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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma polyps can be found at the end of a normal pregnancy. Following NaF and MJA-intoxication, there is an extreme increase of plasma polyps. This accelerated formation can be prevented by the injection of Na-pyruvate and often the number of polyps can be reduced below the norm. 2,4-Dinitrophenol intoxication and breathing of hypoxic gas mixture (2,5% O2, 5% CO2, 92,5% N2) do not lead to increased plasma polyp formation. This proves, that it is not hypoxia, not an energy deficit secondary to separation of oxydative phosphorylation and not cardiac insufficiency leading to secondary ischemia which are responsible for the extreme increase in the number of plasma polyps following the injection of MJA and NaF.
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PMID:[The effect of 2,4-dinitrophenol, monoiodine acetate, sodium fluoride and hypoxia on the formation of plasma polyps in the placenta of guinea pigs (author's transl)]. 99 63

Responses of heart rate (HR), mean arterial blood pressure (MAP) ventilation (VE), and forearm blood flow (FBF) to different degrees of leg muscle ischemia were measured in eight subjects in a four-part experiment. Part I. Total circulatory occlusion (OCCL) of resting legs for 15 min had little or no effect on HR, MAP, VE, or FBF. Part II. OCCL of the legs for 3 min immediately after exercise at 50-250 W did not affect HR or end-tidal CO2; it lowered VO2 and VE and prevented recovery of MAP. Part III. OCCL beginning at end and 10, 20, 30 s before end of 7-min exercise (100-150 W) and continuing 3 min into recovery period produced sustained and graded increments (5-10 mmHg) in MAP, only small changes in HR, and accelerated recovery of VE while end-tidal CO2 remained constant. Part IV. OCCL at end and 30 s before end of exercise increased FBF 2.5-3.5 times; both skin and muscle vasodilated. Thus muscle ischemia preceded by exercise can raise MAP without affecting VE, whereas baroreflexes may lower HR and raise FBF. The results suggest the presence of muscle chemoreceptors whose major effect is on MAP.
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PMID:Human cardiovascular and respiratory responses to graded muscle ischemia. 99 57

The fetal mouse heart (FMH) in organ culture continues to beat for a period of weeks, but degenerative changes occur. Electron microscopy revealed formation of autophagic vacuoles containing damaged organelles in some cells after the first day, indicating focal cytoplasmic injury. This process was accelerated by transient deprivation of oxygen and glucose followed by resupply of oxygen and glucose. FMHs were maintained for up to four hours in glucose-free media in an atmosphere of 95% N/5% CO2 followed by resupply of O2 and glucose. Twenty-four hours later, many cells recovered without residual injury. Many others revealed autophagic vacuoles ranging from those in which organelles were readily identified to those characteristic of residual bodies. It appears that focal injury stimulates the endoplasmic reticulum to enclose the damaged components, permitting localized lysosomal digestion without causing injury to the entire cell. Autophagy has not been emphasized as an important mechanism in transient ischemia in adult myocytes, but it may play a role in repair of sublethal injury. The FMH organ culture provides an excellent model for studying the sequential autophagic changes in a system in which these events can be accelerated.
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PMID:Autophagy in cardiac myocytes. 103

A comparison of regional cerebral blood flow measurements made with beta- and gamma-emitting isotopes revealed good correspondence in areas of normal perfusion and reactive hyperemia but poor correspondence in areas of focal ischemia. After middle cerebral artery occlusion at normocapnia, there was a 65% reduction in regional cerebral blood flow from 1.40 plus or minus 0.27 ml/g min--1 to 0.49 plus or minus 0.10 ml/g min--1 in monkeys studied with 85Kr but only a 27% reduction in regional cerebral blood flow from 0.84 plus or minus 0.09 ml/g min--1 to 0.61 plus or minus 0.08 ml/g min--1 in monkeys studied with 133Xe. The lack of correlation within areas of focal, incomplete ischemia was attributed to an impairment of isotope delivery to the area of ischemia coupled with the inherent lack of spatial resolution of determinations made with 133Xe. This finding may partly explain the numerous discrepancies in experimental and clinical studies of the effects of alterations in the arterial partial pressure of CO2 on regional cerebral blood flow in areas of ischemia; it may also explain the failure of such studies to reflect the true severity of focal ischemia.
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PMID:Comparison of 85krypton and 133xenon cerebral blood flow measurements before, during, and following focal, incomplete ischemia in the squirrel monkey. 111 19

In isolated perfused rabbit hearts, coronary vasodilation, produced by reduced oxygen tension seems to be independent of myocardial prostaglandin biosynthesis. a) Anoxia (N2: CO2 95: 5 %) produced coronary vasodilation without causing prostaglandin-like substance (PLS) biosynthesis and release; b) the decrease in coronary resistance during hypoxia (N2:02:CO2 - 80:15:5 %) was sustained during myocardial perfusion with the low oxygen media despite the transitory nature of its PLS release; and c) indomathacin, which abolished basal or ADP stimulated myocardial PLS release, did not abolish the coronary vasodilation produced by ischemia, hypoxia, or anoxia.
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PMID:Relationship between oxygen tension, coronary vasodilation and prostaglandin biosynthesis in the isolated rabbit heart. 113 23

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79

Tracer kinetic studies on the effect of i.v. infused adrenaline and angiotensin, and a hyperglycemia induced by glucose application, upon glucose metabolism of the rat brain under ischemic and normoxic conditions are reported. in the ischemic brain, the initial glycolytic rate proved dependent on the glucose content being kept at various levels by glucose administration or hormone infusion prior to the onset of ischemia. The typical saturation kinetics revealed a maximal glucose conversion only from a definite initial content of brain glucose, being equivalent to a glucose level of approximately 13 mumole/ml in plasma, and appeared to depend on the presence of glucose in the cellular space. The early cessation of anaerobic lactate formation even with high glucose in the cellular space. The early cessation of anaerobic lactate formation even with high glucose depot in the brain tissue is referred to inhibition of glycolytic key enzymes by increasing tissue azidosis. The aerobic glucose conversion, as calculated from the Cglucose flux in amino acids associated with the citrate cycle was unaffected by the cerebral glucose content (hyperglycemia by hormone or glucose application). During glucose infusion the cerebral levels of NH3, total NH2 and glutamine rose; the Cglucose flux into aspartate and glutamine was increased and almost proportionally reduced in glutamate and gamma-aminobutyrate. These flux shifts are interpreted as a switching of C-chains from pyruvate owing to increased CO2 fixation, and as a biochemical correlate of an increased irritation level of the experimental animals.
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PMID:[Effect of increased plasma levels of glucose, adrenaline, and angiotensin upon glucose metabolism of totally ischemic and normally perfused rat brain]. 123 36

The effect of hypothermic ischemia on alpha-1 and -2 adrenergic receptor mediated vasoconstriction has been studied in an in vitro perfused canine tibia preparation. Bones were perfused at a constant rate with aerated (95% O2, 5% CO2) modified Krebs Ringer solution and the effect of bolus injections of norepinephrine (0.025-6.4 nmol) on the perfusion pressure was studied. For all bones the first dose-response curve was produced under control conditions. In one group the second dose-response curve was generated during a constant infusion of prazosin (alpha-1 adrenergic antagonist); in another it was produced during a constant infusion of rauwolscine (alpha-2 adrenergic antagonist); in the control group it was generated under control conditions. The results demonstrate that, after 48 h of hypothermic ischemia, alpha-1 adrenergic-mediated vasoconstriction was significantly attenuated (p less than 0.001). However, alpha-2 adrenergic-mediated vasoconstriction was unaffected by increasing periods of hypothermic ischemia.
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PMID:The effect of hypothermic ischemia on the alpha-adrenergic mechanisms of the canine tibia vascular bed. 130 85

The purpose of this study was to assess whether proximal renal tubules generate excess hydroxyl radical (.OH) during hypoxia/reoxygenation or ischemia/reperfusion injury, thereby supporting the hypothesis that reactive oxygen species contribute to the pathogenesis of postischemic acute renal failure. In the first phase of the study, rat isolated proximal tubular segments (PTS) were subjected to hypoxia (95% N2- 5% CO2) for 15, 30, or 45 min, followed by 15 to 30 min of reoxygenation in the presence of sodium salicylate, a stable .OH trap. Cellular injury after hypoxia and reoxygenation was assessed by lactate dehydrogenase release; .OH production was gauged by hydroxylated salicylate by-product generation (2,3-, 2,5-dihydroxybenzoic acids (DHBA); quantified by HPLC/electrochemical detection). Continuously oxygenated PTS served as controls. Despite substantial lactate dehydrogenase release during hypoxia (8 to 46%) and reoxygenation (8 to 11%), DHBA production did not exceed that of the coincubated, continuously oxygenated control PTS. In the second phase of the study, salicylate-treated rats were subjected to 25 or 40 min of renal arterial occlusion +/- 15 min of reperfusion. No increase in renal DHBA concentrations occurred during ischemia or reperfusion, compared with that in sham-operated controls. To validate the salicylate trap method, PTS were incubated with a known .OH-generating system (Fe2+/Fe3+); in addition, rats were treated with antioxidant interventions (oxypurinol plus dimethylthiourea). Fe caused marked DHBA production, and the antioxidants halved in vivo DHBA generation. In conclusion, these results suggest that exaggerated .OH production is not a consequence of O2 deprivation/reoxygenation tubular injury.
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PMID:Evidence against increased hydroxyl radical production during oxygen deprivation-reoxygenation proximal tubular injury. 131 20

Zinc is a potent inducer of the 72 kD heat shock protein (HSP72). In brain, pathological conditions such as ischemia and seizures increase extracellular zinc. The present study examines the effect of zinc on HSP72 expression in rat primary cortical astrocyte culture. Astrocytes were grown to confluence and exposed to zinc chloride in CO2-equilibrated Earle's buffered salt solution. Expression of HSP72 was examined using immunocytochemistry. HSP72 was induced with zinc concentrations of 5 to 100 microM after 4 h exposures, or 200 to 300 microM after 15 min exposures. At the lower concentrations expression occurred in small clusters of contiguous cells. At concentrations high enough to cause cell death, HSP72-positive astrocytes formed a continuous margin around patches of dead cells. These patterns of HSP72 expression are similar to the patterns seen after cerebral ischemia in vivo. Exposure to zinc at 100 microM for 4 h or 400 microM for 15 min caused greater than 90% cell death. Increases in extracellular zinc may contribute to HSP72 induction and astrocyte death under ischemia and other pathological conditions in brain.
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PMID:Zinc toxicity and induction of the 72 kD heat shock protein in primary astrocyte culture. 133 69


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