The Cardiac Troponin T and I are highly cardiac specific biochemical markers of myocardial injury. They are very sensitive markers to detect all kinds of myocardial injury, and are able to distinguish myocardial injury and skeletal injury. Furthermore, They are independent predictor of future cardiac events. Such markers are now widely used in the clinic practice. It is prospective to use them in Forensic Medical Science.
Biomarkers ; Forensic Medicine ; Humans ; Myocardial Infarction/blood* ; Myocardium/metabolism* ; Troponin I/blood* ; Troponin T/blood*

The purpose of this study was to test whether oxygen carriers could decrease tissue injury in a rat model of acute myocardial infarct. The study included 3 groups: SD rats in group II and group III were subjected to permanent occlusion of their left anterior descending coronary arteries; SD rats in group I were subjected to sham-operation. The success of modeling was assartained by ECG. Then the rats were given drug via caudal veins for 2 days. A quantitative evaluation was made with an automatic device for interpretation of cardiac troponin T (cTnT); heart staining was made for the calculation of myocardial infarction size (MIS); and myocardial tissue was taken and subjected to routine pathological hematoxylin-eosin (HE) staining for showing myocardial cell injury. cTnT in the sham-operation group was significantly lower by comparison with that in the model group (P < 0.01), and it was slightly lower in the oxygen carriers group than that in the model group, but there was no statistically significant difference (P = 0.18); MIS was significantly smaller in the sham-operation group than that in the model group (P < 0.01), and it was greater in the model rats than that in the oxygen carriers rats (P < 0.05). HE staining of myocardicum in the oxygen carriers group was significantly better than that in the model group (P < 0.01). The evidence suggested that oxygen carriers increased oxygen supply to ischemic myocardium, reduced the myocardial injury, and thus might offer a novel treatment of myocardial infarction.
Animals ; Blood Substitutes ; pharmacology ; Hemoglobins ; metabolism ; Male ; Myocardial Infarction ; metabolism ; Oxygen ; metabolism ; Rats ; Rats, Sprague-Dawley ; Troponin T ; metabolism

OBJECTIVETo observe the influence of aminoguanidine on cardiac troponin (cTnI) and nitric oxide (NO) levels in serum and myocardium in severely scalded rats.

METHODSSeventy-two Wistar rats were subjected to 30% TBSA full-thickness scald and randomly divided into scald group(S) and aminoguanidine group (A, with intraperitoneal injection of 40 mg/kg aminoguanidine before scald). The venous blood and myocardial tissue of the rats were harvested for the determination of the level of cTnI and nitrite in both serum and myocardium before scald and at 1, 3, 6, 12 and 24 post-burn hours(PBH). Six sham scalded rats served as control group. The changes in the cTnI level and myocardial function were determined among control group, A and S groups at 6PBH.

RESULTSThe serum level of NO in S group [(59.6 +/- 5.4) micromol/L] was obviously higher than that before scald [(24.6 +/- 0.8) micromol/L, P < 0.01], and it peaked at 6 PBH, then decreased obviously at 24 PBH, which was still markedly higher than that in A group (P < 0.01). The changes in NO level in myocardium were similar to the above tendency. Compared with S group, the level of cTnI was significantly increased in A group at each time-point. Compared with A group at 6 PBH, the inhibition of the cardiac function was relatively reduced in S group at 6 PBH.

CONCLUSIONInhibition of NO synthesis by aminoguanidine aggravates cardiac damage and impairment of cardiac function of scalded rats, indicating that NO exerts protective effect on myocardium at early stage after a scald injury.

Animals ; Burns ; metabolism ; Disease Models, Animal ; Myocardium ; metabolism ; Nitric Oxide ; blood ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; Troponin T ; blood

OBJECTIVE: To study the postmortem stability of cTnT as well as its expression alteration, and to evaluate it in the diagnosis of early myocardial ischemia in forensic practice. METHODS: Animal model of early myocardial ischemia was established by rabbit coronary artery ligation. The expression of cTnT in myocardium at different postmortem intervals was detected using immunohistochemistry and analyzed using imaging technique and statistics. The results were then compared between the experimental and control groups. RESULTS: In ischemic myocardium, the expression of cTnT showed prominent focal or flaky depletion in myocardial cytoplasm with no expression detected in interstitium. The expression level showed a linear decrease with prolonged postmortem interval, and disappeared completely on day 14 after death while stored at 4 degrees C. However, there were significant differences in the expression levels of cTnT between experimental and control groups from day 1 to day 7 after death. CONCLUSION Immunohistochemical detection of cTnT for diagnosis of early myocardial ischemia in corpses stored at 4 degrees C must be performed within 7 days after death.
Animals ; Female ; Immunohistochemistry ; Male ; Myocardial Ischemia/metabolism* ; Myocardium/metabolism* ; Postmortem Changes ; Rabbits ; Random Allocation ; Time Factors ; Troponin T/metabolism*

Cardiomyopathy, Dilated/metabolism* ; Humans ; Microfilament Proteins/metabolism* ; Models, Cardiovascular ; Mutation ; Myocytes, Cardiac ; Pluripotent Stem Cells/metabolism* ; Transcription Factors/metabolism* ; Troponin T/metabolism*

OBJECTIVE: To compare the changes in muscle enzyme between children with myocarditis and Duchene/Becker muscular dystrophy (DMD/BMD), and to seek the explanations for variation.
 METHODS: The retrospective analysis for 83 myocarditis children (myocarditis group) and 69 DMD/BMD children (DMD/BMD group), who were collected from Department of Pediatric of Shengjing Hospital affiliated to China Medical University since January 2008 to May 2015, was carried out. At the same time, 24 healthy children from the Department of Pediatric Development served as a control group. The examination indexes included creatine kinase (CK), creatine kinase-isoenzyme MB (CK-MB), creatine kinase isoenzyme MB mass (CK-MB mass), cardiac troponin I (cTnI) and high-sensitive-cTnT (hs-cTnT).
 RESULTS: 1) In the myocarditis group, the CK increased from 100 to 1 000 U/L, reached a peak after 5 days, which lasted for a week and then dropped to the normal; the CK-MB reached a peak after 5 to 7 days and dropped to the normal a month later; the CK-MB mass reached a peak on the first day and dropped to the normal after 3 weeks; the cTn reached to a peak after 5 days and dropped to the normal after about 17 days; hs-cTnT reached to a peak on the first day and dropped to the normal after about 19 days. 2) In the DMD/BMD group, the CK increased significantly and 27 cases had a CK value of more than 10 000 U/L. After the treatment for 1 to 2 weeks, their enzyme rose again after a slight drop. In terms of cTnI, 6 cases showed a moderate increase, 5 of them couldn't drop to the normal level until more than 3 weeks later; the hs-cTnT increased in the 45 cases, which lasted for more than 3 weeks in the 31 cases of them and showed a tendency of persisting increase.
 CONCLUSION The cTnI and hs-cTnT rise significantly and possess wider observation window than CK and CK-MB mass in myocarditis children, with more sensitive and specific changes. The myocardial damage can occur before myasthenia and keep this trend for a long time in the DMD/BMD children. The trend of cTnI change in myocarditis children is similar to hs-cTnT, while hs-cTnT in DMD/BMD children is more sensitive than cTnI.
Biomarkers ; Child ; China ; Creatine Kinase ; blood ; metabolism ; Creatine Kinase, MB Form ; blood ; metabolism ; Female ; Humans ; Male ; Muscle Weakness ; enzymology ; Muscular Dystrophy, Duchenne ; enzymology ; therapy ; Myocarditis ; enzymology ; therapy ; Retrospective Studies ; Time Factors ; Troponin I ; blood ; metabolism ; Troponin T ; blood ; metabolism

OBJECTIVETo study the protective effect of intensive insulin treatment on the myocardium of severely scalded rats, and to primarily explore its mechanism.

METHODSEighteen SD rats were divided into three groups, with 6 rats in each group. The rats in burn and intensive insulin group were inflicted with 30% TBSA full-thickness injury on the back. Isotonic saline containing 0.12 U/ml insulin solution, and 100 g/L glucose solution were infused into the rats in the intensive insulin group to keep plasma glucose at the level of 4.0 - 6.6 mmol/L (the total fluid amount was 2 ml x kg(-1) x 8h(-1)). In sham burn group,fluid was given according to physiological demand. The same amount of isotonic saline was infused into the rats in burn group. The venous blood was obtained for the detection of plasma glucose contents, and the left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) were recorded via aortic ventricle cannula before scald and at 1, 2, 3, 4, 5, 6 post-scald hours (PSH). The tissue of the left ventricle was harvested at 6 PSH for the detection of troponin T expression in myocardiocytes.

RESULTSPlasma glucose level was increased to (7.6 +/- 1.7) mmol/L - (8.4 +/- 4.7) mmol/L in burn group during 1-6 PSH, which was significantly higher than that in intensive insulin group (4.5 +/- 0.9) mmol/L - (5.2 +/- 1.3) mmol/L, P < 0.01). Compared with the intensive insulin group, LVSP was markedly decreased in the burn group (60 +/- 11 mm Hg vs 72 +/- 8 mm Hg, P < 0.05) at 1 PSH,whereas LVEDP was increased significantly (21.3 +/- 11.3 mmHg vs 11.7 +/- 5.2 mmHg, P < 0.05). Intensive insulin treatment could significantly inhibit the loss of troponin T protein in myofilaments of myocardium.

CONCLUSIONIntensive insulin treatment possesses a protective effect on myocardia function after severe burns, and it may be related to its preventive effect on the loss of contractile protein in cardiocytes.

Animals ; Blood Glucose ; metabolism ; Burns ; drug therapy ; metabolism ; Insulin ; administration & dosage ; therapeutic use ; Male ; Myocardial Contraction ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley ; Troponin T ; metabolism

OBJECTIVETo study the relation of the structural remodeling processes and activation of calpain I.

METHODSFifteen dogs were randomly divided into three groups. The dogs in pacing group (n=5) and inhibitor group (n=5) were subjected to 3 weeks of rapid atrial pacing at 600 beats/min, control dogs (n=5) were in sham-operated group. The dogs in inhibitor group were administered intravenous N-Acetyl-Leu-Leu-Met (ALLM), a calpain inhibitor, and in pacing group and sham-operated group were administered intravenous DMSO. The activity of calpain I was measured by hydrolyzing Suc-Leu-Leu-Val-Tyr-7-amino-4-methyl-coumarin. The ultrastructure of atrium was examined by light and electron microscopy. TnT expression was assessed by Western blot. Echocardiography examination was performed in all the three groups.

RESULTSCalpain I activity was significantly increased in pacing group (2.3-fold, P<0.01), and decreased in inhibitor group (1.1-fold, P>0.05), compared to sham-operated group respectively. The percentages of myolysis were (76.7 +/- 5.9)% and (20.8 +/- 8.1)% in pacing group and inhibitor group respectively (P<0.01). TnT expression decreased in the rapid pacing-induced persistent atrial fibrillation, and these effects were inhibited by calpain I inhibitor ALLM. The area and volume of left atrium tended to increase after 3 weeks ALLM treatment in inhibitor group, but the change was not as prominent as in pacing group (P<0.05).

CONCLUSIONSALLM can decrease calpain I activity, and prevent canine atrial cardiomyocyte structural remodeling during atrial fibrillation. This study provided a capacity of atrial cardiomyocyte protection.

Animals ; Atrial Fibrillation ; metabolism ; physiopathology ; Atrial Function, Left ; Calpain ; antagonists & inhibitors ; metabolism ; Cardiac Pacing, Artificial ; Disease Models, Animal ; Dogs ; Heart Atria ; ultrastructure ; Myocardium ; metabolism ; Troponin T ; metabolism

OBJECTIVE: To study the depletion of cardiac troponin T in Rats of early myocardial ischaemia. METHODS: Immunohistochemical method (LSAB) was used and the depletion area of CTnT in myocardial ischaemia were measured by the computer image analysis. RESULTS: There is obviously depletion of CTnT after 15 min in myocardial ischaemia of rats, the mean of CTnT depletion of myocardial ischaemic group is significant difference compared with that of the control group (P < 0.01), and the depletion area increased with the prolongagtion of ischaemic time. CONCLUSION The depletion of CTnT is one of sensitive signs of early myocardial ischaemia.
Animals ; Female ; Forensic Medicine ; Image Processing, Computer-Assisted ; Immunohistochemistry ; Male ; Myocardial Ischemia/metabolism* ; Myocardium/metabolism* ; Rats ; Rats, Sprague-Dawley ; Troponin T/metabolism*

OBJECTIVETo investigate the changes of cardiac T troponin (cTnT) and high-sensitivity C reactive protein (hs-CRP) in children with viral myocarditis (VMC).

METHODSForty children with VMC were examined for cTnT, hs-CRP, and creatine kinase MB (CK-MB) levels.

RESULTSChildren with VMC had significantly higher cTnT, hs-CRP and CK-MB levels than the control group on admission (P<0.01), but obviously decreased after two weeks of treatment. The positivity rate of cTnT and hs-CRP were significantly higher in children with VMC than the control group on admission, and decreased significantly after treatment (P<0.01). The positivity rate of cTnT and hs-CRP were significantly higher than that of CK-MB (P<0.05).

CONCLUSIONSerum cTnT and hs-CRP are sensitive indices for diagnosis of VMC, and their detection have important value in estimation of the patients' condition.

Biomarkers ; blood ; C-Reactive Protein ; metabolism ; Child ; Child, Preschool ; Creatine Kinase, MB Form ; blood ; Female ; Humans ; Male ; Myocarditis ; blood ; virology ; Troponin T ; blood ; Virus Diseases ; blood