Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From all mammals investigated so far only in rabbits diamine oxidase could not be detected in any tissue except the gut. Thus this species was chosen for studying the physiological and pathophysiological function of this enzyme in the gastrointestinal tract. By gel filtration on Sephadex G 50 and G 200 the enzyme was purified 100-fold, separated from a soluble monoamine oxidase, and the properties of the two enzymes were determined. Diamine oxidase from rabbit small intestine deaminated putrecine (Km = 1.3 times 10(-4) M, pH-optimum 6.4-6.9) and histamine (Km = 8 times 10(-5) M, pH-optimum 7.5), but not serotonin, and was inhibited by aminoguanidine, but not by pargyline. Soluble monoamine oxidase from rabbit small intestine catabolized serotonin (Km = 1.8 times 10(-4) M, pH-optimum 8.8) but not putrescine and histamine, and was inhibited by pargyline, but not by aminoguanidine. Based on its properties in vitro intestinal diamine oxidase could inactivate the vasoactive biogenic amine histamine in vivo. To confirm this hypothesis, in rabbits the small intestine was damaged severely by inducing total intestinal ischemia, which occurs as mesenteric infarction also in human subjects and is accompanied by histamine release. Treatment with aminoguanidine and ischemia killed the animals 3-times faster than ischemia alone, which supported our hypothesis on a protective role of intestinal diamine oxidase against histamine.
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PMID:Diamine oxydase in rabbit small intestine: separations from a soluble monoamine oxidase, properties and pathophysiological significance in intestinal ischemia. 0 54

Geriatric patients are preferentially involved in ischemic bowel disease. The sudden occlusion of the large mesenteric arteries (a. mesenterica superior (more frequently) and inferior) is followed by intestinal gangrene and peritonitis with a poor prognosis and a high letality (greater than 90%). In chronic intestinal ischemia the leading clinical symptom is postprandial pain ('claudicatio intestinalis'). In some cases of acute mesenteric artery occlusion no embolus or thrombus will be found. In these cases the circulation in the arteriosclerotic vessels falls below a critical value due to cardiac insufficiency, shock, digitalis overdose and others. In less severe ischemia the mucosa is involved being most sensitive to O2 deprivation. It usually regenerates within a few days. This form is found more frequently in the colon than in other parts of the gut (about 40%): ischemic colitis. The therapy - if possible in acute, fulminant ischemia or if necessary in chronic intestinal ischemia - is surgical consisting in reconstructive procedures of the mesenteric circulation.
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PMID:[Ischemic bowel disease (author's transl)]. 1 31

We compared the effectiveness of three pharmacologically and chemically dissimilar vasodilators (histamine, glucagon, and perhexiline) in reversing the hemodynamic and metabolic deficits of intestinal ischemia produced by hemorrhage. With intraarterial infusion into the superior mesenteric artery of anesthetized control dogs, all three agents increased mesenteric blood flow and oxygen consumption without altering systemic arterial blood pressure. Similarly, in the ischemic gut following moderate hemorrhage all three vasodilators increased mesenteric flow and oxygen consumption while reducing vascular resistance and not affecting systemic arterial blood pressure. On a molar basis glucagon was the most potent dilator drug. In severely hemorrhaged dogs whose intestinal blood flow had been reduced nearly 80%, glucagon restored oxygen uptake and vascular resistance to control levels. These findings demonstrate the efficacy of three different vasodilators in reversing the mesenteric ischemia and hypoxia produced by hemorrhage.
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PMID:Effects of vasodilators on mesenteric ischemia and hypoxia induced by hemorrhage. 49 29

Starch microspheres, degradable by endogenous blood amylase were selectively injected into the femoral and superior mesenteric arteries, respectively, to obtain temporary local ischemia in foot and gut of the rat. The experimental models are described. Studies with tracer microspheres demonstrated, that the blood flow in the foot and the small intestine immediately declined to near zero, but latter resumed control levels.
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PMID:Transient blood flow reduction induced by intra-arterial injection of degradable starch microspheres. Experiments on rats. 73 62

Previous studies have been shown that intravenous cardiac glycosides produce mesenteric vasoconstriction (MVC). The possibility that this might critically compromise blood flow in patients with mesenteric vascular disease was suggested. To evaluate whether MVC occurs with intravenous cardiac glycosides in the presence of proximal mesenteric artery stenosis, blood flow in the superior mesenteric artery (SMA) of thirteen dogs was measured with a Doppler flowmeter. The SMA was constricted and pressures were measured in the aorta, SMA, and superior mesenteric vein. Superior mesenteric vascular resistance (SMVR) was calculated by dividing the pressure difference between the SMA and superior mesenteric vein by the total blood flow to the superior mesenteric vasculature and was reported as mm Hg/cc-min. Blood flow was measured simultaneously by a drop rate meter in the vein of a surgically isolated intestinal segment supplied by a single arterial arcade. Venous outflow pressure from this segment was also monitored, which allowed calculation of isolated gut segment resistance (IGSR) in mm Hg/cc-min per 100 g gut. Stenosis of the SMA produced pressure gradients of 10 to 75 mm Hg and decreased resting blood flow by as much as 82%. Digoxin produced an increase in both SMVR and IGSR throughout the 30 to 120 minute period of the study in thirteen dogs despite the presence of severe grades of SMA stenosis. There was no relationship between the degree of proximal SMA stenosis and the magnitude of resistance change due to digoxin. To determine if this MVC was reversible, glucagon was administered to eleven dogs 30 to 60 minutes after digoxin and completely overcame the constriction. Thus, digoxin produced MVC in the presence of proximal SMA stenosis. This MVC was pharmacologically reversible. These data suggest that intravenous digoxin might contribute to intestinal ischemia in patients with preexisting vascular disease.
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PMID:Digoxin induced intestinal vasoconstriction. The effects of proximal arterial stenosis and glucagon administration. 80 76

The major regulatory factors in the mesenteric circulation include general hemodynamic forces, the autonomic nervous system, circulating vasoactive substances, tissue metabolites and intrinsic characteristics of vascular smooth muscle. During mesenteric ischemic states smooth muscle spasm elevates resistance to blood flow and aggravates intestinal tissue hypoxia leading to mucosal necrosis. Close intraarterial infusion of potent vasodilator drugs holds the promise of reversing intestinal ischemia and preserving viability of the gut.
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PMID:Control of the splanchnic circulation. 88 58

Under the aspect of systemic diseases and their manifestation in the gut the following conclusions can be drawn: 1. The skin is the mirror of the intestinal tract; not only in primary gastroenterological disorders one should look for dermatological complications, but should also think in chronic skin lesions of concomitant intestinal alterations. 2. In all patients with collagen diseases a gastrointestinal involvement is very common. 3. In all endocrine disorders except in hypothyroidism diarrhea is a very common finding. 4. Infiltrations of gastrointestinal tract can be demonstrated in many cases by gastric, small bowel or rectal biopsy. 5. In all forms of dysgammaglobulinemia giardiasis is very common. 6. In right heart failure protein-losing enteropathy should be considered, in left ventricular insufficiency bowel ischemia.
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PMID:[Manifestations of systemic diseases in the gastrointestinal tract]. 96 97

Pneumatosis intestinalis in association with connective tissue diseases is an unusual combination whose pathogenesis is not yet understood. Furthermore, steroid medication, often used to treat these diseases, may itself cause pneumatosis. Three cases of scleroderma, systemic lupus erythematosus, and amyloidosis in association with pneumatosis and without prior steroid therapy are presented. The small vessel occlusive pathologic processes in these diseases may cause focal areas of mucosal ischemia resulting in small, perhaps transient ulcerations that allow gas to enter the gut wall from the lumen.
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PMID:Pneumatosis intestinalis in association with connective tissue disease. 101 66

A patient with primary amyloidosis and the nephrotic syndrome had diarrhea and gastrointestinal bleeding probably due to intestinal ischemia. He died with extensive intestinal infarction. The infarction was most likely caused by decreased splanchnic perfusion secondary to the chronic hypotension of the nephrotic syndrome and to amyloid deposition within the walls of the small blood vessels supplying the gut. Although amyloidosis was suspected prior to death, a fixation artifact probably prevented the correct antemortem biopsy diagnosis.
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PMID:Persistent hypotension and intestinal infarction in a patient with primary amyloidosis. 113 38

A comparison study of several vasoconstrictor and vasodilator agents was conducted measuring changes in intestinal blood flow and oxygen consumption during 10-min periods of intra-arterial infusion. Blood flow was measured in a branch of the superior mesenteric artery of anesthetized dogs with an electromagnetic blood flow meter, and the arteriovenous oxygen content difference across the gut segment was determined photometrically. Vasopressin (4 x 10(-3) and 7x 10(-4) U/kg-min) diminished blood flow 60 and 28% and reduced oxygen consumption 54 and 22%, respectively (all P less than 0.001). In a dose which did not lower blood flow, vasopressin still caused a decline in oxygen consumption (P less than 0.01). Epinephrine (5 x 10(-2) mug/kg-min) decreased blood flow 19% (P less than 0.001) but did not reduce oxygen consumption. After beta-adrenergic blockade, however, the same dose of epinephrine decreased blood flow 41% and oxygen consumption 33% (both P less than 0.001). Responses to angiotension II, calcium chloride, and prostaglandin F2alpha resembled effects of vasopressin rather than those of epinephrine, namely decreased blood flow and decreased oxygen consumption. The vasodilator agents, prostaglandin E1, is isoproterenol, and histamine, increased (P less than 0.001) both blood flow (130, 80, and 98%, respectively) and oxygen consumption (98, 64, and 70%, respectively). Vasopressin, angiotensin II, calcium chloride, and prostaglandin F2alpha appear to contract arteriolar and precapillary sphincteric smooth muscle indiscriminately to evoke both intestinal ischemia and hypoxia. Epinephrine is the exceptional constrictor in this case, producing diminished blood flow without a reduction in oxygen uptake.
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PMID:Effect of vasoactive agents on intestinal oxygen consumption and blood flow in dogs. 115 Aug 81


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