Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.27 (lactate dehydrogenase)
 29,211 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to evaluate the effects of a single dose of nifedipine on myocardial stunning in isolated rabbit hearts. Hearts from rabbits pretreated with a single dose of 20 mg of nifedipine (NIF group) 1-4 h before isolation were compared to control hearts in their response to 15 min of global ischemia (37 degrees C) followed by 30 min of reperfusion. Both experimental groups showed similar baseline cardiac contractility. At the end of the reperfusion period in the control group, isovolumic left ventricular developed pressure (LVDP) and +dP/dtmax had stabilized at 45 +/- 2 and 48 +/- 2% of preischemic values respectively and in the NIF group LVDP stabilized at 63 +/- 6 and +dP/dtmax at 66 +/- 6% (P < 0.05 with respect to the control group). Left ventricular end diastolic pressure (LVEDP) values were significantly lower at the end of reperfusion in the NIF group compared to the controls (36.8 +/- 5.5 mmHg vs 53.4 +/- 3.9 mmHg, P < 0.05). The early impairment of the time constant of relaxation (tau) observed in control hearts was attenuated by pretreatment with nifedipine (control delta tau = 55 +/- 10 ms; NIF group delta tau = 29 +/- 5 ms, P < 0.05). Tissue ATP and creatine phosphate (CP) levels in the control group at the end of reperfusion were 6.9 +/- 0.7 and 8.7 +/- 0.7 mumol/g dry tissue, respectively; in the NIF group ATP and CP levels were significantly higher, 9.2 +/- 0.7 and 11.5 +/- 0.9 mumol/g dry tissue respectively (P < 0.05). Creatine kinase (CK) and lactate dehydrogenase (LDH) leakage during reperfusion were significantly higher in the control group (CK = 120 +/- 15 mU/ml and LDH = 60 +/- 8 mU/ml) compared to the NIF group (CK = 82 +/- 5 mU/ml and LDH = 41 +/- 2 mU/ml, P < 0.05). Our results demonstrate that pretreatment with a single oral dose (20 mg) of nifedipine attenuates systolic and diastolic functional alterations as well as the metabolic impairment associated with stunning in the isolated rabbit heart.
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PMID:Protective effect of nifedipine on myocardial stunning in isolated rabbit hearts: role of high energy phosphates stores. 879 16

Fibroblast cultures were used to study the effect of crude venom and six venom protein fractions (F2-F7) from Walterinnesia aegyptia on their metabolic activity. This was done by incubation of six fibroblast cultures with 10 micrograms of crude venom for 3 h at 37 degrees C. The activities of phosphofructokinase, lactate dehydrogenase, and citrate synthase were significantly lowered upon incubation with all fractions except F2. Glycogen phosphorylase activity was significantly increased, leading to a significant concurrent drop of glycogen content. This effect was only seen for fractions F3 and F5. Creatine kinase activity and cellular ATP levels rose significantly upon incubation with all venom proteins except fractions F2 and F7. Increases were seen for aspartate and alanine aminotransferases by all venom proteins except fractions F2 and F4. Incubation of cell sonicates with all the venom proteins did not significantly alter activities of any of the parameters. Thus, fibroblasts in culture under such conditions appear to mobilize glycogen, phosphocreatine, and protein for ATP production to compensate for decreased glucose.
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PMID:The effect of the desert cobra (Walterinnesia aegyptia) crude venom and its protein fractions on the metabolic activity of cultured human fibroblasts. 881 58

After acute myocardial infarction (AMI) cardiac enzymes and proteins are released into plasma and are used as biochemical markers of cardiac muscle injury. We studied the completeness of the release of troponin T, a cardiac protein that is largely bound to myofibrillar structures and compared it with the release of cytoplasmic cardiac enzymes in 22 patients with AMI, who were treated with thrombolytic therapy. Creatine kinase (CK; EC 2.7.3.2), hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LDH; EC 1.1.1.27) and troponin T were assayed serially in plasma samples obtained frequently and for at least 168 h after the start of thrombolytic therapy. Cumulative release of enzymes and troponin T in plasma were calculated by using a two-compartment model for circulating proteins. In order to express the cumulative plasma releases in gram equivalent (g-eq) healthy myocardium per litre plasma (infarct size), we determined HBDH, LDH and total troponin T contents per gram net weight of tissue in 17 human hearts obtained post-mortem from patients who died from non-cardiac causes. Mean (SD) tissue contents per gram wet weight of, respectively, 156 +/- 25 U/g, 385 +/- 59 U/g and 234 +/- 65 micrograms/g were found. For the cardiac enzymes CK, HBDH and LDH the mean (SEM, n = 22) total release over 72 h, was, respectively, 5.9 +/- 1.5, 5.9 +/- 1.6 and 6.1 +/- 1.7 g-eq/L. There was no further increase after 72 h and the differences between enzymes were not significant. The mean (SEM) cumulative troponin T release, expressed in gram equivalents of myocardium per litre of plasma was only 0.30 +/- 0.09 g-eq/L after 72 h and 0.51 +/- 0.61 g-eq/L after 168 h. After 72 h total recovery of troponin T in g-eq/L was only 5% and after 168 h only 8.5% of the total recovery of cytoplasmic cardiac enzymes after 72 h. Cumulative troponin T release after 72 h and after 168 h correlates well with infarct size, estimated from cumulative cytoplasmic enzyme release. However, quantification of infarct size should preferably be performed from plasma release curves of cytoplasmic cardiac enzymes or proteins in order to prevent underestimation of infarct size, caused by incomplete release of the non-cytoplasmic proteins.
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PMID:Cardiac troponin T release into plasma after acute myocardial infarction: only fractional recovery compared with enzymes. 883 89

The electrophoretic patterns of the serum enzymes lactate dehydrogenase and creatine kinase from water buffalo calves are described. Differences in total activities as well as their relative distribution were seen at ages ranging from 1 to 10 weeks. While total lactate dehydrogenase activity increased by over 100%, total creatine kinase increased by almost 400%. The relative activities of lactate dehydrogenase 1 and 5 decreased with age. Lactate dehydrogenase 2 and 3 increased and lactate dehydrogenase 4 did not change. In relation to creatine kinase, the prevalent isoenzyme was creatine kinase-MM, but it's relative activity gradually decreased in comparison to the other two isoenzymes (creatine kinase-MB and creatine kinase-BB). Creatine kinase-BB was completely absent until the 3rd week of age. The percentage modifications of creatine kinase isoenzymes were correlated to age. The results suggest that isoenzymatic separation and characterization of lactate dehydrogenase and creatine kinase in relation to the various tissues can significantly contribute to the diagnosis of diseases which are linked to tissue damage.
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PMID:Age-dependent variations of lactate dehydrogenase and creatine kinase activities in water buffalo calf serum. 898

Creatine kinase (CK) MB and lactate dehydrogenase (LDH) isoenzyme 1 are not heart-specific. By contrast, the regulatory proteins troponin I and troponin T are expressed in three different isoforms, one for slow-twitch skeletal muscle fibers, one for fast-twitch skeletal muscle fibers, and one for cardiac muscle (cTnI, cTnT). cTnI and cTnT are usually not detectable in patients without myocardial damage, which is a prerequisite for high diagnostic performance. After acute myocardial infarction (AMI) cTnI, cTnT, and CKMB mass have a comparable early sensitivity. cTnI and cTnT usually peak in parallel except for patients without reperfusion in whom cTnI peaks about 1 day and cTnT approximately 3-4 days after onset of AMI. Both stay increased for at least 4-5 days. cTnT tends to stay increased longer than cTnI. Because the sensitivities of cTnI and cTnT for myocardial injury are comparable, their specificities are the main topic of current debate. Recent reports on mismatches of cTnI and cTnT in patients with renal failure and myopathy without other evidence for myocardial injury suggest that cTnT could be reexpressed similar to CKMB and LDH-1 in chronically damaged human skeletal muscle. In contrast to cTnT, CKMB, and LDH-1, cTnI is not expressed in skeletal muscle during fetal development. So far, an increase in cTnI has been reported only after myocardial damage. Because of currently higher costs, troponin measurement should be restricted at present to clinical settings that really require their high specificity. Based on its distinct functional association with the metabolism of acute ischemic myocardium and according to initial clinical results, glycogen phosphorylase isoenzyme BB is a promising enzyme for the early detection of ischemic myocardial damage.
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PMID:Cardiac troponin I and troponin T: are enzymes still relevant as cardiac markers? 902 28

Myoglobin (M(r) 18,000) and fatty acid-binding protein (M(r) 15,000), are low molecular mass cytoplasmic proteins that are considered useful biochemical markers for early detection or exclusion of acute myocardial infarction, and also for early estimation of infarct size. As each of these proteins shows renal clearance, we studied the influence of renal function on the estimation of infarct size from their plasma concentration curves. For this, infarct size estimated from plasma myoglobin or fatty acid-binding protein release curves was compared with that estimated with the established infarct size markers hydroxybutyrate dehydrogenase and creatine kinase, which are not influenced by changes in renal function. The discordance between infarct size estimates was related to renal function. Creatine kinase (EC 2.7.3.2), hydroxybutyrate dehydrogenase (EC 1.1.1.27), myoglobin, fatty acid-binding protein and creatinine were assayed serially in plasma samples obtained frequently and for at least 72 hours after the start of thrombolytic therapy in 20 patients with acute myocardial infarction. Cumulative release of the different cardiac markers was calculated by using a two-compartment model for circulating proteins. Mean tissue contents of 156 U/g for hydroxybutyrate dehydrogenase, 2163 U/g for creatine kinase, 2.79 mg/g for myoglobin and 0.57 mg/g wet weight for fatty acid-binding protein, were used to express infarct size in gram-equivalents of healthy myocardium per litre of plasma (g-eq/l). Mean plasma creatinine was obtained by averaging the creatinine concentrations measured in all plasma samples taken during the first 24 hours after acute myocardial infarction. A relation was found between the mean plasma creatinine concentration during the first 24 hours after acute myocardial infarction and the discordance between infarct size estimated from cumulative hydroxybutyrate dehydrogenase release, compared to infarct size estimated from cumulative myoglobin or fatty acid-binding protein release. For patients with mean plasma creatinine concentrations within the reference interval for creatinine (group 1, n = 15) a good agreement was found between infarct size estimated from myoglobin or fatty acid-binding protein plasma curves and that estimated with either hydroxybutyrate dehydrogenase or creatine kinase. However, for patients with a mean creatinine concentration above the upper reference limit (group 2, n = 5), infarct size calculated from plasma myoglobin or fatty acid-binding protein release curves was markedly overestimated, especially for larger infarcts. Estimation of infarct size from serial plasma myoglobin or fatty acid-binding protein concentrations is possible in the first 24 hours after the onset of symptoms, but only in patients with normal renal function, as estimated from plasma creatinine concentrations.
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PMID:Estimation of myocardial infarct size from plasma myoglobin or fatty acid-binding protein. Influence of renal function. 912 40

This study was designed to evaluate whether the addition of potassium channel blockers, tetraethylammonium, 4-aminopyridine or glibenclamide, to St Thomas' cardioplegia improved myocardial preservation over that achieved by St Thomas' cardioplegic solution alone. Initially, isolated rat hearts were subjected to 30 min of continuous normothermic hypoxic cardioplegia. Control hearts were arrested with St Thomas' cardioplegia followed by tetraethylammonium, glibenclamide or 4-aminopyridine-enriched cardioplegia. Subsequently, in a second experiment, hearts were subjected to 45 min of normothermic global ischaemia, after 3 min of cardioplegia with either tetraethylammonium-enriched or standard St Thomas' cardioplegia. In both regimens, hearts arrested with tetraethylammonium-enriched St Thomas' cardioplegia showed better recovery of contractile function than controls (P<0.001). Creatine kinase levels were significantly lower in the tetraethylammonium group (P<0.001). 4-Aminopyridine treatment caused similar contractility to that of the control group but raised creatine kinase and lactate dehydrogenase levels (P<0.001). Glibenclamide diminished coronary flow autoregulation, and increased lactate dehydrogenase leakage in reperfusion (P<0.05) with similar contractility to controls. The results of this preliminary in vitro study demonstrate that, in rat heart, St Thomas' cardioplegia enriched with tetraethylammonium improves post-ischaemic contractile function and reduces creatine kinase release. It is concluded that high potassium blocks the membrane at the rapid depolarization phase with rapid sodium influx and tetraethylammonium further prevents repolarization by blocking voltage-dependent potassium channels.
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PMID:Benefits of supplementing St Thomas' Hospital cardioplegic solution with tetraethylammonium on functional and metabolic recovery of isolated rat hearts. 915 33

We investigated the effects of selenium (Se) deficiency on differentiation, protein degradation, and cell lysis in cultured skeletal muscle cells, using L8 rat skeletal muscle cells cultured in serum-free (SF) medium to induce differentiation and to maintain myotubes. Creatine kinase activity was reduced (p < 0.05) by approximately 15% without Se supplementation for 96 h. Confluent myoblasts were treated with SF media with four different levels of vitamin E (0, 10, 35, and 100 microM) in the absence and presence of Se (0 and 0.25 microM, respectively). After 96 h, vitamin E at a high dose (100 microM) was effective in the prevention of the decrease of differentiation caused by Se deficiency (p < 0.05). Following differentiation, the effects of three Se concentrations (0, 0.25, and 2.5 microM) on degradation of proteins as assessed by release of 3H-labeled free amino acids secreted into the media were studied. Selenium supplementation did not affect (p > 0.05) total protein degradation. However, Se deficiency increased (p < 0.05) lactate dehydrogenase released from lyzed dead cells. The results indicate that Se is required to maintain an optimal rate of muscle cell differentiation and health of myotube cultures.
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PMID:The effects of selenium deficiency on differentiation, degradation, and cell lysis of L8 rat skeletal muscle cells. 1038 95

A 24 year old male with varicella myocarditis was admitted with chest pain and fever up to 39 degrees C. The ECG showed J point and ST elevation in leads V2-V4, and inverted T waves in leads V5 and V6. Creatine kinase (CK) was raised to 435 U/l (CK-MB 36 U/l), troponin I was 63.4 microgram/l, and lactate dehydrogenase was 359 U/l, suggesting cardiac involvement of varicella infection. The left ventricle was dilated (58 mm) and left ventricular ejection fraction was globally reduced (ejection fraction 45%). Myocarditis was confirmed by endomyocardial biopsy. The patient was treated with specific varicella hyperimmunoglobulins, aciclovir, and a non-steroidal anti-inflammatory drug. During two months follow up the patient recovered completely. This case report is a reminder that a varicella infection can cause myocarditis in adults. Early diagnosis and appropriate treatment of this rare form of myocarditis may lead to complete recovery.
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PMID:Varicella myocarditis in an adult. 1111 80

The Olympus AU400 analyser (Olympus, Tokyo, Japan) is an automated chemistry instrument for turbidimetric, spectrophotometric and ion selective electrode measurements. Overall analytical performances of the AU400 and the reagents provided by Olympus were evaluated according to the French Society of Clinical Biology guidelines. Twenty parameters including specific proteins, substrates, enzyme activities and electrolytes were tested. The linearity exceeded the specifications given by the manufacturer. Within- and between-run imprecision (CV%), evaluated at two levels, was below 1.5% for ion selective electrode parameters and 3% for other analytes, except for CO2, alkaline phosphatase at low levels and magnesium. Results compared well with those obtained with the analysers routinely used in our laboratory (Behring BNII, Olympus AU800 and Beckman CX3 Delta). The usual positive interferences from lipaemia and haemoglobin on total protein measurement were observed. Creatine kinase and alkaline phosphatase assays were the subject of positive and negative interference by haemoglobin, respectively. There was a negative interference by bilirubin in the uric acid, aspartate-amino transferase, creatine kinase and lactate dehydrogenase assays and a positive interference in the calcium assay. The system was found to be very easy to use and the workstation is user-friendly.
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PMID:Evaluation of the clinical chemistry analyser Olympus AU400. 1143 99


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