OBJECTIVE: To investigate changes of LDH and HBDH activity in rabbit serum after non-thermal low voltage electrical injury and to provide diagnostic criteria for non-thermal low voltage electrical injury. METHODS: Forty New Zealand rabbits were randomly distributed into control group and electrical injury group (EI-groups; designated 7 time points: 0 h, 2 h, 4 h, 12 h, 1 d, 2 d, 3 d), 5 rabbits per each group. EI-groups were treated with the method of non-thermal low voltage electrical injury established in our laboratory. Ventricular blood (5 mL) was obtained under anesthesia at designated time points after electrical injury. The activities of LDH and HBDH were measured. RESULTS: Dynamic changes were observed with certain patterns from target serum enzyme activities after electrical injury. Compared with control group, the activities of LDH increased markedly at 4 h, 12 h, and on days 1, 2, and 3 after injury (4 h, 12 h, and day 1 P<0.01; day 2 and day 3 P<0.05). Activities of HBDH increased markedly at day 2 and day 3 after injury (P<0.05). The ratio of HBDH/LDH decreased markedly at 2 h, 4 h, and 12 h after injury (P<0.01). CONCLUSION Dynamic changes of LDH and HBDH activities may be useful in diagnosis of non-thermal low voltage electrical injury and in estimation of post injury intervals.
Animals ; Electric Injuries/enzymology* ; Female ; Forensic Pathology ; Hydroxybutyrate Dehydrogenase/blood* ; L-Lactate Dehydrogenase/blood* ; Male ; Rabbits ; Random Allocation

OBJECTIVETo observe the heart damage in 10 patients with acute fluoroacetamide poisoning.

METHODSMonitoring serum activities of myocardial enzymes [creatine kinase (CK), asparate aminotransferase (AST), lactate dehydrogenase(LDH) and hydroxybutyrate dehydrogenase(HBDH)] and recording ECG on these 10 patients were performed during the period of their hospitalization. In the mean while, 24 hour dynamic ECG were also recorded and analysed using GP7000L Holter.

RESULTS(1) Urinary fluorine ion concentrations were increased in 9 patients before therapy and in all these 10 patients during therapeutic period. (2) The activities of serum CK in 2 patients and that of serum HBDH in one patient were increased before therapy. However, the serum activities of one or more than one myocardial enzymes were increased in all these 10 patients during therapeutic period. (3) Four patients had abnormal change of ECG before therapy and 5 patients during therapeutic period. (4) 24 hour dynamic ECG records showed that there were heart electrical alternans in 9 patients. One patient had wandering pacemaker and 6 patients had arythmia.

CONCLUSIONFluoroacetamide may cause obvious heart damage, and also heart electrical alternation.

Acute Disease ; Alanine Transaminase ; blood ; Creatine Kinase ; blood ; Electrocardiography ; drug effects ; Fluoroacetates ; poisoning ; Heart ; drug effects ; Humans ; Hydroxybutyrate Dehydrogenase ; blood ; L-Lactate Dehydrogenase ; blood

OBJECTIVETo study the clinical significance of changes of serum myocardial enzymes in patients with acute carbon monoxide poisoning.

METHODSTo determine the dynamic changes of the activity of myocardial enzymes and ECG in 62 patients with acute CO poisoning.

RESULTSIn patients with acute CO poisoning 5 kinds of myocardial enzymes begin to increase within 24 hours, the activities of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH), CPK isoenzyme (CK-MB) were (20.2 +/- 12.3), (151.6 +/- 91.8), (146.8 +/- 50.4), (154.8 +/- 47.7), (13.8 +/- 8.1) U/L respectively, while those in control group were (12.1 +/- 6.7), (90.6 +/- 17.3), (118.7 +/- 13.5), (89.9 +/- 27.9), (5.9 +/- 3.3) U/L respectively. There was significant difference between two groups (P < 0.01); 3 d later, the activities of 5 enzymes were still increased [(21.3 +/- 12.3), (105.8 +/- 51.4), (144.8 +/- 51.4), (159.8 +/- 35.4), (16.2 +/- 9.1) U/L respectively]. 7 and 12 d later, the activities of alpha-HBDH and CK-MB were still higher than those of control (P < 0.01). LDH(1) and LDH(2) increased to peak value in 24 h after poisoning (35.3 +/- 5.8), (43.8 +/- 5.7) U/L vs (24.8 +/- 3.9), (36.9 +/- 4.3) U/L, P < 0.01. The abnormal rate of serum LDH(1) was 78.7%, LDH(2) 58.3%, LDH 45.2%, CK-MB 37.1%, alpha-HBDH 33.6% and the abnormal rate of ECG was less than 10%.

CONCLUSIONAcute carbon monoxide poisoning may cause myocardial injury. Determination of serum myocardial enzymes may contribute to showing myocardial injury, early diagnosis and treatment, results of treatment and prognosis.

Adult ; Carbon Monoxide Poisoning ; blood ; enzymology ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; Female ; Humans ; Hydroxybutyrate Dehydrogenase ; blood ; Isoenzymes ; blood ; L-Lactate Dehydrogenase ; blood ; Male ; Middle Aged ; Myocardium ; enzymology

OBJECTIVETo investigate the clinical significance of myocardial enzymes in patients with acute tetramine (TEM) poisoning.

METHODSThe dynamic changes of the activity of myocardial enzymes and ECG were observed in 67 patients with acute TEM poisoning as well as in 67 healthy people for medical checkup at outpatient department as the control group.

RESULTSMyocardial enzymes of the patients with acute TEM poisoning were increased to different extents on the first day. There was significant difference in the activity of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) and CPK isoenzyme MB (CK-MB) between the patients and the healthy people in the control group (P < 0.01). There was significant difference in the myocardial enzymes at different time points among the patients with mild, middle and severe poisoning (P < 0.01). The severer the TEM poisoning was, the higher the activity of myocardial enzymes and the abnormal rate of ECG were. The activity of CPK was the earliest to rise with the highest aptitude of fluctuation and the longest time of elevation. The change of the myocardial enzymes was earlier than that of ECG. The abnormal rate of AST, CPK, CK-MB, LDH, alpha-HBDH was 86.57%, 98.51%, 94.03%, 89.55% and 79.10% respectively. The abnormal rate of ECG was 49.3% on the third day of poisoning. Measurement of myocardial enzymes was better than ECG in sensitivity.

CONCLUSIONAcute tetramine poisoning can damage myocardium, which is reversible. CPK is a typical marker for the damage and can serve as one of the important clinical monitoring indices.

Acute Disease ; Adolescent ; Adult ; Aspartate Aminotransferases ; metabolism ; Bridged-Ring Compounds ; poisoning ; Child ; Child, Preschool ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; metabolism ; Electrocardiography ; Female ; Humans ; Hydroxybutyrate Dehydrogenase ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Male ; Middle Aged ; Myocardium ; enzymology