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)

Taurine and glutamine are the most abundant intracellular free amino acids in mammalian hearts where changes in their intracellular concentrations are likely to influence a number of cellular activities. In this study we investigated the effects of ischaemia and reperfusion on the intracellular concentrations of taurine and glutamine in the hearts of patients undergoing coronary artery bypass surgery using cold crystalloid or cold blood cardioplegic solutions. Ischaemic arrest (30 min), using cold crystalloid cardioplegic solution (n = 19), decreased the intracellular concentrations (micromol/g wet weight) of taurine (from 9.8 +/- 0.8 to 7.7 +/- 0.7, P < 0.05) and glutamine (8.7 +/- 0.5 to 7.2 +/- 0.6). After 20 min of normothermic reperfusion the fall in taurine and glutamine was maintained (7.5 +/- 0.5 and 7.4 +/- 0.7 for taurine and glutamine respectively). Myocardial ischaemic arrest with cold blood cardioplegic solution (n = 16) did not cause a significant fall in tissue taurine or glutamine. However, on reperfusion there was a marked fall in the intracellular concentrations of taurine (9.4 +/- 0.5 to 6.5 +/- 0.7) and glutamine (8.0 +/- 0.7 to 5.8 +/- 0.4). The fall in amino acids was associated with a fall in ATP and a rise in tissue lactate. This work demonstrates that irrespective of the cardioplegic solution used to arrest the heart, there is a marked fall in tissue taurine and glutamine which may influence the extent of recovery following surgery. The fall in taurine is largely due to efflux whereas changes in glutamine are due to both transport and metabolism. Ischaemia, hypothermia and changes in the transmembrane concentration gradients are the likely factors responsible for the changes in tissue amino acids.
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PMID:Effect of ischaemia and reperfusion on the intracellular concentration of taurine and glutamine in the hearts of patients undergoing coronary artery surgery. 909 9

Taurine has been shown to be essential for neuronal development and survival in the central nervous system. The release of preloaded [3H]taurine was studied in hippocampal slices from seven-day-, three-month- and 18-22-month-old mice in cell-damaging conditions. The slices were superfused in hypoxic, hypoglycemic and ischemic conditions and exposed to free radicals and oxidative stress. The release of taurine was greatly enhanced in the above conditions in all age groups, except in oxidative stress. The release was large in ischemia, particularly in the hippocampus of aged mice. Potassium stimulation was still able to release taurine in cell-damaging conditions in immature mice, whereas in adult and aged animals the release was so substantial that this additional stimulus failed to work. Taurine release was partially Ca2+-dependent in all cases. The massive release of the inhibitory amino acid taurine in ischemic conditions could act neuroprotectively, counteracting in several ways the effects of simultaneous release of excitatory amino acids. This protection could be of great importance in developing brain tissue, while also having an effect in aged brains.
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PMID:Enhanced taurine release in cell-damaging conditions in the developing and ageing mouse hippocampus. 921 47

In order to investigate the influences of taurine on thrombolysis serum endothelin (ET) concentration was determined in patients with acute myocardial infarcation (AMI) without urokinase (UK) treatment (group 1) and after treatment with UK (group 2) or UK combined with taurine (group 3). In a rat model with abdominal aorta thrombosed by FeCl3, the changes of serum ET, malodialdehyde (MDA) and intravascular thrombosis were observed in three groups same as in patients. The results were as follows: (1) Serum ET levels of group 1 patients at early phase of onset (6 hours) were significantly higher than those of the controls (47.3 +/- 6.3 ng/L vs 20.4 +/- 9.7 ng/L, P < 0.001). After two days serum ET decreased to normal level. Serum ET levels were significantly higher from 6 to 10 hours after the onset of AMI in group 2 than in group 1 (70.8 +/- 6.6 ng/L vs 56.9 +/- 8.6 ng/L, P < 0.01, at 8 hours). Serum ET levels were significantly lower from 8 hours to a week after onset of AMI in group 3 than in group 2 (33.3 +/- 8.2 ng/L vs 70.8 +/- 6.6 ng/L, P < 0.01, at 8 hours). (2) In the rat model with thrombosis of abdominal aorta, the changes of serum ET were similar to those of AMI patients. In addition serum MDA levels were significantly decreased (20.85 +/- 3.05 mumol/L vs 25.18 +/- 3.53 mumol/L after combined treatment with UK and taurine, P < 0.05). The ratio of cross area of vascular lumen and thrombus was lower after treatment with combination of UK and taurine than treatment with UK alone (0.4650 +/- 0.0928 vs 0.6176 +/- 0.1179, P < 0.05), the results suggested that taurine can decrease significantly serum ET levels, potentiate UK-induced vascular recanlization and reduce ischemia reperfusion injury. Taurine might be useful clinically as an adjunct of thrombolytic therapy.
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PMID:[Influences of taurine on thrombolysis]. 938 24

1. Taurine has recently been known to protect against ischemia and heart failure. Taurine possesses plenty of actions on the ion channels and transports, but is very non-specific. 2. Taurine may directly and indirectly help to regulate the [Ca]i level by modulating the activity of the voltage-dependent Ca2+ channels (also dependent on [Ca]i/[Ca]o), by regulation of Na+ channels, and secondly via Na-Ca exchange and Na(+)-taurine cotransport. 3. Taurine can prevent the Ca2+ ([Ca]o or [Ca]i)-induced cardiac functions. 4. Therefore, it seems possible that taurine could exert the potent cardioprotective actions even under the condition of low [Ca]i levels as well as under the Ca2+ overload condition. 5. The electrophysiological actions of taurine on cardiomyocytes, smooth muscle cells, and neurons from recent studies are summarized.
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PMID:Review of some actions of taurine on ion channels of cardiac muscle cells and others. 952 60

The releases of endogenous glutamate, aspartate, GABA and taurine from hippocampal slices from 7-day-, 3-, 12-, and 18-month-old mice were investigated under cell-damaging conditions using a superfusion system. The slices were superfused under hypoxic conditions in the presence and absence of glucose and exposed to hydrogen peroxide. In the adult hippocampus under normal conditions the basal release of taurine was highest, with a response only about 2-fold to potassium stimulation (50 mM). The low basal releases of glutamate, aspartate, and GABA were markedly potentiated by K+ ions. In general, the release of the four amino acids was enhanced under all above cell-damaging conditions. In hypoxia and ischemia (i.e., hypoxia in the absence of glucose) the release of glutamate, aspartate and GABA increased relatively more than that of taurine, and membrane depolarization by K+ markedly potentiated the release processes. Taurine release was doubled in hypoxia and tripled in ischemia but K+ stimulation was abolished. In both the mature and immature hippocampus the release of glutamate and aspartate was greatly enhanced in the presence of H2O2, that of aspartate particularly in developing mice. In the immature hippocampus the increase in taurine release was 10-fold in hypoxia and 30-fold in ischemia, and potassium stimulation was partly preserved. The release processes of the four amino acids in ischemia were all partially Ca2+-dependent. High concentrations of excitatory amino acids released under cell-damaging conditions are neurotoxic and contribute to neuronal death during ischemia. The substantial amounts of the inhibitory amino acids GABA and taurine released simultaneously may constitute an important protective mechanism against excitatory amino acids in excess, counteracting their harmful effects. In the immature hippocampus in particular, the massive release of taurine under cell-damaging conditions may have a significant function in protecting neural cells and aiding in preserving their viability.
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PMID:Release of endogenous glutamate, aspartate, GABA, and taurine from hippocampal slices from adult and developing mice under cell-damaging conditions. 956 93

During ischemia, hypoxia and cardiac failure, the heart undergoes several adverse changes, including a reduction in taurine (2-aminoethanesulfonic acid). Oral administration of taurine under these disease conditions would be expected to act like a mild cardiac glycoside. Taurine would exert improvement in the accumulation of [Na]i and the loss of alpha-amino acids. Nonetheless, when intracellular taurine content is raised, there would be the benefit of increased Ca2+ release from the sarcoplasmic reticulum and increased Ca2+ sensitivity of the contractile proteins, as well as possible changes in the action potential associated with the actions of taurine on ion channels. In fact, intracellular application of taurine produces the opposite actions to extracellularly administration of the amino acid. From our previous experiments, the electrophysiological actions of taurine on cardiac muscle cells include the following. (a) Prolongation of action potential duration (APD) at high [Ca]i and shortening of APD at low [Ca]i. In multicellular preparations, however, taurine did not always prevent [Ca]o-induced effects. (b) Stimulation of spontaneous activity at low intracellular and extracellular Ca2+ concentrations ([Ca]i and [Ca]o), and vice versa. (c) Inhibition of the L-type Ca2+ current (ICa(L)) at high [Ca]i, and vice versa. (d) Enhancement of the T-type Ca2+ current (ICa(T)). (e) Inhibition of fast Na+ current (INa). (f) Enhancement of TTX-insensitive slow Na+ current. (g) Inhibition of delayed rectifier K+ current (IKrec) at high [Ca]i, and vice versa. (h) Enhancement of the transient outward current (Ito). (i) Inhibition of the ATP-sensitive K+ current (IK(ATP)). Since taurine acts on so many ion channels and transporters, it is clearly non-specific. Although it is very difficult to understand the diversity of taurine's actions, it is possible that taurine can exert its potent cardioprotective actions under the conditions of low [Ca]i, as well as Ca2+ overload. Thus, although taurine-induced modulation of ion channels located on the cardiac cell membrane is complex, the multiple effects may combine to yield useful therapeutic results.
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PMID:Cardiac actions of taurine as a modulator of the ion channels. 963 23

Taurine release in the hippocampus is markedly potentiated in various cell-damaging conditions, including ischemia and excitotoxic damage produced by glutamate. The increase in the levels of taurine may provide an important protective mechanism against excitotoxicity. The mechanisms of the enhanced release were now studied in mouse hippocampal slices using a superfusion system. The basal release of [3H]taurine was significantly increased in Na+-deficient media in normal conditions, whereas the ischemia-evoked release was decreased, indicating the participation of Na+-dependent transport processes. The involvement of taurine transport carriers in the release was confirmed with the structural analogs, hypotaurine and beta-alanine. These amino acids potentiated the release by trans-stimulation in normoxia. In Na+-free conditions, this heteroexchange was not discernible, the carriers not being functional without Na+. In ischemia, the marked potentiation of taurine release by hypotaurine and beta-alanine further indicates that the Na+-requiring transporters also operate in ischemia. The effects of membrane disruption on taurine release due to activation of phospholipases were estimated using phospholipase and protein kinase inhibitors, which had no marked effects on hippocampal taurine release. The chloride channel blockers, 4-acetamido-4'-isothiocyanostilbene-2, 2'-disulphonate (SITS) and diisothiocyanostilbene-2,2'-disulphonate (DIDS), reduced the ischemia-induced release, suggesting that taurine diffusion through an anion channel is partially responsible for the enhanced release in ischemia.
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PMID:Mechanisms of ischemia-induced taurine release in mouse hippocampal slices. 975 14

We aimed to investigate the cardio-protective role of taurine with low calcium level against reperfusion damage by adding taurine to extracellular fluid. Guinea-pig hearts were mounted on Langendorf perfusion apparatus and different compositions of perfusion solutions were prepared for each experimental group. After 20 min of normothermic ischemia the hearts were reperfused. Pre-ischemic, post-ischemic and post-reperfusion percentage changes of heart rate and contractile force were compared. Post-reperfusion tissue weight, malondialdehyde (MDA) and prostaglandin E-like activity (PGE-like activity) were assessed. Taurine-added low-calcium perfusion solution significantly decreased the postischemic myocardial injury.
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PMID:Taurine and calcium interaction in protection of myocardium exposed to ischemic reperfusion injury. 1046 51

In an evaluation of the contribution of swelling-induced amino acid release, through the regulatory volume decrease (RVD) process, to cerebral ischemic injury, studies of the role of phospholipases and protein kinases in the response to hyposmotic stress were undertaken using an in vivo rat cortical cup model. Hyposmotic stress induced significant releases of aspartate, glutamate, glycine, phosphoethanolamine, taurine and GABA from the rat cerebral cortex. Taurine release was most affected, exhibiting a greater than 9-fold increase during the hyposmotic stimulus. The phospholipase A2 (PLA2) inhibitors 4-bromophenacyl bromide (1 microM) and 7,7-dimethyleicosadienoic acid (5 microM) had no significant effects on hyposmotically induced amino acid release. AACOCF3 (50 microM), an inhibitor of cytosolic PLA2 decreased taurine release to 84% of DMSO controls. The release of the other amino acids was not affected. The phospholipase C inhibitor U73122 (5 microM) had no significant effects on amino acid release. The protein kinase C (PKC) inhibitor chelerythrine (5 microM) significantly reduced hyposmotically induced taurine release to 72% of saline controls but had no significant effects on the other amino acids. Stimulation of PKC with phorbol 12-myristate, 13-acetate (10 microM) did not significantly change taurine, glutamate, glycine or phosphethanolamine release. The releases of aspartate and GABA were enhanced 2 to 3 fold. Phorbol 12,13-didecanoate (10 microM), another potent stimulator of PKC, significantly increased taurine release to 122% of DMSO controls. The releases of aspartate, glutamate and glycine were enhanced 2.5 to 3.5 fold. Similarly, stimulation of protein kinase A with forskolin (100 microM) significantly increased taurine, aspartate, and glycine release 1.5- to 2-fold compared to DMSO controls. In summary, phospholipases may play a minor role in volume regulation. These studies also support the hypothesis that protein kinases play a modulatory role in the RVD response. The results show that although RVD may play a role, additional mechanisms, including phospholipase activation, must be involved in the ischemia-evoked release of excitotoxic amino acids.
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PMID:Hyposmotically induced amino acid release from the rat cerebral cortex: role of phospholipases and protein kinases. 1053 55

Taurine release in the developing hippocampus is markedly potentiated in ischemia. The mechanisms of the ischemia-induced release were studied in hippocampal slices from seven-day-old mice using a superfusion system. The basal release of [3H]taurine was significantly increased in media under normal conditions, but the ischemia-evoked release decreased in Na+ -free media, indicating the participation of Na+ -dependent transport processes. The involvement of taurine transporters in the release was confirmed with the structural analogs, hypotaurine and beta-alanine. These amino acids potentiated the release by trans-stimulation, but not in Na+ -free media. In the absence of Ca2+, the basal taurine release was markedly increased in normoxia but diminished in ischemia, indicating that a part of basal taurine release in ischemia is Ca2+ dependent. On the other hand, the K+ stimulation of taurine release was preserved in Ca2+ -free medium. The phospholipase and protein kinase inhibitors had no effect on ischemia-induced taurine release, nor did the chloride channel blockers 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (2 mM) and diisothiocyanostilbene-2,2'-disulfonate (0.1 mM) affect the release in ischemia. The increase in extracellular levels of taurine in the immature hippocampus in ischemia may serve as an important protective mechanism against excitotoxicity, to which the developing brain is particularly vulnerable, and contribute to the resistance of the immature brain to hypoxia.
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PMID:Characteristics of ischemia-induced taurine release in the developing mouse hippocampus. 1057 87


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