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

Griffiths' point is defined as the site of (a) communication of the ascending left colic artery with the marginal artery of Drummond, and (b) anastomotic bridging between the right and left terminal branches of the ascending left colic artery at the splenic flexure of the colon. It is upon this critical point at the splenic flexure that collateral circulation between the superior mesenteric artery and the marginal artery branch of the inferior mesenteric artery supplying the descending colon is dependent. Analysis of arteriographic studies shows that anastomosis at Griffiths' point is present in 48%, poor or tenuous in nine percent, and absent in 43%. This critical point is of significance in occlusive vascular impairment of the left colon, both in spontaneous instances and following surgical ligation of the inferior mesenteric artery, and in "nonocclusive" ischemic colitis. Its relationship to arteriosclerotic stenoses and low flow states is discussed. Individuals with absence of dependable anastomoses at Griffiths' point at the splenic flexure may be particularly vulnerable to low perfusion states and develop the syndrome of ischemic colitis. Complete arteriographic evaluation is necessary in ischemia of the colon. This includes particularly assessment of atherosclerotic changes at or near the ostia of the major visceral arteries and the vascular arrangement at Griffiths' point.
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PMID:Griffiths' point: critical anastomosis at the splenic flexure. Significance in ischemia of the colon. 17 88

We describe our observations on abdominal roentgenograms without preparation in two cases of segmental colon infarct and eighteen cases of ischemic colitis. In both infarct cases a colic ileus was noted. In one patient the infarcted loop appeared as gas contrasted. In the ischemic cases there were, in addition to the bowel ileus: a colectasis in two patients, a collapsed segment in thirteen and a gas-filled segment in three. When associated to a significant clinical situation the two latter images have some diagnostic value. In the majority of patients, the contrast enema made possible a diagnosis of ischemic colitis; in three it shaved the sigmoid narrowing responsible for the ischemia.
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PMID:[Plain film findings and contrast enema in colon ischemia (author's transl)]. 66 84

Three cases of double left colic stenosis revealed at one month of age by subobstruction are reported. Recovery was obtained by surgery. The evolution of radiological data in one case, and of histological changes observed on the resected sigmoid colon in the two other cases favor the assumption that cicatricial stenosis occurred likewise. These cases also confirm the existence of a benign expression of necrotising enterocolitis, most common with a colonic localization. Such stenosis due to submucous connective sclerosis strengthens the hypothesis that a transitory mesenteric ischemia is responsible for the necrotizing enterocolitis in newborns.
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PMID:[Colonic stenosis following necrotizing enterocolitis in newborn infants. Apropos of 3 cases]. 93 13

Regional ischemia may induce cervical anastomosis leakage or stenosis or graft necrosis after esophageal reconstruction by retrosternal interposition of an ileocolic graft. These complications may be related to systemic or local hemodynamic alterations. This study was designed to evaluate the relationship between immediate postoperative arterial blood supply to the graft, arterial patency monitored by angiography, and clinical outcome. Eight patients (mean age 30 +/- 4 years; standard deviation) were studied. Miniaturized Doppler implantable microprobes were sutured to the single artery supplying the graft and connected to an 8 MHz pulsed Doppler flowmeter. Systemic hemodynamic parameters and mesenteric hemodynamic data were collected 3 hours after the end of the surgical procedure. These data were compared with the angiogram of the right superior colic artery supplying the graft, systematically performed on the fifteenth postoperative day, and with the clinical course of follow-up for 3 months. Five patients (group 1) had excellent clinical and angiographic results. Mean mesenteric blood flow in these patients was 51 +/- 49 ml.min-1 (+/- standard deviation, ranging from 9 to 122). Three patients (group 2) had a poor clinical outcome. One had early complete graft necrosis and the two others had leakage of the cervical anastomosis with poor distal arterial vascularization of the graft on the angiogram. Mean mesenteric blood flow was nul in the first patient and, respectively, 24 and 28 ml.min-1 in the two others. Cardiac output and mean arterial pressure were in the same range for all patients. Phasic velocity shape analysis revealed that the three group 2 patients had an end-systolic or end-diastolic reverse flow pattern that was not observed in the five group 1 patients, which suggested a submaximal increase in downstream vascular resistance. This reverse flow pattern seems to be a good predictor of ischemia-related complications. We conclude that perioperative pulsed Doppler blood flow monitoring in an ileocolic graft may be useful for the diagnosis and prevention of ischemic complications.
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PMID:Usefulness of perioperative pulsed Doppler flowmetry in predicting postoperative local ischemic complications after ileocolic esophagoplasty. 149

Disturbances in intestinal circulation for even short periods of time can produce mucosal injury, translocation of gut bacteria, and multiple organ failure. We recently reported a model of intestinal ischemia that included occlusion of the superior mesenteric artery (SMA) and interruption of collateral arcades from the right colic and jejunal arteries for 20 min. This present study was designed to characterize further our model of intestinal ischemia by quantitatively assessing changes in intestinal permeability (plasma to luminal clearance of 51Cr-labeled EDTA) and intestinal blood flow (IBF) (microspheres). A total of 89 rats were included for study; mean arterial blood pressure and acid-base balance were not significantly altered by intestinal ischemia or reperfusion. Baseline measurements of 51Cr-labeled EDTA were not significantly different among the experimental animals, and clearance did not change throughout the experimental period in the sham-ischemic group (N = 14). Clearance of 51Cr-labeled EDTA at the end of 20 min of intestinal ischemia (0.194 +/- 0.057 ml/min/100 gm, N = 17) was significantly greater than that measured at control (0.079 +/- 0.006 ml/min/100 gm, P less than 0.05). In addition, clearance measurements during reperfusion (20 min, 0.362 +/- 0.051; 60 min, 0.267 +/- 0.084 ml/min/gm) were significantly higher than those measured at the end of ischemia. Baseline IBF was similar in all rats (N = 42); SMA occlusion reduced IBF by 99% from baseline (from 1.4 +/- 0.27 to 0.014 +/- 0.001 ml/min/gm, N = 20). Removal of the SMA clip returned intestinal perfusion to baseline values (1.72 +/- 0.51 ml/min/g).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in intestinal permeability and blood flow in a new model of mesenteric ischemia. 158 4

Endotoxemia remains the leading cause of death in horses, being intimately involved in the pathogenesis of gastrointestinal disorders that cause colic and neonatal foal septicemia. Endotoxins, normally present within the bowel, gain access to the blood across damaged intestinal mucosa, or endotoxemia occurs when gram negative organisms proliferate in tissues. Endotoxins are removed from the circulation by the mononuclear phagocyte system, and the response of mononuclear phagocytes to these lipopolysaccharides (LPS) play an important role in determining the severity of clinical disease. Macrophages become highly activated for enhanced secretory, phagocytic and cidal functions by LPS. Macrophage-derived cytokines are responsible for many of the pathophysiologic consequences of endotoxemia. The arachidonic acid metabolites, prostacyclin and thromboxane A2 likely mediate early hemodynamic dysfunction and the leukotrienes may potentiate tissue ischemia during endotoxemia. Interleukin 1 (IL-1) induces fever and is responsible for the inflammatory cascade, which constitutes the acute phase response. Tumor necrosis factor (TNF), an important proximal mediator of the effects of LPS, acts to initiate events and formation of other molecules that affect shock and tissue injury. Systemic administration of TNF produces most of the physiologic derangements that are associated with endotoxemia and antibodies that are directed against TNF significantly reduce LPS-induced mortality in experimental animals. In response to endotoxins, mononuclear phagocytes express thromboplastin-like procoagulant activity (PCA), which initiates microvascular thrombosis. Both IL-1 and TNF induce PCA expression, creating a positive feedback loop for LPS-induced coagulopathy. A macrophage-derived platelet activating factor contributes to coagulation dysfunction and further stimulates arachidonic acid metabolism. The ultimate consequences of endotoxemia are multiple system organ failure and death. The numerous feedback loops and intertwining cascades of mediators during endotoxemia defy simplistic methods of treatment. The optimal therapy likely involves methods to alter the generation of inflammatory mediators by mononuclear phagocytes.
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PMID:Endotoxemia in horses. A review of cellular and humoral mediators involved in its pathogenesis. 192 Feb 54

Protein C content and plasminogen activity were measured in plasma from 100 horses with signs of colic. Data were analyzed by grouping horses 4 ways. Each horse was allotted to 1 of 2 outcome groups (survivors and nonsurvivors), 1 of 3 broad-category diagnosis groups (inflammatory disorders, strangulating obstructions, and all other gastrointestinal disorders), and 1 of 2 clinical management groups (medical and surgical). In a fourth grouping, all horses (although numbers of horses included in each subgroup were small) were assigned either to specific diagnostic groups that had high expectation for activated hemostasis (intestinal ischemia, endotoxemia, jugular thrombosis, peritoneal adhesions, and laminitis) or to a control group, in which active hemostasis was unlikely. Within 2 to 24 hours after admission, nonsurvivors developed lower protein C content than did survivors. Protein C content and plasminogen activity became low during hospitalization in horses with strangulating obstructions and in horses having surgery. The results from the grouping by specific diagnosis must be considered pilot data because the numbers of horses in each subgroup were small. Although not statistically significant, trends were noticed in protein C and plasminogen: (1) horses with intestinal ischemia and endotoxemia developed low protein C content and plasminogen activity, (2) protein C content became low in horses that developed peritoneal adhesions or laminitis, and (3) plasminogen activity became low in horses that developed jugular thrombosis. Low protein C content or low plasminogen activity, or both, may be useful as predictors for outcome and for these specific complications of equine colic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of newly developed assays for protein C and plasminogen in horses with signs of colic. 201 48

Pelvic pain is often a difficult differential diagnosis in the emergency department. For physiologic reasons, pain in the pelvis is difficult to localize to a specific organ, and pelvic peritonitis is hard to recognize. On the other hand, differences in types of pain can be very useful in arriving at a correct diagnosis. The clinician must learn to recognize superficial and deep somatic pain, and differentiate between various types of visceral pain which originate from inflammation, ischemia, or colic. A review of the anatomy and physiology of pelvic pain helps identify some of the problems as well as potential aids in approaching the patient with pelvic pain.
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PMID:Pelvic pain: lessons from anatomy and physiology. 221 63

Many models of intestinal ischemia in the rat have been described yielding mortality rates of 8-80% following superior mesenteric artery (SMA) occlusion for periods of 1-85 min. These results have been difficult to reliably reproduce in our lab. Based on our theory that these inconsistent findings are secondary to individual variability in collateral circulation, we have developed a new model for intestinal ischemia with reproducible and consistent mortality. Male Sprague-Dawley rats weighting 300-400 g underwent celiotomy and evisceration. Occlusion of the superior mesenteric artery just distal to the right colic artery was achieved. Collateral arcades from the right colic artery and the jejunal arteries proximal to the site of occlusion were ligated and the bowel was returned to the abdomen for the remainder of the ischemic period. SMA occlusion alone and SMA occlusion with interruption of collateral flow were evaluated and compared for severity of ischemic injury reflected by mortality and for reproducibility of ischemia and mortality. Quantitative measurements of blood flow for each technique were made using radiolabeled microspheres, and a survival curve for SMA occlusion with collateral ligation was constructed. SMA occlusion alone in the rat is not a reliable model for mesenteric ischemia because the resulting ischemic injury is inconsistent and not reproducible. SMA occlusion with collateral ligation produced more severe and reproducible ischemia with greater mortality than did SMA occlusion alone. This technique produced mortality rates that were reproducible and were more consistently related to duration of ischemia.
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PMID:A new model for intestinal ischemia in the rat. 238 Dec 6

1. The relationship of the mesenteric inflammation with intestinal loop deformities was made clear and changes of these deformities were examined with time, using experimental model rabbits. 2. The above rabbit was laparotomized and was caused to develop mesenteritis by applying acetic acid onto sigmoid mesentery and descending colic mesentery, then the abdomen was closed. Subjects were divided into 2 groups (A and B); A group and B group were re-laparotomized 3-7 and 21 days later, respectively and were observed for mesentery and loop appearance, then were extirpated for sigmoid colon and descending colon with mesenterium attached thereto. Roentgenograms were taken first with attachment of mesentery, secondly there-without. Then, the intestinal canal was opened and the mucosal surface was observed, together with bleeding and blood flow disturbance in the depth of the wall in transmitted light. 3. As a result, the following conclusions were obtained: 1) Macroscopically, mesentery was marked with redness for A group and with thickening and twitch due to cicatricial contraction for B group. 2) A group near to the third day showed remarkable shortening, narrowing and marginal irregularity of the loop, which disappeared with time and were scarcely observed for B group; these deformities were considered to involve mesenteric inflammations and ischemia caused by secondary blood flow disturbance. 3) A group near to the 7th day and B group showed remarkable angulation, distortion and coil-like appearance; these deformities are considered to have been caused by thickening (stiffness) of the mesentery and its attachment and twitch-distortion due to cicatricial contraction. 4) Coil-like appearance disappeared upon cutting off the mesentery from the loop.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An experimental study on mesenteritis and deformities of the intestinal canal; with special reference to the changes with time of deformities (angulation, distortion, coil-like appearance)]. 262 49


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