People are admitted to the hospital for resuscitation with intravenous fluids, careful monitoring of laboratory tests, and optimization of their cardiovascular function. NG tube decompression and heparin anticoagulation may also be used to limit stress on the bowel and optimize perfusion, respectively.Surgical revascularisation remains the treatment of choice for intestinal  ischaemia related to an occlusion of the vessels supplying the bowel, but thrombolytic medical treatment and vascular interventional  radiological techniques have a growing role.If the ischemia has progressed to the point that the affected intestinal segments are gangrenous, a bowel resection of those segments is called for. Often, obviously dead segments are removed at the first operation, and a second-look operation is planned to assess segments that are borderline that may be savable after revascularization. Methods for revascularization
Open surgical thrombectomy
Intestinal bypass
Trans-femoral antegrade intestinal angioplasty and stenting
Open retrograde intestinal angioplasty stenting
Trans-catheter thrombolysis

Prognosis
The prognosis depends on prompt diagnosis (less than 12–24 hours and before gangrene) and the underlying cause:
venous thrombosis: 32% mortality
arterial embolism: 54% mortality
arterial thrombosis: 77% mortality
non-occlusive ischemia: 73% mortality.In the case of prompt diagnosis and therapy, acute intestinal ischemia can be reversible. History
Acute intestinal ischemia was first described in 1895 while chronic disease was first described in the 1940s. Chronic disease was initially known as angina abdominis. Terminology
The related term mesenteric ischemia generally defined as ischemia of the small bowel specifically. It has also been defined as poor circulation in the vessels supplying blood flow to any or several of the mesenteric organs, including the stomach, liver, colon and intestine.
Pharmacology
Systemic absorption of the globular tetradecapeptide is minimal.Linaclotide, like the endogenous guanylin and uroguanylin it mimics, is an agonist that activates the cell surface receptor of guanylate cyclase 2C (GC-C). The medication binds to the surface of the intestinal epithelial cells. Linaclotide is minimally absorbed and it is undetectable in the systemic circulation at therapeutic doses. Activation of GC-C increases cyclic guanosine monophosphate (cGMP). Elevated cGMP stimulates secretion of chloride and bicarbonate and water into the intestinal lumen, mainly by way of cystic fibrosis transmembrane conductance regulator (CFTR) ion channel activation. This results in increased intestinal fluid and accelerated transit. By elevating cGMP, linaclotide is also considered to reduce activation of colonic sensory neurons, reducing pain; and activates colonic motor neurons, which increases smooth muscle contraction and thus promotes bowel movements. Chemistry
Linaclotide is a hybrid peptide design of the E.coli heat-stable enterotoxin (STa) and the endogenous peptide hormones endogenous guanylin and uroguanylin.