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)

Thrombolytic agents are being used with increasing frequency to produce reperfusion of acute myocardial infarction in humans. This study was designed to assess the potential of a magnetic resonance (MR) contrast agent, the manganese chelate of N,N'-bis(pyridoxal-5-phosphate) ethylenediamine-N,N'-diacetic acid (DPDP), in differentiating between reversible and irreversible myocardial injury during reperfusion. Ischemia was produced in rats by occlusion of the left coronary artery for either 15 minutes (n = 10) or 2 hours (n = 10), followed in both cases by 30 minutes of reperfusion. Signal intensity (SI) was measured before and after (every 15 minutes for 1 hour) the administration of Mn-DPDP. Prior to intravenous injection of the contrast agent, no significant difference in SI was observed between normal and reversibly or irreversibly injured myocardium. Mn-DPDP produced greater enhancement of SI of the irreversibly injured region compared with normal myocardium. There was no differential enhancement of the reversibly injured region compared with normal myocardium. Thus, Mn-DPDP is useful in discriminating reversible from irreversible injury in reperfused myocardium.
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PMID:Reversible and irreversible injury in the reperfused myocardium: differentiation with contrast material-enhanced MR imaging. 211 68

Fibroblast viability of the allograft valve leaflet has been suggested to affect clinical durability. Warm ischemic time is thought to be one of the critical determinants of cell viability. We assessed cell viability of allograft valves by flow cytometry, using a fluorescein diacetate-propidium iodide stain to characterize the effects of warm ischemia and cryopreservation on viability. Twelve human pulmonary valves with harvest-related warm ischemic times (range, 70 to 520 minutes; mean +/- standard deviation, 225 +/- 157 minutes) were studied by flow cytometry. We assessed cell viability of the allograft valve leaflets before and 30 days after storage. A significant negative correlation was found between warm ischemic time (x minutes) and cell viability (y%) before (y = -0.024x + 96.7; r2 = 0.62; p = 0.002) and after 30 days of storage (y = -0.036x + 94.0; r2 = 0.86; p = 0.001). Cell viability of the cryopreserved allograft valves was well preserved (> 70%) with a warm ischemic time less than 520 minutes (8.7 hours).
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PMID:Effect of warm ischemia and cryopreservation on cell viability of human allograft valves. 764 40

This study was conducted to determine the beneficial effects of treating digestive disorders of (6E,12E)-tetradecadiene-8,10-diyne-1,3-diol diacetate (TDEYA) detected in the plasma in hydrolyzed form: (6E,12E)-tetradecadiene-8,10-diyne-1,3-diol (TDEY), following the oral administration of a decoction of Atractylodes rhizome to rats. Assessment was also made of the efficacy of TDEYA in experimental gastric disorder models. Oral administration of TDEYA at doses of 300 to 500 mg/kg suppressed the formation of gastric lesions induced by indometacin in a dose-dependent manner. TDEYA at a dose of 200 mg/kg suppressed gastric lesions induced by an ischemia-reperfusion injury model. TDEYA at doses of 100 to 300 mg/kg did not show suppressive effects on water immersion stress-induced gastric lesions. TDEYA showed no active oxygen species scavenging action, nor did it have any effect on superoxide dismutase activity in the stomach tissue. TDEYA at doses of 200 to 500 mg/kg significantly suppressed xanthine oxidase (XO) activity in the stomach tissue following its oral administration. The suppressive effects of TDEYA on lesion formation induced by indometacin and ischemia-reperfusion injury models would thus appear to be due in part to the inhibition of XO activity in the stomach tissue.
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PMID:Effects of the acetylene compound from Atractylodes rhizome on experimental gastric ulcers induced by active oxygen species. 787 60

In order to study the possible role of C kinase (PKC) on sodium pump of cerebral vessels, we used diacylglycerol (diC8: sn-1,2-dioctanoylglycerol) and phorbol esters (PMA: phorbol 12-myristate 13-acetate; PDA: phorbol 12,13-diacetate; 4 alpha-P: 4-alpha phorbol) as PKC activators, and examined their effects on Na,K-ATPase activity in rat brain microvessels (MVs). Rats were divided into non-treated (control; n = 9), four-vessel occlusion (4VO; 30-30 minutes ischemia and recirculation, n = 5), and middle cerebral artery occlusion (MCAO, n = 3) groups. MVs were passed through nylon meshes and were obtained by ultracentrifuge at 58000 g. Na,K-ATPase activity in MVs was determined by the phosphomolybdate method. DiC8 enhanced Na,K-ATPase activity at 10(-4) M in the control group, the 4VO group and the contralateral hemispheres of the MCAO group (139% +/- 0.06, 135% +/- 0.2, 133% +/- 0.18, mean +/- SE, p < 0.05, p < 0.01, Wilcoxon rank sum) respectively, but had no effects on MVs in the ipsilateral hemispheres of MCAO group (74% +/- 0.04). This activation by diC8 was inhibited by PKC inhibitors, staurosporine (3 x 10(8) M) and H7 (10(-6) M) in the control MVs. By contrast, PMA suppressed Na, K-ATPase at 10(-5) M in the control group (-25% +/- 0.07), but it tended to activate Na,K-ATPase activity in the ipsilateral hemispheres of the MCAO groups (33% +/- 0.09). PDA and 4 alpha-P did not have any consistent effects at the concentration examined. The cause of difference between the effects of diC8 and PMA is unclear at present, but it may stem from the mode of lipid-membrane interaction in these agents and the difference in the condition of cells as well.
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PMID:Effects of protein kinase C activators on Na, K-ATPase activity in rat brain microvessels. 797 18

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

We have determined the kinetics of the cellular viability ratio (CVR), defined as the number of living cells over the total cell count, in pig kidneys using propidium iodide and fluorescein diacetate staining, as a function of time and preservation conditions. The kidneys were preserved in warm or cold ischemia in order to mimic the conditions of transplantation from non-heart-beating donors or multiple removal with optimal preservation of the graft, respectively. To determine the CVR, the cells were obtained by a fine-needle aspiration biopsy, which minimizes the damage to the graft. A biometric analysis by regression enabled the determination of the time dependence for warm ischemia (CVR(t) = 80.0 x e(-0.733-t)(+2.7/-0.36)) and for cold ischemia (CVR(t) = 80.0 x e(-0.022-t)(+1.57/-0.64)) with a confidence interval of 95%. These master curves allow us to predict, under the described conditions, the CVR after a given ischemia time. The half-life of the cells can be deduced from the time-dependent CVR(t), and is 0.64 hr (38 min) for warm ischemia and 21.4 hr for cold ischemia. Further, the CVR for a given kidney can be used to assess its condition at removal: if the CVR is below 48% at 2 hr after removal, one can conclude that the organ has suffered a period of warm ischemia.
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PMID:Kinetics of cellular viability in warm versus cold ischemia conditions of kidney preservation. A biometric study. 877 93

Polymorphonuclear leukocytes (PMN), atrial natriuretic peptide (ANP) and leukotriene B4 (LTB4) reportedly play a major role in ischemia/reperfusion states of coronary artery disease. We sought to determine whether ANP and LTB4 cooperate in inducing PMN activation with consequent modulation of membrane molecules required for adherence to endothelium and myocardial cells, namely CD11b and L-selectin and the release of toxic oxygen radicals. ANP (from 10(-16) to 10(-8) M), LTB4 (from 10(-10) to 10(-6) M) and combinations of the two were incubated with normal PMN at 37 degrees C for 15 minutes. Membrane molecules modulation was measured by flow cytometry using specific monoclonal antibodies. Hydrogen peroxide production, an indicator of the capacity of PMN to release toxic oxygen species was quantified by flow cytometry using the peroxide-sensitive fluorescent probe dichlorofluorescein diacetate. ANP, uneffective when used alone, dose-dependently potentiated the PMN response to LTB4 (10(-9) M) as evidenced by an up-regulation of CD11b expression and peroxide production, and a down-regulation of L-selectin expression. These effects were prevented dose-dependently by the protein kinase C (PKC) inhibitor staurosporine (from 10 to 160 microM). Two carnitine congeners, palmytoylcarnitine (tested from 125 pg to 2 micrograms/ml) that also possesses an established ability to antagonise PKC and L-carnitine (tested from 12 to 200 ng/ml) were also effective. These data indicate that ANP potentiates LTB4 in inducing PMN mobilization and activation with a possible consequent detrimental effect on cardiac tissue and evisages the usefulness of PMN metabolism modulators.
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PMID:Potentiation of human polymorphonuclear leukocyte activation by atrial natriuretic peptide. Inhibitory effect of carnitine congeners. 892 47

Myocardial protection is usually studied in vitro on perfused heart preparations, but never directly on cultured cardiomyocytes. We evaluated a model of cultured newborn rat cardiomyocytes to study both the cytotoxicity and the protective effect against chemical hypoxia of three cardioplegic solutions (St Thomas' I, Bretschneider, St Thomas' II) under normothermic (37 degrees C) and hypothermic (4 degrees C) conditions. Cytotoxicity was evaluated in 50% and 100% concentrations of the cardioplegic solutions with incubation times from 90 to 360 min. Myocardial protection was studied in 50% cardioplegic solution with metabolic inhibitors. Immediate and late viabilities, after 24 h of recovery in the medium, were evaluated by simultaneous staining with fluorescein diacetate and propidium iodide. At 37 degrees C, the 50% concentration of the three cardioplegic solutions did not modify cell viability. At 37 degrees C, with 360 min of incubation, the 100% concentration of the St Thomas' I and Bretschneider solutions diminished immediate viability (mean +/- SD; medium 87% +/- 2%; St Thomas' I 58% +/- 5%; Bretschneider 37% +/- 8%; St Thomas' II 89% +/- 3%) as well as late viability (medium 69% +/- 2%; St Thomas' I 32% +/- 3%; Bretschneider 24% +/- 7%; St Thomas' II 65% +/- 4%). At 4 degrees C, immediate and late viabilities were unaffected by cardioplegic solutions. At 37 degrees C, after 360 min incubation time, metabolic inhibitors diminished immediate viability to 29% +/- 1% and late viability to zero. None of the three cardioplegic solutions used at 50% concentration prevented this effect. At 4 degrees C, immediate viability was not significantly affected by metabolic inhibitors (73% +/- 10%), but the use of Bretschneider cardioplegic solution seemed to be detrimental (53% +/- 9%). On the other hand, recovery phase after pretreatment with metabolic inhibitors with or without cardioplegic solutions for 360 min significantly diminished late viability (medium 63% +/- 7%; metabolic inhibitors 17% +/- 8%; St Thomas' I 17% +/- 6%; Bretschneider 8% +/- 6%; St Thomas' II 15% +/- 3%) and again cardioplegia was inefficient. In conclusion, in this in vitro model for the study of cardioplegic solutions, only pure concentrations of the St Thomas' I and Bretschneider solutions under normothermic conditions were cytotoxic. The well-known protective effects of hypothermia against ischemia and reperfusion injury were both reproduced. Therefore, and even though cardioplegia failed to have any protective effect, probably owing to a severe metabolic inhibition, this model may be useful for studying myocardial protection.
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PMID:Validity of a model of cultured myocardial cells for assessment of cardioplegia. 935 21

The arterial ketone body ratio (AKBR) has been proposed as an accurate indicator of liver mitochondrial redox potential. However, the efficacy of the AKBR as a biochemical marker has been recently called into question. To resolve this issue, we studied the effect of temporary vascular occlusion on the AKBR during hepatectomy. Twenty patients undergoing hepatectomy were divided into two groups: those with hepatocellular carcinoma with a history of hepatic cirrhosis (n = 10; cirrhotic group) and those with liver disease without cirrhosis (n = 10; non-cirrhotic group). To minimize blood loss during hepatectomy, temporary vascular occlusion was applied using the Pringle maneuver. Acetoacetate and beta-hydroxybutyrate concentrations in the arterial blood and the AKBR were determined before and after vascular occlusion. In 25% of the two groups combined, the AKBR increased following normothermic ischemia, as compared with the levels prior to clamping; in 20% of cases in the cirrhotic group, it increased immediately following reperfusion, as compared with the levels prior to clamping. Changes in the AKBR during hepatectomy did not correlate with preoperative hepatocellular function. An AKBR of less than 0.7 prior to clamping which persisted during surgery was not a consistent risk factor for postoperative complications. The AKBR was not a useful predictor of liver viability in partial liver resection with temporary vascular occlusion.
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PMID:Arterial ketone body ratio during hepatectomy. 935 69

In this study, we determined whether the retina cell death observed in response to an ischemic-like insult is related to an overactivation of the ionotropic glutamate receptors and/or to a collapse of the energy levels. Cultured chick retina cells were submitted to 'chemical ischemia' by metabolic inhibition with sodium cyanide and iodoacetic acid, which block oxidative phosphorylation and glycolysis, respectively. The assessment of neuronal injury was made spectrophotometrically by quantification of cellularly reduced MTT, which gives information about mitochondrial function, or by staining with fluorescein diacetate (FDA), which correlates with changes in the plasma membrane permeability. 'Chemical ischemia' induced both an acute and a delayed time-dependent degeneration of chick retina cells. We observed that 2 min after the ischemic insult, the levels of ATP were reduced to a minimum. On the other hand, the metabolic inhibition induced the release of aspartate, glutamate and gamma-aminobutyric acid, and the activation of AMPA/kainate receptors during the period of metabolic arrest was partially responsible for the loss of mitochondrial function. However, the NMDA and non-NMDA receptor antagonists (MK-801 and CNQX) did not prevent the plasma membrane damage caused by sodium cyanide and iodoacetic acid. The results show that the collapse of the energy levels, rather than the increase in excitatory amino acids, appears to underlie the observed cell injury, suggesting an important relationship between ischemia-induced depletion of high-energy metabolites and retina cell degeneration.
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PMID:'Chemical ischemia' in cultured retina cells: the role of excitatory amino acid receptors and of energy levels on cell death. 936 12


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