Superior Mesenteric Artery Embolus

Ra, McCready; Lh, Hollier; Pc, Pairolero; Ta, Orszulak

doi:10.1097/00007611-198406000-00037

Cited by 5 publications

(1 citation statement)

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“…The mortality of acute mesenteric ischemia in adults has been reported at 60-80 % (Debus et al 2011), primarily because of the difficulty of making an early diagnosis before bowel infarction occurs. Surgical intervention (e.g., embolectomy, intestinal resection) (McCready et al 1984) and local intra-arterial infusion of vasodilators (e.g., papaverine) (Boley et al 1981) are used to treat acute mesenteric ischemia, but the mortality of this disease continues to be significant. Experimental nonocclusive mesenteric ischemia in dogs has been treated successfully with intravenously administered vasodilators that are selective for the mesenteric circulation (e.g., urotensin I, sauvagine, and corticotropin-releasing factor) (MacCannell et al 1986), thereby potentially obviating the risk of an indwelling angiographic catheter, but the potential therapeutic effectiveness of these drugs in humans remains unclear.…”

Section: Consequences Of Intestinal Ischemia and Reperfusionmentioning

confidence: 99%

Intestinal Ischemia and Reperfusion: Consequences and Mechanisms

Granger¹,

Seifert²,

Senchenkova³

2014

PanVascular Medicine

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Ischemia and reperfusion of the ischemic intestine can result in significant tissue injury that is manifested as vascular dysfunction and mucosal barrier failure. The injury response to ischemia per se can be attributed to hypoxia and the cellular alterations brought about by this condition. Several protective mechanisms, including intramural and extramural collaterals, arteriolar dilation, and capillary recruitment, exist to minimize the reduction in tissue oxygen tension that accompanies partial occlusion of the arterial supply to the intestine. Reperfusion of the ischemic intestine is accompanied by a more profound injury response that has been linked to the generation of reactive oxygen species that are derived from the enzyme xanthine oxidase. The accumulation of these reactive species at the time of reperfusion, coupled with the inactivation of nitric oxide, creates an inflammatory phenotype within the vasculature and mucosal membrane. The resulting recruitment of leukocytes and platelets and the activation of resident inflammatory cells that normally reside in the perivascular space (mast cells, macrophages) lead to further oxidative stress and a more intense inflammatory condition, ultimately resulting in capillary and mucosal membrane failure and organ dysfunction.

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Section: Consequences Of Intestinal Ischemia and Reperfusionmentioning

confidence: 99%