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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to assess the extent of collateral blood flow provided by the celiac and inferior mesenteric arteries to the intestines during total occlusion of the superior mesenteric artery (SMA). In anesthetized cats, blood flow to the pancreas, duodenum, jejunum, ileum, and colon was measured with radioactive micropheres (15 microns in diameter) before and during occlusion of the SMA. Superior mesenteric artery occlusion significantly decreased (by 63%) blood flow to the head of the pancreas. Flow to the neck and tail of the pancreas was not altered. Blood flow to the proximal and distal duodenum was significantly reduced by 35% and 61%, respectively. Along the entire jejunum and ileum, SMA occlusion markedly decreased blood flow by an average of 71%. In the proximal colon, blood flow decreased by 63%, whereas flow to the middle and distal colon was not affected by SMA occlusion. Reduction in total wall blood flow to the small and large intestines was largely due to a marked reduction in mucosa/submucosa blood flow; muscularis/serosa flow was not affected. The results of this study suggest that total occlusion of the SMA does not compromise blood flow to the neck and tail of the pancreas and middle and distal colon (tissues that are normally perfused with blood from either the celiac or inferior mesenteric arteries). Perfusion through collaterals maintains flow to the head of the pancreas and gut (from duodenum to proximal colon) to within 30%-65% of control (preocclusion) flow. An important new observation of this study is that collateral blood vessels are much more effective in preventing ischemia in the muscularis/serosa than in the mucosa/submucosa after SMA occlusion.
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PMID:Importance of collateral circulation in the vascularly occluded feline intestine. 355 16

Only 50% of rabbits survive 90 min hepatic ischemia in spite of decompression of the gut. The remainder die within 36 h after operation. A single application of fibronectin before hepatic ischemia delays death for only a few hours. However, three postischemic applications of fibronectin--immediately after operation and 5 h and 24 h later--are associated with a statistically significant rise in the survival rate. Analysis of the transaminases indicates that fibronectin obviously limits the extent of ischemic liver cell necrosis. Of major significance is the fact that fibronectin supplement enables the RES of the liver to improve its phagocytic capacity, as shown by the RES clearance test. The presented experimental model shows that the liver with its RES, located between the splanchnic and the systemic circulation, is of particular significance for the entire organism. Hepatic ischemia or shock, independent of the initial cause, leads to significant reduction of hepatic phagocytosis. The results indicate that substitution of opsonins supports the phagocytic capacity.
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PMID:Protective effect of fibronectin in temporary liver ischemia: an experimental study. 356 Jul 82

Heat stress causes a marked reduction in splanchnic blood flow in order to compensate for the increased flow to the skin. Splanchnic ischemia causes a leakage of endotoxins from the gut lumen into the portal circulation and, especially in the presence of a compromised reticuloendothelial system, may cause severe systemic endotoxemia. Since many of the pathological features of heat stroke are similar to the shock state produced by LPS, we examined whether heat-stress causes endotoxemia. Five anesthetized monkeys were subjected to an environmental temperature of 41 degrees +/- 0.3 degrees C and relative humidity of 100%, until death. Rectal temperatures were recorded continuously, blood pressure and ECG were recorded at 5-min intervals, and arterial blood samples were taken at 15-30 min intervals. A decline in mean arterial pressure and rapid rise in heart rate occurred at about 42 degrees C. Plasma LPS remained at 0.071 +/- 0.006 ng.ml-1 until a rectal temperature of +/- 42 degrees C. Thereafter, it increased slowly until beyond 43 degrees C when it rose rapidly to 0.347 +/- 0.024 prior to death. Endotoxemia may have been a contributing factor in the pathogenesis of heat stroke. If so, then the use of anti-LPS antibodies may be expected to be beneficial.
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PMID:Time course of endotoxemia and cardiovascular changes in heat-stressed primates. 368 71

This study was undertaken to evaluate the relative contribution of ischemia, bacteria, and luminal substrate, the pathogenetic components of necrotizing enterocolitis (NEC), to the development of intestinal necrosis. Sprague-Dawley rats, either germ-free (No. = 25) or conventionally colonized (No. = 20) underwent laparotomy. Isolated ileal segments were created, two per rat. Ischemia was produced in one segment by application of a microaneurysm clip; the other segment served as a control. Segments were injected with 1 mL of either normal saline, dilute Similac formula, or standard formula. Groups were as follows: Group I (germ-free), received saline; Group II (germ-free), dilute formula; Group III (germ-free), standard formula; Group IV (conventional), saline; Group V (conventional), dilute formula; Group VI (conventional), standard formula. At 48 hours, the rats were evaluated for survival, gross bowel integrity, histologic severity of necrosis (graded 0 to 4+), and bacteriology. Gross analysis of bowel integrity showed no lesions in the ischemic segments of the germ-free rats (Groups I, II, and III) and necrosis in 75% of conventionally colonized animals (Groups IV, V, and VI; P less than 0.001). Microscopic necrosis was more common (P less than 0.001) in ischemic segments of conventional rats than in ischemic segments of germ-free rats. There was no difference in necrosis attributable to ischemic time or to the presence of either standard or dilute formula. Of the three pathogenetic factors evaluated, the presence of bacteria was most crucial to the development of bowel necrosis in this model. Improved treatment and prevention of NEC may depend upon suppression and/or modification of the gut flora.
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PMID:Comparative effects of ischemia, bacteria, and substrate on the pathogenesis of intestinal necrosis. 372 7

Ischemia of the intestines damages the permeability of the intestinal wall, allowing lipopolysaccharide (LPS) (endotoxin) to leak from the gut lumen into the blood circulation, causing shock and death. We measured LPS levels associated with corticosteroid treatment vs. no treatment in cats whose superior mesenteric artery had been occluded for 60 min. In untreated cats, the preocclusion mean plasma LPS concentration remained stable at 0.069 +/- 0.015 ng/ml. Toward the end of the occlusion period, mean plasma LPS rose to 0.239 +/- 0.032 ng/ml (p less than .01). Release of the clamp and reperfusion with oxygenated blood was followed within 20 min by a large rise in plasma LPS concentration to 0.825 +/- 0.11 ng/ml (p less than .01), which had returned to preocclusion levels about 80 min later. Methylprednisolone (30 mg/kg) was infused into a second group of cats 1.5 h before SMA occlusion. In these cats there was a complete inhibition of the LPS rise both during and after occlusion. These data suggest that the reported beneficial effect of corticosteroids in the treatment of septic shock may be mediated, in part, by reducing LPS leakage from the gut.
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PMID:Effect of corticosteroid prophylaxis on lipopolysaccharide levels associated with intestinal ischemia in cats. 375 30

A rat model representing segmental intestinal ischemia was used to study the absorption and transport of endotoxin from the ischemic gut. Serial quantitative analyses were made on peritoneal fluid, thoracic duct lymph and arterial and portal vein blood. Significantly increased endotoxin concentrations were found in thoracic duct lymph before transmural leakage took place. After leaking through the devitalized intestinal wall, endotoxin was transported by both lymphatic and portal routes. Kinetic analysis revealed that systemic endotoxemia paralleled the appearance of endotoxins in thoracic duct lymph, preceding a significant increase in the portal vein. The amount transported by the portal vein never exceeded the proposed endotoxin-filtrating capacity of the liver. In intestinal ischemia, consequently, systemic endotoxemia appears to be mediated mainly by lymphatic transport.
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PMID:Endotoxin-transport routes and kinetics in intestinal ischemia. 409 Aug 92

The effect of motility on blood flow varies with the nature of the motility and the initiating stimulus, and the mechanical compressing effect on contractions can be modified by intricate local regulatory mechanisms. Although rhythmic contractions usually decrease instantaneous arterial inflow and increase instantaneous venous outflow, mean blood flow may increase, decrease, or remain unchanged. A decrease in mean flow may indicate the predominance of the mechanical effects whereas an increase may be due to an active muscular hyperemia. Both tonic contractions and gut distention decrease total wall blood flow if mechanical compression overrides compensatory mechanisms; the effect is more pronounced on mucosal than on muscularis flow. Oxygen consumption and the capillary filtration coefficient may increase, decrease, or remain unchanged, depending on the degree of distention. The effects of chemicals depend on the interplay and predominance of their vascular, metabolic, and motility actions. When drawing conclusions regarding the effect of motility on blood flow, one must consider the role of local neural and chemical factors, alterations in the metabolic activity of different layers of the gut wall, collateral blood flow, and the mechanical effects of contractions and increased lumen pressure. Increased blood flow has little effect on motility, but severe or total ischemia and hypoxia produce a transient rise in motility followed by a prolonged paralysis.
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PMID:Blood flow and intestinal motility. 612 5

It has been suggested that histamine contributes to lethal circulatory collapse after acute superior mesenteric artery occlusion. The activity of the histamine inactivating enzyme diamine oxidase, the release of the amine, and the effect of histamine receptor antagonists was therefore studied in rabbits. The main results were: (a) Diamine oxidase activity decreased by 60% after intestinal ischemia and reperfusion. A monoexponential dose-response relationship was found between the specific diamine oxidase inhibitor aminoguanidine and reduced survival time. (b) Plasma histamine levels in the right atrium rose only slightly after ischemia, but considerably during reperfusion of the gut, and remained high for at least 20 min. In sham-operated animals the plasma histamine concentration was unchanged throughout the experiment. The histamine content in the intestinal wall did not fall significantly at any time after mesenteric artery occlusion and reperfusion. (c) The aminoguanidine-induced reduction in survival time was completely reversed by pre-treatment of the animals with the H1-receptor antagonist dimethylpyridine and the H2-receptor antagonist cimetidine. This study provides strong evidence for the protective role of intestinal diamine oxidase in intestinal ischemia.
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PMID:Intestinal diamine oxidase and histamine release in rabbit mesenteric ischemia. 616 12

Acute primary ulcer of the small intestine is an exceptional occurrence. Diagnosis is established only after a complication occurs. In most instances, this complication is perforation of the gut. Acute primary ulcer of the small intestine is accurately defined by specific histologic criteria. It can be unequivocally distinguished from the many other causes of spontaneous perforation of the small intestine. Experimental studies, although numerous, have not improved understanding of pathophysiology. Nosologic classification remains unclear. Many features are similar to those encountered in acute peptic ulcer but stress is usually absent. Other features resemble those of transient necrotizing enterocolitis ; acute primary ulcer of the small intestine may be a very localized form of this latter condition. Ischemia seems to be the most significant factor. However, for an ulcer and finally perforation to occur, ischemia must probably be associated with a number of other factors.
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PMID:[Acute primary ulcer of the small intestine. Present concepts (author's transl)]. 628 93

The severity and distribution of small intestinal ischaemia caused by temporary proximal occlusion of the superior mesenteric artery in cats were evaluated by electromagnetic flowmetry and carbonized microspheres. Average mucosal blood flow was reduced from 0.94 to 0.40 ml/min/g. Mucosal flow in the proximal jejunum and distal ileum was even less affected. Ischaemia induced by proximal occlusion of the superior mesenteric artery in cats was not severe enough to provide optimum conditions for intestinal hypoxic radiation protection, nor was such ischaemia evenly distributed along the gut.
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PMID:Temporary intestinal ischaemia induced by proximal mesenteric artery occlusion. 630 25


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