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The Veterinary clinics of North America. Equine practice1989; 5(2); 247-270; doi: 10.1016/s0749-0739(17)30587-4

The pathophysiology of intestinal damage: effects of luminal distention and ischemia.

Abstract: Intestinal edema, luminal distention, and ischemia are common pathologic processes involved in producing the intestinal damage found during surgical exploration for acute abdominal disorders in the horse. The severity of intestinal edema depends on the degree of altered intravascular forces and changes in capillary permeability. Capillary hydrostatic pressure rises as the less pliable venules and veins become occluded during intestinal obstruction. Concurrently, the production of various endogenous products that damage the vascular wall leads to increases in capillary permeability and protein exudation, causing fluid movement into the interstitium and consequent tissue edema. The information presently available indicates that luminal distention does not produce the morphologic damage observed during natural conditions. However, slight intestinal edema was observed with experimental distention of the equine small intestine. Although the effects of increased luminal pressure appear minor, in the overall scheme of intestine damage, many processes are occurring together, and the luminal distention may be additive in the production of intestinal damage. The intestinal damage occurring during natural obstructions is most likely related to both the severity of the ischemia and the subsequent reperfusion injury. Experimentally, an ischemic insult produces a consistent sequence of mucosal alterations to both the equine small and large intestine. Severity of ischemia may be the limiting factor in determining the clinical outcome in cases in which the ischemic insult is irreversible; however, if the intestinal tissue survives the ischemia, the reperfusion injury may substantially increase the damage, producing an irreversible injury. The proposed mechanisms responsible for the reperfusion injury include the presence of highly reactive cytotoxic oxygen radicals. The intestinal epithelium and vascular endothelium are both capable of producing these unstable compounds. Secondly, the influx and activation of neutrophils may also release oxygen radicals. During experimental ischemia, neutrophils gradually move to the affected area; however, during reperfusion their numbers dramatically increase and may play a significant role in producing intestinal damage. Therapy for intestinal damage involves first determining the viability of the affected intestine. All nonviable bowel should be resected and viable intestine anastomosed. The care and maintenance of intestine of questionable viability are presently based on therapy in humans and experimental information concerning the pathophysiologic mechanisms of intestinal ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
Publication Date: 1989-08-01 PubMed ID: 2670106DOI: 10.1016/s0749-0739(17)30587-4Google Scholar: Lookup
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Summary

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The research focuses on the effects of intestinal swelling, luminal distention, and inadequate blood supply on intestinal damage, particularly during surgery for acute abdominal disorders in horses. The study highlights that the severity of such damage depends on changes in intravascular forces and capillary permeability, along with the production of endogenous substances that harm blood vessels.

Understanding the Impacts on Intestinal Damage

  • The researchers explain that during acute abdominal disorders and surgical interventions in horses, intestinal damage is often a result of edema (swelling), luminal distention (stretching of the intestines), and ischemia (inadequate blood supply).
  • The severity of this intestinal edema depends on altered intravascular forces and changes in the permeability of the capillaries. For instance, capillary hydrostatic pressure increases as less flexible venules and veins become clogged during intestinal obstruction.
  • Alongside this phenomenon, various endogenous (originating within the organism) substances that damage the vascular wall are produced. This damage process intensifies capillary permeability and protein exudation, leading to fluid movement into the interstitial areas of the tissues and causing edema.

Role of Luminal Distention and Ischemia

  • Despite the common occurrence of luminal distention and ischemia, the study suggests that luminal distention does not greatly contribute to intestinal damage observed in natural conditions. Experimental distention in equine small intestines only resulted in slight intestinal edema.
  • However, the researchers postulate that while its impact may seem minor, luminal distention could be additive, exacerbating the overall damage to the intestine when combined with other processes.
  • The most impactful damage during natural obstructions is tied to the severity of ischemia (restricted blood supply) and the resulting reperfusion injury (tissue damage caused when blood supply returns after a period of ischemia).
  • Experimentally, an ischemic event creates a consistent sequence of mucosal alterations in both the small and large intestines of horses. The severity of ischemia could be the deciding factor in outcomes where the ischemic insult is irreversible.
  • If the intestinal tissue survives ischemia, the subsequent reperfusion injury could significantly escalate the damage, leading to irreversible injury.

Proposed Mechanisms and Therapy

  • Reperfusion injury is proposed to be caused by the generation of highly reactive, cytotoxic oxygen radicals. Both the intestinal epithelium and vascular endothelium can produce these unstable compounds.
  • Additionally, the migration and activation of neutrophils (a type of white blood cell) may also release these oxygen radicals, contributing to tissue damage.
  • For treatment, the study suggests first assessing the viability of the affected intestine. Any nonviable bowel should be removed, and viable intestine should be sewn together.
  • Care for intestines with questionable viability is currently based on human therapies as well as experimental information related to the pathophysiological mechanisms of intestinal ischemia.

Cite This Article

APA
Snyder JR. (1989). The pathophysiology of intestinal damage: effects of luminal distention and ischemia. Vet Clin North Am Equine Pract, 5(2), 247-270. https://doi.org/10.1016/s0749-0739(17)30587-4

Publication

ISSN: 0749-0739
NlmUniqueID: 8511904
Country: United States
Language: English
Volume: 5
Issue: 2
Pages: 247-270

Researcher Affiliations

Snyder, J R
  • Department of Surgery, University of California, Davis School of Veterinary Medicine.

MeSH Terms

  • Animals
  • Colic / physiopathology
  • Colic / veterinary
  • Edema / physiopathology
  • Edema / veterinary
  • Horse Diseases / physiopathology
  • Horses
  • Intestinal Diseases / physiopathology
  • Intestinal Diseases / veterinary
  • Intestinal Obstruction / physiopathology
  • Intestinal Obstruction / veterinary
  • Intestines / blood supply
  • Intestines / physiopathology
  • Ischemia / physiopathology
  • Ischemia / veterinary

Citations

This article has been cited 6 times.
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    doi: 10.1007/s11259-007-3450-5pubmed: 17225087google scholar: lookup
  6. Delesalle C, Deprez P, Schuurkes JA, Lefebvre RA. Contractile effects of 5-hydroxytryptamine and 5-carboxamidotryptamine in the equine jejunum.. Br J Pharmacol 2006 Jan;147(1):23-35.
    doi: 10.1038/sj.bjp.0706431pubmed: 16230998google scholar: lookup