Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q16637 (SMA)
 8,107 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mucosal diamine oxidase (DAO) decreases during intestinal ischemia and may be a useful marker of intestinal ischemic injury. Tissue DAO activity and histologic changes were studied in intestinal segments taken from the midpoint of the small intestine before and 2, 4, and 24 hr after manipulation of the intestinal blood supply in 24 mongrel dogs. Intestinal DAO activity decreased significantly (17 +/- 21% of control value) 24 hr after SMA ligation and was associated with abnormal histology (histology score 7.8 +/- 2.9 at 24 hr vs 0.3 +/- 0.5 at 0 hr). SMA occlusion for 2 hr resulted in a significant decrease in DAO activity (45 +/- 36% of control value) 4 hr after manipulation which returned to normal at 24 hr, as did the histologic injury. Ligation of both the mesenteric arteries and veins resulted in a more rapid decrease in DAO activity. Decreased DAO activity correlated with the extent of histologic injury. Intestinal ischemia is associated with decreased intestinal DAO activity, which is influenced by the mechanism and duration of intestinal ischemia.
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PMID:Intestinal diamine oxidase levels reflect ischemic injury. 190 Mar 39

Advanced age and cardiovascular diseases cause of SMA occlusion. Shock is triggered and maintained by bowel ischemia. Since lactate is the end product of anaerobic glycolysis, lactacidosis is a valuable clinical parameter. Lactate values above 4-5 mmol/l are conclusive evidence in the presence of symptoms of acute SMA occlusion. Chance of survival are poor in stages II and III with advanced shock and non reversible gangrene. Revascularisation of the SMA combined with adequate bowel resection reduces the production of toxic and lethal substances in the intestinal mucosa, thus increasing the chance of survival. Determination of serum lactate should be an integral part of the diagnostic procedure and the close followup for it is both an adequate index of the grade of intestinal ischemia and a means of assessing whether a second-look is warranted.
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PMID:[Acute mesenteric vascular occlusion: pathophysiology, clinical stages, diagnosis]. 198 61

Perfusion of ischemic tissue with glucose has been shown to be deleterious to heart, spinal cord, and kidney. Observations that glucagon improves survival after acute mesenteric ischemia, however, suggest that hyperglycemia may not be deleterious during bowel ischemia. This experiment examined the effect of glucose infusion on survival in an established rat model of acute mesenteric ischemia. The superior (cranial) mesenteric artery (SMA) was occluded for 85 min in 36 anesthetized Sprague-Dawley rats. Animals were randomized to receive 5% glucose in normal saline (n = 15; 16.5 mL/kg.min iv), normal saline alone (n = 13; 16.4 mL/kg.min iv), or no intravenous fluid (n = 8). Ninety-minute intravenous infusions were initiated 10 min after SMA occlusion. Survival to 48 h was 47% in glucose-saline-treated rats, 31% in saline-only-treated rats, and 12.5% in control rats. These results demonstrate no deleterious effect of glucose infusion on mortality after acute mesenteric ischemia in this model.
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PMID:The effect of glucose infusion on survival after acute mesenteric ischemia/reperfusion. 228 46

Escape of endotoxin from the intraintestinal site was investigated in experimental models of intestinal ischemia and during intraabdominal infection in rats. Following the instillation of Salmonella abortus equi endotoxin (S-form) into the proximal large bowel, we recorded the presence of the lipopolysaccharide molecule in the bowel wall, the intestinal lymph nodes, the peritoneal cavity, and in the liver sinusoids by immunohistochemical methods. At 3, 6, 12, 24, and 48 hr after the operative procedure, peritoneal fluid, blood, and tissue samples were taken. Survival rates were similar between the two test-groups (occlusion of the superior mesenteric artery [SMA] and cecal ligation and puncture [CLP]) and were not influenced by the amount of the injected endotoxin. There was no detectable morbidity in the sham-operated control animals with endotoxin doses up to 20 mg. Endotoxin could only be detected at 24 and 48 hr in the SMA group in the liver as well as in the peritoneal sediment and in intestinal lymph nodes. CLP and control samples remained negative throughout the observation period. Bacteria were found intraperitoneally within 12 to 24 hr in the SMA group and within 3 to 12 hr in the CLP group.
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PMID:The role of intestinal endotoxin in experimental peritonitis. 291 75

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

From 1979 to 1984 39 patients were operated on for acute mesenteric ischemia. The purpose of this retrospective study was the documentation of the therapeutic results and discussion of the value of a second-look operation and postoperative angiography. Proximal occlusion of SMA in 33 patients (85%) resulted in extended bowel infarction, whereas segmental infarction due to peripheral occlusion was found in 15%. The hospital mortality was 85%. Operative procedure consisted of revascularisation (18%), bowel resection (18%), revascularisation and resection (10%) and explorative laparotomy (18%). The second-look operation as a routine procedure has been replaced by a postoperative angiogram. Laparotomy was performed in case of reocclusion of SMA or clinical signs.
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PMID:[Results of therapy of acute mesenteric vascular occlusion]. 405 94

The records of 60 patients with acute intestinal ischemia treated between 1969 and 1982 were studied retrospectively. Fifty-three patients (88%) had thrombosis or embolus of the superior mesenteric artery and 7 patients (12%) occlusion of the superior mesenteric vein. Initial symptoms were obscure, although 25% presented with signs of peritonitis. The most frequently used investigation was plain abdominal X-ray with a positive finding in only 1/3. Forty-three patients (72%) were operated on. In 18 patients irreversible changes were found. Total mortality rate was 82%, in SMA-thromboembolism 85% and in SMV-thrombosis 57%. To improve the prognosis clinical awareness of the problem and attempts towards early diagnosis should be raised.
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PMID:Acute intestinal ischemia. A 14-year retrospective investigation. 646 24

Prevention of ischemic bowel complications following abdominal aortic reconstruction requires identification of the patient at high risk for developing the complication; on precise, gentle, meticulous operative technique; on knowledge of bowel blood supply; on determining when the IMA must be reconstructed or when it can be safely ligated; and on methods of preserving or preventing damage to bowel blood supply. Patients at greatest risk for developing bowel ischemia following aortic reconstruction include those with a history of visceral angina, those with a patent IMA (40% to 52%), those being treated for ruptured aneurysm, those whose postreconstructive IMA stump mean blood pressures are less than 40 torr, those in whom Doppler flow signals cease following division or occlusion of the IMA, and those who have SMA occlusive disease and arteriographic documentation of IMA to SMA flow in the MMA (Table II). Patients at least risk include those in whom the IMA is already occluded (48% to 60%), those whose postreconstructive IMA stump pressures are more than 40 torr, those in whom Doppler flow signals persist after IMA occlusion, those who have flow in the MMA from the SMA to the IMA (provided this vessel is not injured), and those undergoing aortic reconstruction for aortoiliac occlusive disease.
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PMID:Prevention of intestinal ischemia following abdominal aortic reconstruction. 684 80

To elucidate the critical role of superoxide dismutase (SOD) and nitric oxide in brain injury and systemic circulation during brain ischemia, we performed bilateral carotid artery ligation (BCAL) on rats and evaluated the effects of NG-monomethyl-L-arginine (L-NMMA) and a long-acting SOD derivative (SMA-SOD). After administration of L-NMMA, specific inhibitor against nitric oxide synthase (NOS), most of BCAL rats died within 6 h while no BCAL rats without L-NMMA died at all. Administration of SMA-SOD exhibited no effect on the life span of BCAL rats. Magnetic resonance imaging (MRI) and microscopic analysis for the ischemic brain revealed that, although administration of L-NMMA showed no significant effect on the ischemic brain of BCAL rats, SMA-SOD effectively prevented the ischemic changes based on permeability edema in the frontal lobe. Measurement of changes in the blood flow of the ischemic brain revealed that administration of L-NMMA decreased the blood flow in the BCAL rats while no remarkable changes were seen after administration of SMA-SOD. Urinary secretion of NO2-/NO3-, the metabolites of nitric oxide, was increased by challenging BCAL, and the presence of L-NMMA or SMA-SOD diminished this elevation. Blood pressure was increased by performing BCAL to rats, and administration of L-NMMA showed further elevation of the blood pressure. On the contrary, administration of SMA-SOD decreased post-ischemic hypertension. These results suggest that SOD may play a protective role for brain ischemia by suppressing increased vascular permeability, while nitric oxide showed beneficial effect on the ischemic brain by increasing the blood flow in the ischemic brain.
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PMID:Role of superoxide dismutase and nitric oxide on the interaction between brain and systemic circulation during brain ischemia. 752 76

Adult respiratory distress syndrome (ARDS) often occurs in response to sepsis, shock, or ischemia/reperfusion (I/R) of a remote organ and is a frequent cause of mortality in the ICU patient. Pulmonary vascular resistance (PVR) increases during ARDS, yet direct observations of the pulmonary microcirculation are needed to characterize the vascular response. The purpose of this study was to quantitate the changes in hemodynamic variables, subpleural arteriolar diameters (AD), and alveolar cross-sectional areas (ACSA) during intestinal I/R-induced lung injury in rats, using a new method of in vivo videomicroscopy. Sprague-Dawley rats were anesthetized and cannulated, and superior mesenteric arteries were looped. A thoracotomy was performed with animals ventilated with air with 1 cm PEEP. Hemodynamic and videomicroscopic data were obtained before and during 45 min of SMA occlusion and after reperfusion, up to 120 min. Maximal vessel dilation was measured using topical 10(-5) M nitroprusside. The ability of vessels to constrict was confirmed by applying topical 10(-6) M endothelin-1. Intestinal I/R produced decreases in arterial pH, mean arterial pressure, and cardiac output. Despite these alterations, subpleural AD remained maximally dilated. Arterioles maintained the ability to constrict as demonstrated by the response to topical endothelin-1. ACSA did not change, indicating a uniform inflation of the lung. Using a unique method of in vivo pulmonary videomicroscopy, we have shown that AD do not change following 120 min of intestinal I/R, despite systemic hemodynamic instability. It appears that pulmonary arteriolar vasoconstriction does not contribute to increased PVR during the early phase of lung injury.
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PMID:Pulmonary subpleural arteriolar diameters during intestinal ischemia/reperfusion. 763 Jan 36


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