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 investigate the diagnostic value of carbon dioxide arteriograms in patients with peripheral vascular disease, ten patients in whom standard contrast arteriography was contraindicated underwent carbon dioxide digital subtraction arteriography. Lower extremity ischemia or severe hypertension with renal insufficiency were the indications for arteriography. Standard contrast arteriography was precluded by chronic nondialysis-dependent renal insufficiency, severe congestive heart failure or contrast hypersensitivity. All critical arterial segments were well visualized with the exception of the infrapopliteal arterial tree in three patients. Adequate imaging of this segment required the addition of 20 cc of dilute nonionic contrast. Guided by carbon dioxide digital subtraction arteriography, four percutaneous transluminal angioplasties and three reconstructive procedures were successfully performed. One patient did not have surgically reconstructible disease and two had renal arteries without critical stenoses. Renal function transiently deteriorated in one patient who received 20 cc of nonionic contrast. No adverse events occurred due to carbon dioxide. Clinically useful diagnostic arteriograms are possible using carbon dioxide as the contrast agent.
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PMID:Carbon dioxide digital subtraction arteriography: a pilot study. 212 Dec 15

The effect of anoxia and reoxygenation on the synthesis and secretion of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) was studied in primary cultures of human umbilical vein endothelial cells. Sublethal anoxia, determined by trypan blue dye exclusion and lactate dehydrogenase release, was produced by cell culture under a 95% N2, 5% CO2 atmosphere for 2-24 h and was followed by reoxygenation with 95% air, 5% CO2 for 24 or 48 h. Anoxia did not alter the levels of mRNA for t-PA or PAI-1 in the cells or the secretion of t-PA or PAI-1 into the medium. At 24 h, t-PA secreted into conditioned medium was 7.0 +/- 1.4 ng/2 x 10(6) cells (n = 9) and PAI-1 was 300 +/- 13 IU/2 x 10(6) cells (n = 9), whereas the content of t-PA mRNA was 2.2 pg/micrograms of RNA and PAI-1 mRNA was 180 pg/micrograms of RNA. During reoxygenation, however, t-PA antigen and PAI-1 activity as well as mRNA for PAI-1 decreased proportionally to the duration of anoxia, to reach 27 +/- 1.0, 49 +/- 2.0, and 47 +/- 14% of control values, respectively, within 24 h of anoxia. t-PA mRNA also decreased significantly during reoxygenation following anoxia, but the extent could not be accurately quantitated. Addition, during anoxia, of a 200 micrograms/ml concentration of the superoxide anion radical scavenger superoxide dismutase or of a 5 mM concentration of the iron chelator deferoxamine mesylate prevented the subsequent decrease of t-PA antigen during reoxygenation; addition of these compounds during reoxygenation had no effect. Superoxide dismutase, but not deferoxamine mesylate, when added during anoxia prevented the subsequent decrease in PAI-1 activity. These studies suggest that the marked alteration of endothelial cell fibrinolysis during anoxia followed by reoxygenation is most likely mediated by a mechanism dependent on oxygen radicals. Impaired endothelial cell fibrinolysis may contribute to the pathophysiology of ischemia/reperfusion injury.
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PMID:Oxygen radicals generated during anoxia followed by reoxygenation reduce the synthesis of tissue-type plasminogen activator and plasminogen activator inhibitor-1 in human endothelial cell culture. 212 75

The effect of pH regulation on the function of the isolated neonatal heart during continuous hypothermic perfusion and arrest was tested in 3- to 6-day-old piglet hearts. Three groups of hearts were perfused from an adult support pig, with pH varied by a carbon dioxide/oxygen gas exchanger and temperature controlled by a heat exchanger. After control function studies were obtained at normothermia with a pH of 7.4, the hearts were cooled over 15 minutes to 10 degrees C. Hypothermic perfusion was maintained for 1 hour, followed by rewarming to 37 degrees C. In group 1 (n = 5), the alpha stat (neutral) model, the blood perfusate was maintained at a pH of 7.4 (calculated at 37 degrees C). In group 2, the alkaline model, the pH was maintained at 7.9, and in group 3, the pH-stat (acid) model, the pH was maintained at 7.0. In addition, the effect of 1 hour of hypothermic ischemia after hypothermic perfusion at a pH of 7.0 was evaluated in five hearts (group 4). After rewarming no significant difference was noted in functional recovery (group 1 = 93% +/- 5%, group 2 = 92% +/- 6%, group 3 = 96% +/- 5%, and group 4 = 95% +/- 2%), oxygen consumption, coronary resistance, lactate extraction, and myocardial extravascular water content. We conclude that neonatal heart function is resistant within the range of this study to changes in pH caused by changes in carbon dioxide tension during hypothermic perfusion and ischemia.
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PMID:Effect of PCO2-adjusted pH on the neonatal heart during hypothermic perfusion and ischemia. 212 78

1. The aim of this study was to examine the rapid changes in extracellular hydrogen ion activity [( H+]o or pHo) which are associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion. Two parallel studies were performed with different rat models of ischemia: repetitive severe ischemia produced in anesthetized animals by occlusion of the vertebral and carotid arteries and temporary interruption of blood flow in isolated brain. [H+]o and direct current potential (DC potential) were recorded simultaneously in all experiments. Examination of these two parameters was supplemented by recording tissue concentration of carbon dioxide (PtCO2) in the four-vessel occlusion model and assaying major metabolites involved in energy production in experiments with isolated brains. 2. Measurements of [H+]o during ischemia consistently revealed a steady increase of [H+]o on which was superimposed an abrupt and transient fall in [H+]o closely related to the occurrence of the fast negative shift of DC potential characterizing brain-cell depolarization. Analysis of the relationship between the magnitude of the transient fall in H+ and the level of [H+]o at which this occurred showed that the amplitude of the transient fall in H+ increased with tissue acidosis. 3. We propose that this phenomenon is indirect evidence that rapid transfer of acid equivalents occurs across the plasmalemma, concomitantly to its depolarization. Both events probably result from a common cause, i.e., nonspecific increase of the cell-membrane permeability to ions subsequent to opening of membrane channels. 4. Early on during recirculation, an acidotic [H+]o shift associated with membrane repolarization was clearly visible whenever the ionic gradients recovered rapidly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A rapid redistribution of hydrogen ions is associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion. 212 59

The effects of non-competitive N-methyl-D-aspartate receptor antagonists on amnesia induced by carbon monoxide (CO) were investigated, since they have neuroprotective effects on delayed degeneration induced by ischemia. In the mice exposed to CO, acute and delayed amnesia were induced. (+)-MK-801 and (-)-MK-801 improved the delayed amnesia, but the effects of phencyclidine (PCP) were weak. (+)-MK-801 and PCP potentiated the acute amnesia. From these results, it is suggested that there is a stereoselectivity in the effects of MK-801 on CO-induced amnesia and that CO-induced delayed amnesia animals could be used as an ischemic amnesia model.
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PMID:MK-801 ameliorates delayed amnesia, but potentiates acute amnesia induced by CO. 215 27

With the use of microelectrodes, intracellular pH (pHi), surface pH (pHs), and intracellular Na+ activity (aiNa) were measured in isolated guinea pig papillary muscles during normal superfusion and during a reversible condition of simulated ischemia. Acid loading by NH+4 prepulse or by CO2-HCO3- addition during superfusion with pH 7.4 solutions caused internal acidification followed by a recovery of pHi, which could be inhibited by amiloride. pHi recovery was associated with an amiloride-sensitive peak rise of aiNa and membrane hyperpolarization, indicative of Na(+)-H+ exchange. Peak increase of aiNa was absent if the pH of the superfusion solution was concomitantly lowered. Imposed ischemia after control superfusion caused membrane depolarization and acidification of pHi and pHs. The change of pHs consistently was larger than that of pHi. aiNa decreased from 5.5 to 4.6 mM after 10-min ischemia. Enlarging the pHi (and pHs) decrease in ischemia by prior reduction of the tissue buffer capacity (CO2-HCO3(-)-free superfusion) was unable to induce a rise of aiNa during the subsequent ischemic period. Amiloride had no significant effect on aiNa during ischemia. It is concluded that the important acidification of pHs reduces the rate of pHi regulatory Na(+)-H+ exchange and thereby contributes to a longer maintenance of the Na+ electrochemical gradient in ischemic cardiac muscle.
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PMID:Acidification and intracellular sodium ion activity during stimulated myocardial ischemia. 216 81

The effect of ischemia reperfusion or hypoxia reoxygenation on pulmonary vascular permeability and resistance was studied in 25 isolated blood-perfused dog lungs. Vascular permeability, assessed by determining filtration coefficient (Kf), and vascular resistances were measured at the beginning and end of the experiment. Ischemia reperfusion was produced by occluding blood flow to the lung for 3 h and reperfusing for 1 h, whereas hypoxia reoxygenation was obtained by ventilating the lung with 95% N2-5% CO2 for 3 h and then ventilating with 95% O2-5% CO2 for 1 h with no interruption of perfusion. There was a significant increase in Kf in both ischemia reperfusion and hypoxia reoxygenation groups (51 and 85%, respectively), and total vascular resistance increased greatly in both groups (386 and 532%, respectively). Two additional groups were also studied in which the ischemia reperfusion or hypoxia reoxygenation lungs were pretreated with allopurinol (20 micrograms/ml). The Kf did not significantly increase in either the allopurinol ischemia reperfusion or the allopurinol hypoxia reoxygenation groups (22 and 6%, respectively). However, total vascular resistance significantly increased in both groups (239 and 224%, respectively). Although vascular permeability is modestly increased by both ischemia reperfusion and hypoxia reoxygenation, the predominant change in these conditions is the increased vascular resistance, which predominantly affects the postcapillary resistance and would result in a greater tendency for edema to develop in these slightly damaged lungs. Allopurinol, which inhibits xanthine oxidase, attenuated the permeability changes in both groups and may be useful in preventing ischemia reperfusion injury in certain conditions.
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PMID:Effect of ischemia reperfusion or hypoxia reoxygenation on lung vascular permeability and resistance. 222 71

We tested the hypothesis that 1- to 2-wk-old pigs (piglet) have improved recovery of cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and somatosensory-evoked potentials (SEP) compared with 6- to 8-mo-old pigs (pig) after transient global cerebral ischemia. All animals were anesthetized with pentobarbital sodium. After tracheostomy ventilation was adjusted to maintain normoxia (arterial oxygen pressure, 100-150 mmHg) and normocarbia (arterial carbon dioxide pressure, 35-40 mmHg). Arterial blood gases, blood pressure, and hemoglobin concentration remained within physiological limits throughout the experiment. Cerebral ischemia was produced by sequentially tightening ligatures around the inferior vena cava and ascending aorta. During ischemia the electroencephalogram and SEP became isoelectric within 40 and 120 s, respectively. At 10 min of reperfusion hyperemia occurred in most brain regions (e.g., whole brain: piglet, 270 +/- 45%; pig, 316 +/- 48%). In pigs delayed hypoperfusion occurred in all regions except white matter. In contrast, piglets only had delayed hyperperfusion to the brain stem and caudate nucleus. Throughout reperfusion CMRO2 was decreased in pigs (3.3 +/- 0.4 to 1.9 +/- 0.2 ml.min-1.100 g-1) but was not different from control (2.7 +/- 0.3 ml.min-1.100 g-1) in piglets. By the end of reperfusion SEP amplitude was closer to control in piglets than pigs (55 +/- 9 vs. 32 +/- 4% of control). We conclude that 1- to 2-wk-old piglets have quicker return of CBF, CMRO2, and SEP to control values after global ischemia, which mechanistically may explain previous reports of improved neurological recovery in young animals after transient ischemia.
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PMID:Age-related cerebrovascular response to global ischemia in pigs. 224 Feb 52

The protective effect of KB-2796, a new calcium antagonist possessing a selective vasodilator activity on cerebral vessels in cerebral hypoxia and ischemia, was investigated in both in vivo and in vitro. KB-2796 showed an apparent protective potency against complete ischemia induced by decapitation, normobaric hypoxia and KCN-induced death in mice. KB-2796 (50 mg/kg, p.o.) significantly prolonged survival time in gerbils with bilateral carotid ligation. In guinea-pig hippocampal slices, the amplitude of the population spike recorded from the dentate granule cell layers, in response to electrical stimulation of the perforant path, gradually decreased during mild hypoxia (20% O2 + 75% N2 + 5% CO2), with a tendency to recover to pre-hypoxic levels during reoxygenation (95% O2 + 5% CO2). Pretreatment with KB-2796, at a concentration of 1 microM, significantly accelerated the recovery of the population spike during the reoxygenation period. These results suggest that the protective effect of KB-2796 in cerebral hypoxia and ischemia is due in part to a mechanism independent of its effects as a cerebral vasodilator.
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PMID:Protective effect of KB-2796, a new calcium antagonist, in cerebral hypoxia and ischemia. 224 12

The aim of this study was to investigate the oxygenation of the gastrointestinal tract mucosa using indirect pH measurements in a porcine septic model (intravenous infusion of live E. coli). By means of intraluminally placed balloon catheters (Tonomitior) permeable to CO2, intramucosal pH (pHi) was calculated using the Henderson-Hasselbalch equation. Cardiopulmonary hemodynamics and portal blood flow were measured using Swan-Ganz catheters. Samples were taken from the gastrointestinal tract for histological examination. Nine pigs were given i.v. E. coli infusion while six pigs served as sham controls and were given an equivalent amount of Ringer's solution only. All septic animals developed hemodynamic signs of septic shock. Gastric, small intestinal and sigmoid colonic pHi decreased gradually during the four hour observation period. In the small intestine and the sigmoid colon the decrease was significant already after one hour (p less than 0.01 and p less than 0.02, respectively). Microscopic examination of tissue specimens obtained 4 hours following induction of sepsis revealed normal or close to normal findings in all the sham and in more than half of the septic animals. These findings indicate that abnormally low gastrointestinal intramucosal pH may be found early in septicemia, preceding microscopically detectable damage by several hours. It is concluded that the tonometer technique does provide early detection of gastrointestinal ischemia in septic shock.
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PMID:Early detection of gastrointestinal mucosal ischemia in porcine E. coli sepsis. 226 40


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