfoxide (dmso; 1 g/kg of body weight) were investigated in 18 ponies, using light microscopy and scanning and transmission electron microscopy. Ponies were allotted to 4 groups: group 1—control (n = 3); group 2—dmso (n = 3); group 3—ischemia (n = 6); and group 4—ischemia and dmso (n = 6). In each pony, 2 jejunal sections were evaluated. The first section was obtained prior to induction of ischemia, and the second was obtained 2 hours later after reperfusion. Mucosal lesions were graded from 0 (normal) to 5 (most severe).

Combined ischemia and reperfusion of 2 hours’ duration induced moderately severe mucosal injury to the equine jejunum (group 3; grade 1.5 to 2.5), characterized principally by disruption of enterocyte attachment from the basement membrane and lamina propria. Fluid accumulation disrupted enterocyte cell-to-cell adhesion toward cell bases, while apical tight junctions and desmosomal junctions toward the luminal surface remained intact. Intracytoplasmic organellar changes within enterocytes were not a prominent feature of the injury. The aforementioned processes were marked at the villus tip and progressed down the villus sides. These findings support the importance of mechanisms leading to early sub-epithelial fluid accumulation rather than that of direct severe enterocyte injury. Further, fluid accumulation does not appear to arise from intercellular migration from the luminal surface. In this model, a pathomechanical effect caused by vigorous villus retraction appears to exacerbate epithelial lifting toward the villus tip. Systemic administration of dmso (1 g/kg) prior to reperfusion failed to improve the appearance of the mucosa (group 4; grade 1.5 to 4.0), suggesting that it was ineffective in preventing this form of ischemia-reperfusion injury.

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