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)

Creatine kinase isoenzyme I(BB) is generally not detectable in normal serum, and its occurrence in serum has been documented in only a few disease states. In particular, increased activity of this isoenzyme has been reported in association with chronic renal failure, hemodialysis, and renal transplantation. The present study demonstrates that the apparent creatine kinase observed in the serum of such renal patients is an artifact, observed as a result of measuring creatine kinase isoenzymes by fluorescence. Our observations resemble those of McKenzie et al. [Clin. Chim. Acta 70, 333(1976)] concerning an artifact in the fluorometric determination of lactate dehydrogenase isoenzymes in the sera of patients with end-stage renal failure. The artifact binds to albumin, is not a protein, and occurs in some normal sera at very low concentrations. This artifact can be mistakenly identified as isoenzyme I in renal-disease patients if CK isoenzymes are determined fluorometrically.
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PMID:Spurious brain creatine kinase in serum from patients with renal disease. 35 42

We measured creatine kinase (EC 2.7.3.2) activity in 1009 serum samples from 538 patients in the intensive-care units of the University of Texas Medical Branch hospitals. Creatine kinase isoenzymes migrating cathodal to skeletal muscle creatine kinase (CK-MM) on cellulose acetate electrophoresis were found in sera from 14 of the 538 patients. Creatine kinase, lactate dehydrogenase (EC 1.1.1.27), aspartate aminotransferase (EC 2.6.1.1), and alanine aminotransferase (EC 2.6.1.2) activities were abnormally increased in these 14 patients. Liver lactate dehydrogenase isoenzyme (LDH5) and cardiac creatine kinase isoenzyme (CK-MB) were abnormally increased in 12 and eight of these patients, respectively. Ten of the 14 patients died during their hospital admission. We believe the creatine kinase isoenzymes that migrated cathodal to skeletal muscle creatine kinase (CK-MM) were of mitochondrial origin.
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PMID:Creatine kinase isoenzymes of mitochondrial origin in human serum. 44 29

Creatine kinase (CK), lactic dehydrogenase (LDH), and more recently their isoenzyme determinations (CK-MB and LDH1) have been useful adjuncts in verification of myocardial injury. To determine whether DC cardioversion affects these serum enzyme levels, we recorded total CK, total LDH, CK-MB, and LDH1 levels serially during 24 hours following elective DC cardioversion in 18 patients without cardiac ischemia. New postcardioversion elevations in total CK and total LDH levels were small and occasional: CK (one of 18 patients), LDH (four of 18 patients). Elevations of CK-MB or LDH1 following cardioversion did not develop in any of the patients. Therefore, new CK-MB or LDH1 elevations associated with arrhythmias must result from myocardial damage to DC cardioversion.
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PMID:Direct current cardioversion. Effect on creatine kinase, lactic dehydrogenase and myocardial isoenzymes. 57 71

Sera from patients with myocardial infarction and cardiac arrhythmias were analyzed for myoglobin concentration and the activities of total creatine kinase, creatine kinase isoenzyme-2, and lactate dehydrogenase isoenzyme-1 at the time of hospital admission and during the first few days of hospitalization. The nine patients with a final diagnosis of myocardial infarction had abnormally high values for total creatine kinase, creatine kinase-2, lactate dehydrogenase-1, and myoglobin. Myoglobin concentrations were highest on admission in six patients and on the day after admission in the other three patients. Creatine kinase-2 manifested maximum activity on the day after admission for all patients with myocardial infarction. Lactate dehydrogenase-1 did not reach maximal values until the second or third day after admission. The six patients with arrhythmias did not show any significant increases in creatine kinase-2 or lactate dehydrogenase-1. Myoglobin and total creatine kinase, however, were increased in the four patients who had received cardioversion. The specificity and diagnostic usefulness of these serum measurements are discussed.
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PMID:Myoglobin concentrations and muscle-enzyme activities in serum after myocardial infarction and cardiac arrhythmia. 85 91

Serum creatine kinase, aspartate transaminase, and hydroxybutyrate dehydrogenase activities were abnormal in 76, 50, and 28% respectively of 50 patients studied within 26 hours of surgery. No patient showed clinical evidence of myocardial infarction. Creatine kinase MB isoenzyme elevation, and lactate dehydrogenase LD1 activity greater than LD2 (LD) greater than LD2) were infrequent (6 and 10% respectively). No patient showed the combination of transient MB isoenzyme elevation and LD1 greater than LD2, although their rare association without infarction after surgery is to be anticipated.
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PMID:Serum enzymes and isoenzymes after surgery. 92 Dec 11

Creatine kinase(CK), aspartate aminotransferase (AST), alpha-hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LD) and LD isoenzymes, CK-MB isoenzymes and CK-MM isoforms were measured in 17 acute myocardial infarction (AMI) patients treated with thrombolysis resulting in reperfusion and 2 not resulting in reperfusion as well as 71 treated conventionally to assess reperfusion. The results showed that the peak of the ratio of MM3 to MM1 was attained significantly earlier in patients with reperfusion than in those conventionally treated and those without reperfusion, and this ratio is considered to be a good indicator to assess reperfusion. The results were similar to those of previous reports. The peak in all the 17 patients with confirmed reperfusion was attained within 9 hours after onset of AMI, while only 9 of the 73 patients in the group without reperfusion had their peaks within 9 hours. The diagnostic efficiency was 94%. The authors suggested a new indicator for assess reperfusion. An increase of CK-MM3 over 10% from the first to the second hour after treatment with urokinase was found in 15 of the 17 urokinase-treated patients with reperfusion. The diagnostic efficiency was also 94%. We consider that it is an indicator as good as the peak of ratio of MM3/MM1. Furthermore, with this indicator, it is possible to assess reperfusion in two hours after treatment with urokinase.
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PMID:[Determination of serum creatinine kinase MM isoforms in assessing reperfusion after acute myocardial infarction]. 131 15

The effect of nucleoside transport inhibition on 24-hour preservation of canine hearts was studied in 36 hearts arrested either with a cold hyperkalemic cardioplegic solution without (group I) or with supplementation of a specific nucleoside transport inhibitor (R75231, 1 mg/L) (groups II and III). The hearts were excised and stored for 24 hours at 0.5 degrees C. Then they were reperfused for 3 hours with use of a closed perfusion system primed with normal blood (groups I and II) or with blood supplemented with the same nucleoside transport inhibitor (0.32 mg/L) (group III). Serial biopsy specimens for determination of myocardial purines were taken. Creatine kinase and heat-stable lactate dehydrogenase release from the myocardium were examined during reperfusion. Recovery of function was studied during reperfusion by measurement of isometric contraction in a fluid-filled intraventricular balloon. After 24 hours of preservation, without the use of the drug, myocardial inosine and hypoxanthine accumulated to, respectively, 4.05 +/- 1.18 and 0.28 +/- 0.08 mumol/gm dry weight. In the drug-treated groups (II and III pooled), significantly less inosine and hypoxanthine accumulated (1.68 +/- 0.33 and 0.05 +/- 0.02 mumol/gm dry weight, respectively) (p < 0.05 versus group I). Upon reperfusion, intramyocardial adenosine was lost in the control hearts and maintained in the drug-treated hearts. Hypoxanthine accumulated significantly (p < 0.05) during reperfusion in group I (1.08 +/- 0.43 versus 0.16 +/- 0.13 in group II and 0.03 +/- 0.03 mumol/gm dry weight in group III). The rate of creatine kinase and heat-stable lactate dehydrogenase release was significantly lower (p < 0.05) in group III (that is, pretreatment and posttreatment with the drug) than in the control group. Functional recovery of hearts in group III was superior to that in group II (p < 0.05), while hearts in group I showed no recovery at all. We conclude that nucleoside transport inhibition improves long-term preservation of the heart and that the mechanism of this protection may be related to an increase in endogenous adenosine and reduction of myocardial hypoxanthine content.
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PMID:Effects of nucleoside transport inhibition on long-term ex vivo preservation of canine hearts. 145 25

A newly developed troponin T (TnT) test for the detection of myocardial cell necrosis has been reported to be very efficient in the detection of acute myocardial infarction. The aim of the present study was to determine whether cardiac TnT in coronary effluent from isolated heart perfused with albumin-free perfusion medium could be detected using the enzyme-linked immuno-sorbent assay developed by Katus et al. Isolated rat hearts were perfused according to the method of Langendorff. Coronary flow rate was measured by timed collection of the coronary perfusate that dripped from the hearts during 5 h of hypoxia (protocol A) or 4 h of hypoxia followed by 1 h of reoxygenation (protocol B). Creatine kinase (CK) and lactate dehydrogenase (LD) levels were compared with that of TnT. Myocardial adenine nucleotides were measured by HPLC. There was a strong correlation between TnT levels in albumin-free coronary effluent and TnT levels in coronary effluent diluted 1:1 with 5% bovine serum albumin (r = 0.996, N = 72). The coefficients of correlation between TnT and CK or LD during hypoxia and reoxygenation were 0.891 (N = 88) and 0.871 (N = 88), respectively. The coefficient of correlation between CK and LD was 0.993 (N = 88). There were no significant differences in either the decrease of coronary flow or the increase of TnT content between the hearts in the two protocols. There was no significant correlation between sigma TnT and energy charge of adenine nucleotides. These results indicate that cardiac TnT levels can be easily measured in albumin-free coronary effluent of isolated heart preparations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Release kinetics of cardiac troponin T in coronary effluent from isolated rat hearts during hypoxia and reoxygenation. 146 27

The pathophysiology of cold injury was examined by cooling a hind leg of an anesthetized New Zealand white rabbit. A flow probe and a thermocouple were placed in the leg to be cooled to monitor the blood flow and tissue temperature. After baseline measurements, the leg was cooled with a freezing mixture up to 0 degrees C, which was followed by rewarming. The other leg served as control. In the experimental group, liposome-bound superoxide dismutase and catalase were infused through the femoral vein 15 minutes prior to putting the freezing mixture on the leg. Salicylic acid was injected through the femoral vein at the end of some experiments to assay hydroxy radical (OH). Our results demonstrated reduction of local blood flow in cold-exposed leg, indicating development of ischemia. Creatine kinase and lactage dehydrogenase were increased during rewarming in conjunction with hydroxyl radical formation, phospholipid breakdown, and lipid peroxidation. Treatment with superoxide dismutase and catalase reduced OH formation, prevented phospholipid degradation, and decreased creatine kinase, lactate dehydrogenase, and malonaldehyde formation. These results indicate that rewarming of cooled tissue is associated with "rewarming injury" similar to "reperfusion injury", and that oxygen-derived free radicals play a significant role in the pathophysiology of such injury.
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PMID:Reduction of cold injury by superoxide dismutase and catalase. 164 16

The time course of changes in serum proteins and other blood constituents after eccentric exercise of the forearm flexors by six nonweight-trained female subjects (age, 19.7 +/- 1.9 years) was investigated. Eccentric muscle actions are those in which the muscle lengthens as it exerts force, as when a person lowers a weight. Serum levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, myoglobin, as well as urea nitrogen, uric acid, creatinine, calcium, and phosphorus were examined before and for 6 days after exercise. Creatine kinase increased dramatically (peak value ranged from 6740 to 24,200 U/L) and aspartate aminotransferase, lactate dehydrogenase, alanine aminotransferase, and myoglobin followed the same time course as creatine kinase, but their peak values were lower. These proteins did not increase significantly until 48 hours after exercise and reached peak values 3 to 5 days after exercise. Alkaline phosphatase, gamma-glutamyl transpeptidase, uric acid, urea nitrogen, creatinine, calcium, and phosphorus showed no change. There is either a delay in muscle protein release by damaged muscle fibers, or the proteins are unable to leave the interstitial area for the 24 to 48 hour period after exercise. Because of the long delay, care should be taken when blood protein levels are interpreted in persons who have exercised strenuously (even if only for a short period of intense effort) several days before any diagnostic tests are performed.
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PMID:Time course of serum protein changes after strenuous exercise of the forearm flexors. 174 Jun 32


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