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)

Effects of glucagon and prostacyclin (PGI2) were studied in anesthetized dogs during sequential occlusive and postocclusive mesenteric ischemia induced by 90 min of tourniquet stenosis of the superior mesenteric artery (SMA). After 30 min of SMA stenosis, glucagon (1 microgram/kg/min, n = 7), PGI2 (30 ng/kg/min, n = 7), or saline (1 ml/min, n = 3) was infused intravenously for 30 min, followed by 30 min of continued ischemia. SMA flow and distal SMA pressure ( SMAP ) decreased 76% with SMA stenosis (P less than 0.01). Ileal wall flow measured by radiolabeled microspheres decreased from 45 to 13 ml/min/100 g (P less than 0.01); mesenteric AV O2 difference ( AVDO2 ) increased from 5.1 to 10.1 ml/dl (P less than 0.01); and mesenteric O2 consumption (VO2) decreased by 48% (P less than 0.05). Glucagon infusion caused a further decrease in ileal wall flow, to 10 ml/min/100 g (P less than 0.05), and an increase in AVDO2 to 11 ml/dl (P less than 0.05), despite a 22% increase in cardiac output. PGI2 caused a similar decrease in ileal wall flow and an increase in AVDO2 , although these were not statistically significant. Saline infusion caused no change in measured variables. In the second phase of this study, SMA blood flow was restored by tourniquet release. After animals had stabilized for 30 min, a repeat 30-min drug infusion was studied. In this postocclusive period, persistent gut ischemia was indicated by a reduction in VO2 to 76% of original baseline, associated with a 50% decrease in both CO and SMAQ . Intravenous infusion of glucagon at this time increased SMAQ by 195% (P less than 0.05) and resulted in a return of VO2 to its original baseline level. PGI2 infusion caused a 21% increase in SMAQ and a 16% decrease in AVDO2 (NS), but had no significant effect on VO2. Glucagon was effective in the management of postocclusive mesenteric ischemia but appeared to have a detrimental effect on ileal blood flow in severe occlusive ischemia.
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PMID:Effects of glucagon and prostacyclin in acute occlusive and postocclusive canine mesenteric ischemia. 637 91

Data from 722 consecutive causes with intracranial aneurysms were stored in a computer and later retrieved for analysis. Results and complications (including preoperative death and morbidity) of the surgical management of these patients were correlated with the Botterell grade of the patient in individuals with a recent subarachnoid hemorrhage (SAH), with the type of aneurysm, and with the timing of the surgical procedure. Patients with no SAH within 30 days prior to hospital admission were classified as "no SAH." Approximately 30% of all patients had sustained more than one hemorrhage. Death and morbidity rates prior to surgery in good-grade patients with a recent SAH exceeded the risk of surgery itself. Rebleeding was the primary cause for death and morbidity in Grade 1 patients: 3% of Grade 1 patients died from a recurrent hemorrhage and 7% deteriorated to a lower grade. Deterioration from ischemia produced by vasospasm related or unrelated to rebleeding exceeded the risks of rebleeding in Grade 2 patients. There was an operative morbidity of 2% and mortality of 2% in patients who were classified as Grade 1 at the time of surgery, but an overall management morbidity of 3% and mortality of 6% in patients who were in Grade 1 at the time of hospital admission. Early surgery in Grade 1 patients was not associated with an increased incidence of delayed ischemia postoperatively. In Grade 2 patients, the operative morbidity and mortality was 7% and 4%, respectively, and the management morbidity and mortality 16% and 11%, respectively. Early surgery in this group was associated with a high frequency of postoperative delayed ischemia (particularly in patients with more than one SAH). Epsilon-aminocaproic acid appeared to protect against a rebleed, gut was associated with a higher incidence of postoperative pulmonary emboli. Intraoperative complications were related both to the size of the aneurysm and to its location. Repair of multiple aneurysms did not adversely affect the result. The surgical approach, the importance of using a self-retaining brain retractor, and the technical complications in these cases are discussed.
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PMID:Results and complications of surgical management of 809 intracranial aneurysms in 722 cases. Related and unrelated to grade of patient, type of aneurysm, and timing of surgery. 680 8

The challenge presented to the surgeon by infants with NEC is to time an operation to coincide with the finite interval between infarction of gut and perforation. This study describes a new technique for continuous monitoring of peritoneal fluid in a rabbit model of intestinal ischemia to aid in predicting this interval. Color change to brown appears to be a reliable indicator of infarction. A sudden dramatic rise in the WBC of this fluid may also be an easily obtained, useful parameter. Further clinical studies of this method seem warranted to help improve the still dismal outcome of this disease.
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PMID:Technique for continuous sampling of peritoneal fluid for prediction of intestinal gangrene. 722 44

Twenty-six cases of carcinoid-related mesenteric angiopathy and intestinal infarction (three from our institution and 23 previously reported cases) were reviewed. Twenty patients presented with acute abdominal findings, including peritonitis (13 cases), intestinal obstruction (five cases), and bleeding per rectum (two cases). Fifteen patients (75%) experienced antecedent symptoms of abdominal pain and/or diarrhea, averaging 2.5 years in duration. Twelve patients (46%) exhibited symptoms of carcinoid syndrome. Mesenteric angiography in three cases demonstrated encasement and segmental branch narrowing or occlusion of major mesenteric vessels. Eleven patients underwent resection and primary bowel anastomosis with an early survival rate of 91%. Four additional patients who underwent lesser surgical procedures and five patients who did not undergo operation all died. Elastic vascular sclerosis (EVS) was identified in 19 of 22 cases with available histologic material (86%). These changes were observed in proximity to as well as distant to the primary tumor. In general, the severity of EVS did not correlate with the likelihood of gut ischemia. Although not the sole cause of intestinal gangrene in patients with midgut carcinoids, EVS may contribute significantly to the evolution of these ischemic changes.
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PMID:Mesenteric angiopathy, intestinal gangrene, and midgut carcinoids. 728 Oct 10

Administration of lipopolysaccharide (LPS) to experimental animals leads to diminished mesenteric perfusion, increased ileal mucosal [H+] , and increased gut epithelial permeability to hydrophilic solutes. We sought to determine whether these phenomena are causally related. Experiments were performed in anesthetized pigs. Permeability was assessed by measuring the plasma-to-lumen clearance of fluorescein isothiocyanate dextran (4,000 Da; FD-4) by a segment of ileum perfused with Ringer lactate solution. Mucosal perfusion (Qmuc) and [H4+] were estimated using laser-Doppler flowmetry and tonometry, respectively. In an initial series of experiments, we showed that mucosal permeability was linearly correlated with mucosal [H+] in animals subjected to graded degrees of mechanically induced mesenteric ischemia (n = 14, R2 = 0.58, P < 0.002) or injected with graded doses of LPS (n = 11, R2 = 0.93, P < 0.0001). In a second series of experiments, we induced mucosal acidosis in normal pigs by mechanical ventilation with either a hypoxic (n = 7) or a hypercapnic (n = 5) gas mixture. In both groups, ileal mucosal permeability to FD-4 increased significantly (P < 0.05), although transmesenteric release of lactate increased significantly only in the hypoxic group. Qmuc was unchanged in both groups. These data suggest that mucosal acidosis, even in the absence of tissue ischemia or hypoxia, increases intestinal permeability to a macromolecular hydrophilic solute. Tissue acidosis may be an important factor contributing to LPS-induced gut mucosal hyperpermeability.
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PMID:Endotoxin-induced ileal mucosal hyperpermeability in pigs: role of tissue acidosis. 751 59

To study the changes of the bowel-barrier function and its preservation, we developed a new animal model. A specially bred miniswine (Guizhou species) was used with multiple catheterizations for sampling different blood from portal, inferior mesenteric as will as jugular (central) veins. The animals were sustained with 30% III burns of TBSA 7 days after catheterization and divided randomly into early feeding (EF) group, given a complete diet beginning from 2 hours postburn (n = 6) and delayed feeding (DF) group, given the same diet initiating on 4 days postburn (n = 6). The results indicated that the bowel-barrier function was weakened significantly early postburn so that the translocation of both endotoxin and bacteria from the gut to portal vein was evidently increased. However, improving the intestinal mucosa ischemia, preserving mucosal mass and maintaining bowel-microecological balance through early enteral feeding, as revealed in this study, could enhance the barrier function, and the translocation of bacteria and endotoxin would be thus decreased to some extent.
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PMID:[Preserving intestinal function after severe burn injury]. 752 Aug 25

Gut mucosal ischemia has been associated with cardiopulmonary bypass (CPB) and may contribute to postoperative systemic inflammatory response and multiorgan dysfunction. Hypertonic saline/dextran (HSD) has been previously shown to selectively increase mucosal blood flow in circulatory shock. To determine whether adding HSD to the prime solution for CPB improves gut mucosal blood flow and oxygenation, we performed normothermic, non-cross-clamped CPB in pigs with 1 ml/kg of HSD (25% NaCl/24% dextran 70) (HSD group, n = 9) or lactated Ringer's solution (LRS group, n = 9) as control added to a standard prime. Animals were instrumented with ultrasonic flow probes on the superior mesenteric artery (SMA), laser Doppler mucosal flow probes in the ileum, and indwelling portal vein catheters and tonometers for mucosal hydrogen ion measurements and pH calculations in the stomach, ileum, and rectum. The total infused volume and net fluid balance was significantly lower in the HSD than in the LRS group (649 +/- 171 ml vs 2075 +/- 385 ml and 502 +/- 182 ml vs 1891 +/- 363 ml, respectively, P < 0.01). SMA flow in the LRS group increased to 110-123% of baseline during CPB and was significantly higher than that in the HSD group which remained unchanged. Ileal mucosal blood flow decreased significantly to 70-50% of baseline in both groups with no difference between groups. Gut oxygen (O2) delivery decreased during CPB in both groups, but O2 consumption remained unchanged. Gastric, ileal, and rectal mucosal pH decreased progressively, and portal venous blood pH also decreased in both groups, but there was no significant difference between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertonic saline/dextran for cardiopulmonary bypass reduces gut tissue water but does not improve mucosal perfusion. 752 80

During ECC, dogs ventilate spontaneously according to classical physiology. Further, given the CO2 clearance insured by the ECC oxygenator, many hours of reversible apnea are tolerated without sequellae. Surgical removal of the lungs shows that an emptied chest still responds to chemical drives, but the absent lung-recoil causes hyperinflation with lethal failure. Finally, liquid ventilation induces metabolic acidemia through phasic gut ischemia and respiratory muscle strain that destroys the delicate lung structure.
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PMID:[Aspects of pathological physiology of the dog in extracorporeal circulation]. 755 34

Impaired gut mucosal perfusion has been reported during cardiopulmonary bypass. To better define the adequacy of gut blood flow and oxygenation during cardiopulmonary bypass, we measured overall gut blood flow and ileal mucosal flow and their relationship to mucosal pH, mesenteric oxygen delivery and oxygen consumption in immature pigs (n = 8). Normothermic, noncross-clamped, right atrium-to-aorta cardiopulmonary bypass was maintained at 100 ml/kg per minute for 120 minutes. Animals were instrumented with an ultrasonic Doppler flow probe on the superior mesenteric artery, a mucosal laser Doppler flow probe in the ileum, and pH tonometers in the stomach, ileum, and rectum. Radioactive microspheres were injected before and at 5, 60, and 120 minutes of cardiopulmonary bypass for tissue blood flow measurements. Overall gut blood flow significantly increased during cardiopulmonary bypass as evidenced by increases in superior mesenteric arterial flow to 134.1% +/- 8.0%, 137.1% +/- 7.5%, 130.3% +/- 11.2%, and 130.2% +/- 12.7% of baseline values at 30, 60, 90, and 120 minutes of bypass, respectively. Conversely, ileal mucosal blood flow significantly decreased to 53.6% +/- 6.4%, 49.5% +/- 6.8%, 58.9% +/- 11.6%, and 47.8% +/- 10.0% of baseline values, respectively. Blood flow measured with microspheres was significantly increased to proximal portions of the gut, duodenum and jejunum, during cardiopulmonary bypass, whereas blood flow to distal portions, ileum and colon, was unchanged. Gut mucosal pH decreased progressively during cardiopulmonary bypass and paralleled the decrease in ileal mucosal blood flow. Mesenteric oxygen delivery decreased significantly from 67.0 +/- 10.0 ml/min per square meter at baseline to 42.4 +/- 4.6, 44.9 +/- 3.5, 46.0 +/- 3.6, and 42.9 +/- 3.9 ml/min per square meter at 30, 60, 90, and 120 minutes of bypass. Despite the decrease in mesenteric oxygen delivery, mesenteric oxygen consumption increased progressively from 10.8 +/- 1.4 ml/min per square meter at baseline to 13.4 +/- 1.2, 15.9 +/- 1.2, 16.7 +/- 1.4, and 16.6 +/- 1.54 ml/min per square meter, respectively. We conclude that gut mucosal ischemia during normothermic cardiopulmonary bypass results from a combination of redistribution of blood flow away from mucosa and an increased oxygen demand.
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PMID:Gut mucosal ischemia during normothermic cardiopulmonary bypass results from blood flow redistribution and increased oxygen demand. 756 51

Nitric oxide (NO.) plays a central role in the physiology of the gastrointestinal tract and its response to critical illness. Potential sources of NO. in the gut include: intrinsic intestinal tissue (mast cells, epithelium, smooth muscle, neural plexus), resident and/or infiltrating leukocytes (neutrophils, monocytes), reduction of luminal gastric nitrate, and denitrification by commensal anaerobes. The brain and endothelial isoforms of nitric oxide synthase are expressed under resting conditions, whereas inflammatory stimuli are required for the induction of the inducible type. Under resting conditions, mucosal perfusion is regulated by NO. derived from the vascular endothelium of the mesenteric bed. During inflammation, excessive NO. production from the inducible synthase may contribute to mucosal hyperemia. Coordination of peristalsis and sphincteric action is mediated by the release of NO., which acts as the principal neurotransmitter of the nonadrenergic, noncholinergic enteric nervous system. Alterations in bowel motility, such as ileus, result from excessive concentrations of NO. generated during endotoxicosis and inflammatory bowel disease. The role of NO. in the regulation of salt and water secretion is poorly understood. Endotoxin-induced inhibition of gastric acid secretion appears to be mediated by the action of NO. on parietal cells. NO. may protect the gastrointestinal mucosa from a variety of stimuli (caustic ingestion, ischemia, ischemia/reperfusion injury, early endotoxic shock) by maintaining mucosal perfusion, inhibiting neutrophil adhesion to mesenteric endothelium, blocking platelet adhesion, and preventing mast cell activation. Excessive NO., however, may directly injure the mucosa. Barrier function of the intestinal mucosa is protected by NO. in the early stages of injury, when neutrophil adhesion, ischemia, and mast cell activation are relevant. Inhibition of NO. synthesis ameliorates barrier dysfunction during more advanced stages of inflammation, when activation of inducible NOS yields toxic concentrations of NO.. At high concentrations, NO. disrupts the actin cytoskeleton, inhibits ATP formation, dilates cellular tight junctions, and produces a hyperpermeable state. Selective inhibition of the inducible isoform of NOS and maintenance of the constitutive types may be therapeutic.
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PMID:Nitric oxide in the gut. 758 76


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