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)

Resting iodine 123-labeled metaiodobenzylguanidine (123I-MIBG) scintigraphy was performed in 19 patients with unstable angina to determine if it can detect myocardial ischemia and identify the angina-provoking coronary artery. Visual assessment of 123I-MIBG single-photon-emission computed tomograms was related to coronary vessel stenoses revealed by arteriography at each vascular territory. Fourteen (74%) of 19 patients had regional 123I-MIBG-identified defects at areas with preserved thallium-201 perfusion. 123I-MIBG defects were highly positive at areas supplied by angina-provoking coronary arteries. The sensitivity and specificity of 123I-MIBG defects for identifying the angina-provoking coronary vessel were 71% and 78%, respectively. The interval between the most recent angina attack and imaging was shorter and the angina occurred more commonly after admission in patients with 123I-MIBG defects than in those without defects. These data suggest that repetitive myocardial ischemia impairs regional 123I-MIBG uptake and that this impairment persists for several days after perfusion has been restored. Thus resting 123I-MIBG scintigraphy is a useful noninvasive method to detect coronary stenoses provoking repetitive ischemia in patients with unstable angina in its acute phase.
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PMID:Detection of angina-provoking coronary stenosis by resting iodine 123 metaiodobenzylguanidine scintigraphy in patients with unstable angina pectoris. 790 Jun 22

Apoptosis, a form of cell death ("programmed" cell death) in which the nucleus and cytoplasm shrink and often fragment, serves to eliminate excessive or unwanted cells during remodeling of embryonic tissues, during organ involution, and in tumor regression. In acute pathological states, such as ischemia, the cells tend to swell and lyse--a process called necrosis. We hypothesize that the delayed neural death clinically associated with hypoxia may, in part, represent apoptosis. A tissue culture model of 24 hours of hypoxia was employed using sympathetic neurons. Pretreatment with an endonuclease inhibitor (aurintricarboxylic acid) decreased cell death by 53%, depolarizing conditions (55 mM potassium chloride) decreased cell death by 33%, and an RNA synthesis inhibitor (actinomycin D) by 26% (all have been shown to prevent apoptosis). Pretreatment with antisense c-myc had no effect. Fluorescent staining with propidium iodide (a DNA marker) demonstrated chromatin condensation and agarose gel electrophoresis demonstrated a DNA "ladder." These data suggest that apoptosis may play a role in hypoxic cell death and that in this paradigm, expression of c-myc is unnecessary. This would suggest a new approach to our understanding of hypoxia and open new strategies to lessen neuronal damage secondary to this process.
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PMID:Evidence for hypoxia-induced, programmed cell death of cultured neurons. 799 72

Quantitation of myocardial blood flow has been sought by the clinician using a variety of imaging modalities and blood indicator dilution techniques. Ultrafast computed tomography has real potential for clinically useful estimations of regional myocardial blood flow. At the present time, there are limitations with this technique and early washout of indicator (iodine) appears to be the most likely explanation for the inaccuracies observed. Several methods have been tried to correct for early washout without success. Preliminary data based on a new algorithm look promising. Currently available techniques for detecting and quantifying myocardial ischemia have significant limitations. A noninvasive method able to determine wide ranges of flow with accuracy will be essential to understand the pathophysiology of ischemia and for directing better methods of managing ischemic heart disease.
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PMID:Ultrafast computed tomography for the physiological evaluation of myocardial perfusion. 803 87

Previous studies have revealed that the sympathetic nervous system is more vulnerable to ischemia than the myocardium itself. Thus our study was undertaken to detect denervated myocardium in non-Q-wave myocardial infarction (MI) and unstable angina with iodine 123 metaiodobenzylguanidine (123I-MIBG), which can delineate myocardial sympathetic innervation. Eight patients with non-Q-wave MI and 12 with unstable angina were studied. Sequential 123I-MIBG and thallium-201 chloride (201TlCl) imaging and single-photon emission computed tomography (SPECT) were performed at rest 24 +/- 12 days after the last ischemic attack. Myocardial perfusion defect was not detected by 201TlCl in 4 of 8 patients with non-Q-wave MI, whereas 123I-MIBG SPECT imaging revealed defects corresponding to myocardial ischemic areas predicted by coronary angiography in all 8 patients. 123I-MIBG imaging revealed defects in 7 of 12 patients with unstable angina corresponding to coronary angiographic findings, whereas no myocardial perfusion defect was detected by 201TlCl imaging in any of them. In conclusion, 123I-MIBG SPECT is a sensitive method for detecting myocardium exposed to transient ischemia that cannot be detected by 201TlCl imaging.
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PMID:Regional sympathetic denervation detected by iodine 123 metaiodobenzylguanidine in non-Q-wave myocardial infarction and unstable angina. 807 4

To assess the clinical value of simultaneous dual myocardial imaging with iodine-123-beta-methyl-iodophenyl-pentadecanoic acid (123I-BMIPP) and thallium-201 (201Tl), myocardial imaging was performed at rest and during exercise in seven patients with coronary heart disease. When 123I-BMIPP and 201Tl images were compared, the initial exercise and resting images agreed 87% and 64%, respectively. In the initial resting images, the regional uptake of 123I-BMIPP was frequently less than that of 201Tl. The incidence of exercise-induced reversible defects by 201Tl in the Tl > BMIPP regions was significantly higher than that in the Tl = BMIPP regions (57% vs 4%, p < 0.01) and the incidence of coronary narrowing of more than 90% in the Tl > BMIPP regions was also significantly higher than that in the Tl = BMIPP regions (91% vs 38%, p < 0.01). In addition, this disparity (Tl > BMIPP) was found more frequently in regions with abnormal wall motion than in regions with normal wall motion (hypokinetic regions; 68%, severe hypokinetic or akinetic regions; 50%, vs normokinetic region; 4%, p < 0.01). In contrast, the uptake of 123I-BMIPP correlated closely with that of 201T1 in normal myocardium and the uptake of both 123I-BMIPP and 201Tl was severely reduced in myocardium with severe ischemia during exercise and prior infarction. These results indicate that dual myocardial imaging with 123I-BMIPP and 201Tl may provide a unique means of identifying patients with metabolically disturbed myocardium, such as hibernating and stunned myocardium.
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PMID:Simultaneous dual myocardial imaging with iodine-123-beta-methyl iodophenyl-pentadecanoic acid (BMIPP) and thallium-201 in patients with coronary heart disease. 819 52

Effects of hypoxia, substrate deprivation and simulated ischemia (combined hypoxia and substrate deprivation) on cell survival during the insult itself and during a 24 h 'recovery' period were studied in primary cultures of mouse astrocytes and in cerebral cortical neuronal-astrocytic co-cultures. Cell death was determined by release of the cytosolic high molecular enzyme lactate dehydrogenase (LDH) as well as morphologically (retention of staining with rhodamine 123 and lack of staining with propidium iodide as an indicator of live cells). Glutamate concentrations were measured in the incubation media at the end of the metabolic insults. Astrocytes were very resistant to hypoxia, but less so to simulated ischemia; under both conditions the glutamate concentrations in the media remained low. Cerebral cortical neurons were almost equally susceptible to damage by hypoxia and by simulated ischemia, although hypoxia had a faster deleterious effects on some of the neurons and simulated ischemia during a long-term insult (9 h) killed all neurons, whereas a non-negligible neuronal subpopulation survived 9 h of hypoxia. Neuronal cell death after long-term hypoxia (but not after simulated ischemia) was correlated with high concentrations of glutamate in the incubation media. After certain insults, most notably relatively short lasting simulated ischemia (3 h) in neurons (which caused no increased cell death during the insult), there was a large release of LDH during the 'recovery' period.
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PMID:Cell death in primary cultures of mouse neurons and astrocytes during exposure to and 'recovery' from hypoxia, substrate deprivation and simulated ischemia. 819 61

We report a patient with an unruptured, large arteriovenous malformation that was treated by staged, superselective embolization with liquid agents and by an investigation of the hemodynamic changes accompanying embolization. A 29-year-old man presented with headache and left upper quadrantanopsia. A neuroradiological study revealed a large right temporo-occipital arteriovenous malformation, and angiography disclosed poor filling of the adjacent vessels. In the venous phase, marked cortical reflux, suggesting venous hypertension, was also observed. Single photon emission computed tomography scanning with N-isopropyl-p-iodine-123- iodoamphetamine disclosed a low-perfusion area in the ipsilateral occipital and temporal lobes. After embolization, cerebral blood flow and the clinical symptoms attributed to ischemia improved. A follow-up study 1 year later demonstrated that the patient's improvement was stable. Single photon emission computed tomography confirmed that embolization achieves an improved cerebral blood flow.
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PMID:Improvement of cerebral blood flow and clinical symptoms associated with embolization of a large arteriovenous malformation: case report. 823 19

When in some selected patients, a direct arterial surgery (DAS) procedure or an endoluminal surgery (ES) are required for a chronic arterial ischemia (III or IV degrees), and an arteriography with contrast is absolutely contraindicated (because of severe renal failure without hemodialysis program or a severe congestive heart failure or a hyperthyroidism or a seriously demonstrated hypersensibility against the contrast agents); an angiography by digital subtraction with carbon dioxide (DIVAS-CO2) is indicated. This technique provides good quality images with minimal risks for the patient and an adequate study for ulterior treatment. We report a case of a 67-years-old woman, with diabetes-II, ischemic cardiopathy, arterial hypertension and a demonstrated hypersensibility against the iodide compounds. The patient was admitted because of a chronic ischemia (IV degree) with ischemic ulcerations on some fingers from the left foot. High doses of analgesic drugs were needed. Because the hypersensibility against the iodide compounds, an angiography with CO2 was carried out. The good quality images provided by this technique showed the factibility of a revascularization.
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PMID:[Digital subtraction angiography with carbon dioxide in severe arterial ischemia and allergy to iodinated compounds]. 839 9

Peroxide production in cultures of Saccharomyces cerevisiae was measured using the H2O2-sensitive fluorescent probe 2',7'-dichlorofluorescein diacetate (DCFH-DA) and flow cytometry. Aeration of cultures of S. cerevisiae exposed to a period of hypoxia was found to induce elevated levels of peroxide that were 100-fold higher than the levels observed in cultures maintained under exclusively aerated or hypoxic conditions. Simultaneous viability analysis, using the fluorescent DNA-intercalating dye propidium iodide, indicated that the increase in peroxide generation preceded cell damage and death. Various agents were found to influence the effect of peroxides on cell viability. The addition of ethanol to hypoxic stationary cultures dramatically increased the rate of cell death without further increasing the amount of peroxide produced, while glucose inhibited peroxide production and decreased the rate of cell death. Surprisingly, elevated peroxide levels of hypoxic/reaerated cultures were maintained upon addition of KH2PO4, although the cells remained viable for extended periods of time when compared to control and other test cultures. Similarities between our observations and those of other investigators using anoxic/reperfused organs suggest that hypoxic/reaerated yeast cultures may be a useful model system to study ischemia-dependent tissue destruction of mammals.
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PMID:Characterization of hypoxia-dependent peroxide production in cultures of Saccharomyces cerevisiae using flow cytometry: a model for ischemic tissue destruction. 847 5

Synovial perfusion was quantified in milliliters per minute per knee by two quite different clearance methods based on (1) counting tritiated water in serial aspirates of intraarticular saline, and (2) external counting of joints injected with free radioiodide. In each case, the serial counting data determine a rate constant that is multiplied by a distribution volume to provide the clearance in flow terms of milliliters per minute. This report updates and summarizes these data and compares the two methods to each other and to alternative assessments of synovial blood flow. Available methods such as laser Doppler flowmetry (with data output measured in volts) and solute clearance constant determinations (in min-1) are useful for selected purposes but cannot be used to quantify the articular flux (in milligrams per minute) of any solute. Radiolabeled microspheres provide data (in milliliters per minute per g of tissue) but are unsuitable for human use. The two clearance methods provide comparable results, but the free iodide technique seems most suitable for physiologic investigations. The latter potentially includes critical evaluations of synovial blood flow in relation to issues such as palpable warmth, visible erythema, articular ischemia, the permeability of synovial vessels, the genesis of effusions, the delivery and removal of therapeutic agents, and the concentration of every synovial fluid solute from micronutrients through cytokines, plasma proteins, and molecular markers of cartilagenous injury.
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PMID:Synovial perfusion in the human knee: a methodologic analysis. 852 91


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