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)

We wished to determine whether histidine scavenges hydroxyl radical, H2O2, and superoxide anion in vitro and to investigate the protective effect of histidine on isolated perfused rat hearts after global ischemia (40 min) and reperfusion (30 min) (I/R). Left ventricular (LV) function was recorded and coronary effluent was collected for measurement of lactate dehydrogenase (LDH) before ischemia and at 5, 10, 15, and 30 min of reperfusion. At the end of the experiment, a portion of the LV wall was fixed with 2% glutaraldehyde for morphological analysis; the remaining heart was immediately frozen in liquid nitrogen for determination of adenine nucleotides. Histidine effectively quenched hydroxyl radicals and H2O2, but not superoxide anions, in in vitro and in vivo conditions. Hearts treated with histidine exhibited significantly greater functional recovery during reperfusion as compared with nontreated hearts (p < 0.05). Cell morphology was well preserved, and enzyme release was significantly attenuated by histidine treatment (p < 0.05). Histidine raised the ATP level to 73% and the creatine phosphate level to 68% of normal control during reperfusion. Total adenine nucleotide pool and energy charge rate in histidine-treated hearts significantly increased as compared with those in nontreated hearts (p < 0.05), but no effect on ATP and creatine phosphate was noted during ischemia, Histidine prevents postischemic reperfusion injury in isolated heart by inhibiting reactive O2 species and preserving high-energy phosphates (HEP).
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PMID:Antioxidative properties of histidine and its effect on myocardial injury during ischemia/reperfusion in isolated rat heart. 772 45

The aim of this study is to investigate the efficacy of HTK solution in the 120 minutes cross-clamping method in comparison with conventional intermittent cardioplegia using GIK solution. Fifty-four open heart surgery were performed with cardioplegic solution using either HTK solution (HTK) or GIK solution (GIK). In the HTK, HTK (3L) was infused for the initial dose and 1L was added every 60 min after 120 min of cross-clamping. In GIK, 1L of GIK solution was intermittently infused initially and then every 30 min together with continuous cold blood perfusion. The effect of two cardioplegic solution was evaluated by postoperative cardiac function (CI, %SF), released enzymes (CPK), histology and dosage of catecholamine. Postoperative CI was 3.67 +/- 0.76 in HTK, and 4.34 +/- 1.04 in GIK (NS). % SF was 26.0 +/- 5.26 in HTK and 25.6 +/- 0.76 in HTK, and 4.34 +/- 1.04 in GIK (NS). %SF was 26.0 +/- 5.26 in HTK and 25.6 +/- 9.2 in GIK (NS). The CK-MB (IU/dl) level after reperfusion was significantly decreased in HTK at 60 and 180 min after reperfusion. Histology at 60 min of ischemia revealed a significant increase of edema of mitochondria in GIK. Postoperative catecholamine dose was 2.65 +/- 1.3 in HTK and 10.3 +/- 3.4 in GIK (p < -0.01). PH of myocardium was well maintained around 7.4 during cross-clamping in HTK, however, it was decreased in GIK. In conclusion, The HTK method offers a reliable cardiac protection due to effective buffering using Histidine in comparison with GIK.
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PMID:[Efficacy of myocardial preservation using HTK solution in continuous 120 min cross-clamping method--a comparative study with GIK method]. 840 3

We investigated the efficacy of histidine in reducing ischemia-reperfusion (I/R)-induced myocardial injury in isolated perfused rat hearts. In I/R hearts, the contractile function and coronary flow were 59 +/- 10 and 78 +/- 6% of control. Perfusion with histidine resulted in significant increase in contractility (94 +/- 4%) and coronary flow (92 +/- 4%). The incidence of arrhythmias during reperfusion was 100% (10 out of 10) in the I/R hearts with an average duration of 12.22 +/- 1.55 (SE) min. The duration of arrhythmias was shortened to 8.24 +/- 1.46, 2.15 +/- 0.9, and 2.49 +/- 1.50 min with 10, 25, and 50 mM histidine, respectively. The duration of sinus rhythm increased from 6.26 +/- 1.56 min in I/R hearts to 10.66 +/- 1.55, 14.99 +/- 1.61, and 17.18 +/- 0.95, and 11.73 +/- 0.93 min after perfusion with 10, 25, and 50 mM histidine, and superoxide dismutase (SOD)-catalase-mannitol, respectively. Electron microscopy revealed significant ultrastructural damage of myocytes in I/R hearts, which included swelling of the mitochondria and disruption of both the sarcolemma and the myofibrils. Histidine reduced the ultrastructural damage in a dose-dependent fashion. In general, the protective effect of histidine was superior than SOD-catalase-mannitol. We conclude that histidine protects myocardium against I/R damage most likely by a singlet oxygen scavenging mechanism.
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PMID:Protective effects of histidine during ischemia-reperfusion in isolated perfused rat hearts. 849 50

This study was aimed to determine whether singlet oxygen (1O2) attenuates 5'-nucleotidase activity in the ischemic myocardium. Isolated rat hearts were exposed to either exogenous 1O2 produced by irradiating rose bengal or 40-min ischemia and reperfusion. Ecto-5'-nucleotidase activity was inhibited by exogenous 1O2 (3.74 +/- 0.38 mumol/min/g dry weight), when compared with normal control (7.52 +/- 0.41 mumol/min/g dry weight; P < 0.05). The enzymatic activity was significantly preserved by histidine (25 mM)--a 1O2 scavenger (7.04 +/- 0.61 mumol/min/g dry weight; P < 0.05 v rose bengal group). After ischemia, the activity of ecto-5'-nucleotidase was greatly reduced (2.51 +/- 0.25 mumol/min/g dry weight), when compared with normal control. Histidine significantly enhanced ecto-5'-nucleotidase activity (6.55 +/- 0.52 mumol/min/g dry weight, P < 0.05 v ischemic control). Adenosine release was consistent with ecto-5'-nucleotidase activity. The time course studies of effects of 1O2 on coronary flow, cardiac function, and LDH release revealed that the damage by 1O2 to ecto-5'-nucleotidase activity and adenosine release primarily accounted for impaired coronary flow, cardiac dysfunction, and impaired cardiac metabolism. Lipid peroxidation induced by exogenous 1O2 or ischemia was in parallel with ecto-5'-nucleotidase deactivation by 1O2. It is concluded that 1O2 causes inactivation of ecto-5'-nucleotidase and attenuation of adenosine release which could possibly be one of the important mechanisms of oxygen radical-mediated myocardial injury.
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PMID:Interaction of singlet oxygen with 5'-nucleotidase in rat hearts. 859 96

The protective effects of carnosine and related compounds on isolated rat heart were studied under experimental ischemia. The ability of carnosine to suppress significantly the development of ischemic reperfusion contracture and to support the restoration of the contractile force during reperfusion were shown. At the same time, a decrease of myoglobin and nucleoside release from myocytes was observed, this indicating a membrane-protecting effect of carnosine. Methylation of carnosine at the N1 or N3 atom of the imidazole ring significantly decreased the protective effect; the substitution of beta-alanine with gamma-aminobutyric acid (resulting in formation of homocarnosine) actually augmented ischemic damage to the heart. Acetylation of carnosine at the beta-amino group amplified the membrane-protecting properties of the molecule, the acetylated derivative of carnosine also showing the ability to induce contractile activity of the ischemic heart. Histidine alone or in combination with beta-alanine and sodium acetate had no effect, while acetylhistidine showed a significant protective effect during reperfusion. The comparison of the effects of natural histidine-containing dipeptides versus synthetic antioxidants indicates that the anti-ischemic effect of carnosine and acetylcarnosine involves antiradical and membrane-protecting mechanisms; nevertheless, the effect cannot be reduced to these mechanisms alone. The observed phenomena of heart muscle protection by acetylated derivatives of carnosine and anserine under ischemia correlates with the preferential localization of these compounds in high quantities in the myocardium.
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PMID:Effect of histidine-containing dipeptides on isolated heart under ischemia/reperfusion. 911 34

Histidine is an efficient scavenger of highly active singlet oxygen and somewhat weaker scavenger of hydroxyl radicals. And it has been shown to protect against reperfusion injury in the heart. The effects of L-histidine were examined in the forebrain ischemia reperfusion injury of the rat hippocampus (CA-1). Male Wistar rats were treated with the free radical scavenger L-histidine for 30 minutes before transient forebrain ischemia produced by 4-vessel occlusion. The extracellular concentrations of glutamate were measured by cerebral microdialysis. The intravenous (i.v.) administration of 50 mg/kg and 100 mg/kg L-histidine protected the elevation of extracellular glutamate concentrations after transient cerebral ischemia (p < 0.01). And the administration of L-histidine prevented ischemia-reperfusion induced delayed neuronal death in the rats. Morphological changes in the CA-1 sector of the hippocampus were evaluated 7 days after 10 minutes occlusion. The average neuronal density of treated groups showed a statistically significant (p < 0.01) persistence compared with that of control groups. These results indicate that L-histidine can reduce neuronal damage after reperfusion of cerebral ischemia and further suggest that excitatory amino acid and oxygen free radicals may damage the brain by a common pathway.
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PMID:[Protective effect of L-histidine (singlet oxygen scavenger) on transient forebrain ischemia in the rat]. 923 48

A number of imidazole-based compounds were tested for their utility as (1)H NMR molecular probes of intracellular pH. Imidazole, previously found useful as a probe of erythrocyte pH, reported a pH in perfused canine glioma cells that was more than 1 pH unit lower than that reported by inorganic phosphate, consistent with the known lysosomal compartmentation of the molecule. Imidazole acetate, also proposed as an NMR probe of cellular pH, was found not to enter the cells of this study. Histidine was found to be readily taken up by cells and reported a pH consistent with that reported by inorganic phosphate. Using the chemical shift of the histidine H2 proton in cells incubated with 10 mM histidine, cellular pH measurements could be obtained in less than 1 s. This compares quite favorably with the measurement time, typically several minutes, needed to assess in vivo pH by (31)P NMR. The use of histidine as a probe of pH is demonstrated in perfused canine and rat glioma cells subjected to ischemia or to low extracellular pH.
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PMID:A study of imidazole-based nuclear magnetic resonance probes of cellular pH. 968 13

We examined whether histidine can increase the production of interstitial adenosine via noradrenaline (NA) release-mediated activation of ecto-5'-nucleotidase in the ventricular myocardium, with use of microdialysis techniques in in situ rat hearts. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rat hearts and the tissue was perfused with Tyrode's solution containing adenosine 5'-monophosphate (AMP) through the dialysis probe at a rate of 1.0 microl/min. Adenosine in the dialysate collected during perfusion with Tyrode's solution containing 100 microM AMP (through the probe) originated from the hydrolysis of AMP catalyzed by endogenous ecto-5'-nucleotidase, so that the level of adenosine reflected the activity of ecto-5'-nucleotidase in this tissue. In the presence of NA (10 microM), histidine, a scavenger of highly active singlet oxygen (1O2), significantly increased concentration of adenosine. Histidine (5-50 mM) increased the level of AMP-primed dialysate adenosine in a concentration-dependent manner. When histidine (25 mM) was infused to rat myocardium, small increase in the levels of adenosine were observed. However, when corresponding experiments were performed with NA (10 microM)-pretreated animals, a marked elevation of the level of adenosine in rat heart dialysate was obtained. To confirm the possible mechanism of interaction between 1O2 and NA, we examined the effect of histidine in ischemic-reperfused rat hearts. In the presence of histidine (25 mM), a marked elevation of NA and adenosine was observed. However, when corresponding experiments were performed with reserpinized rat hearts, the elevation of both NA and adenosine was not observed in ischemia-reperfused rat hearts. These results indicate that histidine increases interstitial adenosine concentration via NA release-mediated activation of ecto-5'-nucleotidase.
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PMID:An increase of the native interstitial adenosine concentration during histidine application. 1083 7

Inflammatory reactions play an important role in ischemia-reperfusion injury in the brain. Since histamine H(2) action suppresses inflammatory reactions, effects of postischemic loading with histidine, a precursor of histamine, were examined. Focal cerebral ischemia for 15 min was provoked by transient occlusion of the right middle cerebral artery in rats, and delayed neuronal death were evaluated in striatal neurons after 7 days. Histidine was administered four times, immediately, 6, 24, and 48 h after reperfusion of blood flow (1000 mg/kg, i.p., each time). To examine the role of histaminergic action on changes in histologic outcome, effects of mepyramine (3 nmol, i.c.v.), an H(1) antagonist, and ranitidine (30 nmol, i.c.v.), an H(2) antagonist, were evaluated in histidine-treated rats. Transient ischemia for 15 min provoked severe neuronal damage in the saline-injected control group, and the number of striatal neurons decreased to 21% of that on the contralateral side. Administration of histidine alleviated ischemic neuronal damage, and the number of preserved neurons was 76% of that on the contralateral side. Simultaneous administration of mepyramine with histidine did not affect the histologic outcome. However, administration of ranitidine abolished the alleviation by histidine. These findings indicate that the elevation of histamine H(2) receptor stimulation by massive administration of histidine suppresses reperfusion injury in the brain.
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PMID:Alleviation of ischemic neuronal damage by postischemic loading with histidine in the rat striatum. 1472 77

Histidine-tryptophan-ketoglutarate (HTK) preserves rat muscle function during cold storage. We examined the effect of HTK perfusion on preservation of microvascular function during 4 h of warm ischemia and subsequent reperfusion (I/R) in the rat cremaster muscle. Leukocyte-endothelium interactions, capillary perfusion, and arteriole diameters were quantified prior to HTK-perfusion and/or ischemia, and at 0, 1, and 2 h after restoration of blood flow. In all groups, the number of rolling leukocytes increased with time, whereas I/R induced a slight increase in leukocyte adhesion. After ischemia, capillary perfusion rapidly recovered to about 50% and returned to near normal (90%) after 2 h. HTK at 22 degrees C did not affect the assessed microcirculation variables, whereas HTK at 4 degrees C reduced leukocyte rolling, but not adhesion. Therefore, microvascular function of HTK-perfused muscles was not better preserved during warm I/R than that of nonperfused muscles. Contrary to other preservation solutions, HTK perfusion in itself was not detrimental to the microcirculation.
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PMID:Effect of HTK on the microcirculation in the rat cremaster muscle during warm ischemia and reperfusion. 1570 26


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