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)

To monitor free radical scavenging properties of drugs, the 'stable' radical 2,2,6,6-tetramethylpiperidino-1-oxyl (TEMPO) was used. The sydnonimine molsidomine (SIN-1) effectively reduced the ESR signal whereas the nitrate isosorbidemononitrate (ISMN) did not. Thiol reagents like 2-mercaptopropionylglycine (MPG) or glutathione (GSH) only were effective in the presence of Fe2+ or Fe3+. Protein-bound iron in hemoglobin proved about four times more effective in reducing ESR signal height by thiols. It is suggested that the decrease in thiol content adds to the lack in protein bound iron of hemoglobin to induce the burst of free radicals in hypoxia (ischemia) and reperfusion.
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PMID:Free radical scavenging drugs, assessed by ESR studies: influence of hemoglobin. 285 30

Serial measurements of a marker of brain ischemia, creatine kinase isoenzyme BB, were performed in arterial and internal jugular venous blood from 20 infants younger than 1 year of age before and during the first 20 hours after deep hypothermic total circulatory arrest procedures. A two-site monoclonal method was used, and the results were analyzed in relation to age, size, type of cardiac lesion, hemoglobin level, blood glucose level, pH, and duration of the total circulatory arrest. The creatine kinase BB concentrations increased after the arrest, more so in venous than in arterial blood, from 3.2 +/- 0.5 ng/ml to 17.5 +/- 4.5 in arterial blood and from 3.5 +/- 0.5 ng/ml to 18.1 +/- 5.8 in venous blood. Arterial-venous concentration differences correlated with venous concentrations (r = 0.92, p less than 0.01). The duration of the arrest correlated with creatine kinase BB concentrations during reperfusion with correlation coefficients between 0.50 to 0.90 depending of what sequence of the 20-hour sampling period was analyzed. The best correlation was obtained during the first 4 hours of reperfusion. Age, size of the child, and preoperative cyanosis correlated with postoperative creatine kinase BB but were less important than the arrest time, blood glucose level (r = 0.62, p less than 0.01), pH (r = -0.78, p less than 0.01), and hemoglobin level (r = 0.76, p less than 0.01) during reperfusion. It is suggested that a different control of blood glucose level and pH during reperfusion may be of importance to reduce biochemical signs of cerebral dysfunction after deep hypothermic total circulatory arrest procedures.
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PMID:Elective deep hypothermia with total circulatory arrest: changes in plasma creatine kinase BB, blood glucose, and clinical variables. 291 Nov 96

Reflectance spectrophotometry measures indices of mucosal hemoglobin concentration (IHB) and oxygen saturation (ISO2). In the rat colon, characteristic patterns of IHB and ISO2 are associated with ischemia with congestion (increased IHB and decreased ISO2) and ischemia without congestion (decreased IHB and decreased ISO2). Endoscopic measurements with acceptable interobserver variability was demonstrated in the canine stomach. In eight healthy subjects, endoscopic measurement in different areas of the colon and rectum revealed significantly lower IHB values in the splenic flexure. These observations are compatible with reduced flow and increased susceptibility to ischemic damage in this watershed area. The endoscopic measurements in 13 patients with active inflammatory bowel disease revealed an increase in IHB and ISO2 values in the involved areas, indicating an increase in mucosal blood flow. In six patients restudied when the disease remitted, these values returned to normal.
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PMID:Assessment of mucosal hemodynamics in normal human colon and patients with inflammatory bowel disease. 292 Aug 81

In rats with artificial renal hypertension, the amount of erythrocytes in the blood was increased in 43% of cases within 2-3 months after surgery. Diverse changes of the blood oxygen-transport properties indicate several mechanisms of the organism adaptation to changes in oxygen regiment in response to the arterial pressure increase due to ischemia of renal tissue: an increase in the blood oxygen capacity; changes of the hemoglobin oxygen-binding properties. The parameters under study, except the arterial pressure, did not differ from the control ones in a number of experimental animals.
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PMID:[Oxygen transport properties of the blood in experimental renal hypertension in the rat]. 309 88

The mechanism for the prolonged contractile dysfunction observed in myocardium reperfused after reversible regional ischemia ("stunned" myocardium) is unclear. Recent studies suggest that myocardial stunning may be mediated by oxygen-derived free radicals, but the precise molecular species involved remain unknown. Thus we explored the role of the highly cytotoxic hydroxyl radical in regional postischemic dysfunction by using dimethylthiourea (DMTU), an effective and highly permeable hydroxyl radical scavenger. Open-chest dogs undergoing a 15 min occlusion of the left anterior descending coronary artery followed by 4 hr of reperfusion received either DMTU (0.5 g/kg iv over 45 min starting 30 min before occlusion, n = 14) or saline (n = 15). Control and treated dogs were comparable with respect to variables that may affect postischemic dysfunction, including heart rate, aortic pressure, left atrial pressure, arterial blood gases and hemoglobin concentration, size of the occluded bed (determined by postmortem perfusion), and collateral blood flow (determined by radioactive microspheres). Regional myocardial function was assessed by measuring wall thickening with an epicardial Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions and similar degrees of dyskinesis during ischemia. After reperfusion, however, wall thickening (expressed as percent of baseline) was considerably greater in treated as compared with control dogs: 53 +/- 9% (mean +/- SEM) vs 9 +/- 14% (p less than .03) at 1 hr, 55 +/- 9% vs 23 +/- 13% (p less than .05) at 2 hr, 60 +/- 9% vs 28 +/- 14% (p less than .05) at 3 hr, and 67 +/- 5% vs 36 +/- 13% (p less than .05) at 4 hr. Thus DMTU produced a significant and sustained improvement in recovery of contractile function. In concentrations greater than the plasma levels attained in vivo, DMTU did not scavenge either hydrogen peroxide or superoxide anion in vitro. These results suggest that the myocardial dysfunction occurring after a brief episode of regional ischemia is mediated in part by the hydroxyl radical.
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PMID:Attenuation of dysfunction in the postischemic 'stunned' myocardium by dimethylthiourea. 311 44

Effects of three unmodified hemoglobin solutions on myocardial contractile function was evaluated using isolated perfused rabbit interventricular septa. The hemoglobin solutions tested were: a human hemoglobin solution (SFHS-A), a bovine hemoglobin prepared by a column chromatography (SFHS-B), and a bovine hemoglobin obtained by a ultrafiltration method (SFHS-C). Myocardial effects were assessed by comparing contractile parameters; developed tension (DT), resting tension (RT), and perfusion pressure (PP), measured before (control perfusion with Tyrode buffer) and during hemoglobin perfusion. Further, to examine the effects of hemoglobin solutions on myocardial contractility following a period of impaired flow, septal responses to a 10-minute period of ischemia (stopflow) were also studied. After a 10-minute perfusion with hemoglobin solution, SFHS-C increased DT to 124 +/- 12% (paired t-test, p less than 0.05) without causing a significant increase in RT or PP while SFHS-A and SFHS-B decreased DT to 96 +/- 20% (p greater than 0.05) and to 77 +/- 7% (p less than 0.05), respectively. A significant rise in PP (40-50% above baseline) was also noted with these solutions (p less than 0.05). Similarly, after a 30-minute reperfusion following a 10-minute ischemia, SFHS-C allowed significantly better percentage recovery (95 +/- 3%) than septa perfused with SFHS-A (81 +/- 2%) or SFHS-B (63 +/- 6%) (Student's t-test, p less than 0.05). These results indicate that hemoglobin solution, if properly prepared, does not seem to have acute deleterious effects on contractile function of the isolated heart.
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PMID:Effects of hemoglobin perfusion on contractile function of the isolated ventricular septa. 317 74

Hemoglobin solutions were assessed in terms of their ability to promote lipid peroxidation, which was quantitated by measuring the formation of thiobarbituric acid reactive substances (TBARS) under specified conditions in murine brain homogenates. Solutions designed for use in acute treatment of hypovolemic shock and trauma should incorporate ingredients specifically aimed at decreasing oxygen and lipid radical mediated injury occurring secondary to ischemia and reperfusion. A number of strategies aimed at decreasing the oxidant effect of hemoglobin solutions and other blood and plasma substitutes have been evaluated. These include use of the naturally occurring anti-oxidants in human plasma, specifically transferrin and ceruloplasmin. Similarly, certain iron chelators, such as deferoxamine (Desferal, Ciba-Geigy), effectively prevent molecular and cellular damage caused by iron catalyzed formation of oxygen derived radicals.
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PMID:Hemoglobin: a lifesaver and an oxidant. How to tip the balance. 317 98

The view that intracellular changes during oxygen depletion are the primary cause of abnormal function and altered physiology was originally proposed by Paul Bert. From that time it remains a basic assumption that hypoxia in intact animals produces alterations of cell and organ function, and that by measuring the intensity of these disturbances or the intensity of the functional impairment produced by these disturbances, a clearer understanding of the impact and consequences of oxygen depletion should emerge. At present, intracellular changes are inferred from the measurement of extracellular signals such as blood pressure, arterial oxygen tension and pH, or hemoglobin saturation, which provide mean values of changes occurring over the entire body. However, cells and organs in different parts of the body respond differently to a given degree of hypoxia or ischemia, and measurements of extracellular variables cannot provide precise information about abnormalities in any specific organ. Extracellular variables also do not reflect adaptive responses of a specific organ such as autoregulation of its blood flow and the ability to alter energy demand in response to changes in energy production. Other factors include differences in metabolic rates and dependence upon oxidative and glycolytic reactions, cell heterogeneities within a tissue or organ, redistribution of blood flow to various organs during hypoxia, or other insults, and other, yet unknown, cell-specific changes that result in a range of survival capabilities among organs. These considerations suggest the importance of direct monitoring of intracellular changes produced by cardiovascular or respiratory diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracellular monitoring of experimental respiratory failure. Collaborative Group on Intracellular Monitoring. 319 40

In order to assess the changes in the clinical biochemistry of runner's anemia and its evolution during a prolonged period of high-intensity training, 11 male international class distance runners (mean time for 1 mile 4 min, 2.5 sec) were followed over a 10-month period prior to the 1984 U.S. Olympic Trials. Mean values of hemoglobin, hematocrit, and mean corpuscular hemoglobin (MCH) decreased modestly over the period of study. Means of haptoglobin, iron, and total iron binding capacity (TIBC) remained roughly constant. Percentage of saturation of TIBC by iron (% sat) averaged 30% or less in 5 of 11 runners, suggesting mild iron deficiency. Most measured haptoglobin levels were below normal range throughout the study period. The cause of runner's anemia has been demonstrated to be multifactorial, including disordered iron metabolism, iron deficiency, and hemolysis. Other studies have shown absent bone marrow iron in male athletes, secondary to hematuria, ischemia of the intestinal mucosa with bleeding, and iron losses due to heavy perspiring. Cardiorespiratory fitness, evaluated through repetitive treadmill testing, was not adversely affected in our athletes. Total creatine kinase (CK) increased significantly after a training session, while the MB fraction of CK never exceeded 3%. Total lactate dehydrogenase (LD) also rose after exercise, but the fractions represented by isozymes 1-5 were unaltered; specifically, there was no change in the LD-1/LD-2 ratio. Enzyme elevations were thus derived from skeletal muscle and not from heart.
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PMID:An analysis of serum enzyme changes and clinical biochemical abnormalities of the anemia in Olympic runners. 321 6

Endoscopic reflectance spectrophotometry was used to compare the effect of vasopressin and propranolol on gastric mucosal hemodynamics in dogs with surgically induced esophageal varices and prehepatic portal hypertension. Reflectance spectrophotometry provides indices of mucosal hemoglobin concentration (IHB) and oxygen saturation (ISO2). Hyperemia (increased IHB, normal ISO2), ischemia without congestion (decreased IHB, decreased ISO2), and ischemia with congestion (increased IHB, decreased ISO2) are accompanied by characteristic patterns of IHB and ISO2. Under anesthesia, measurements were obtained on separate days from the gastric corpus mucosa of eight dogs before and 2 to 10 min after either 1 to 5 units of intravenous vasopressin or 1 mg of propranolol. Results revealed that vasopressin (in doses that significantly reduced variceal and portal venous pressure in this animal model) produced a reduction in both IHB and ISO2, indicating gastric mucosal ischemia secondary to splanchnic vasoconstriction. On the other hand, propranolol in a dose that significantly reduced pulse rate by 27 +/- 2% had no effect on IHB or ISO2, suggesting that this dose of propranolol has no direct vasoactive effect on the gastric (splanchnic) circulation.
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PMID:Endoscopic demonstration that vasopressin but not propranolol produces gastric mucosal ischemia in dogs with portal hypertension. 326 2


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