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*

Child ; Child, Preschool ; Female ; Heart Defects, Congenital ; metabolism ; Humans ; Male ; Troponin I ; metabolism

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

The aim of the present study was to investigate the expressions of calpain and calpastatin in the myocardium of simulated weightlessness rats, and to elucidate the underlying mechanism of cardiac troponin I (cTnI) degradations. Tail-suspended (SUS) rats were used as a simulated weightlessness model on the ground. The myocardium of rats was homogenized, and the expressions of calpain-1, calpain-2, calpastatin and cTnI were analyzed by Western blotting technique. Calpastatin expression was significantly decreased in 2- and 4-week SUS groups compared with that in the synchronous controls (P<0.05). Calpain-2 expression was slightly decreased, whereas calpain-1 expression was unaltered in SUS groups. However, calpain-1/calpastatin and calpain-2/calpastatin ratios were increased after tail-suspension, being significantly higher in 2- and 4-week SUS groups than those in the synchronous controls (P<0.05, P<0.01). Cardiac TnI degradation was significantly increased after tail-suspension (P<0.01), but cTnI degradation in both SUS and control groups was significantly inhibited by a non-specific inhibitor of calpain, PD150606 (P<0.01). These results suggest that an increase in calpain activity may enhance cTnI degradation in the myocardium of tail-suspended rats.
Animals ; Calcium-Binding Proteins ; metabolism ; Calpain ; metabolism ; Hindlimb Suspension ; Myocardium ; metabolism ; Proteolysis ; Rats ; Troponin I ; metabolism ; Weightlessness Simulation

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*

Actins ; metabolism ; Animals ; Antigens, CD ; metabolism ; Cadherins ; metabolism ; Carotid Artery Injuries ; metabolism ; pathology ; Endothelium, Vascular ; metabolism ; ultrastructure ; Fluorescent Antibody Technique ; Microscopy, Confocal ; Rats ; Troponin ; 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 investigate the changes in aquaporin-1 (AQP-1) expression in myocardium of scalded rats in early stage of a burn injury, and to analyze its relationship with myocardial edema.

METHODSThirty-six healthy Wistar rats were divided into normal control (n = 6, without scald) and scald (n = 30) groups according to the random number table. Rats in scald group were inflicted with 30%TBSA full-thickness scald on the back, and intraperitoneally injected with Ringer's solution for antishock treatment. Myocardium tissue from left ventricle and serum specimen in rats of scald group were collected at post scald hours (PSH) 2, 8, 12, 24, and 48 (with 6 rats at each time point). Myocardial water ratio was determined by dry-wet weight method. The distribution of AQP-1 protein in myocardium was observed with immunohistochemical staining. The expression of myocardial AQP-1 mRNA was assessed with quantitative real-time PCR. The serum content of cardiac troponin-I (cTnI) was determined with ELISA. The rats in normal control group were detected with above-mentioned method. Data were processed with one way analysis of variance and LSD test. Correlation analysis was performed between AQP-1 mRNA and myocardial water ratio, AQP-1 mRNA and the serum content of cTnI in scald group at each time point.

RESULTSCompared with that in normal control group, the myocardial water ratio in scald group was markedly increased during PSH 8-48 (P values all below 0.01), and it peaked at PSH 12 [(80.79 ± 0.12)%]. In both groups, AQP-1 was mainly expressed in endothelial cells of capillaries and pericellular membrane of myocardial cells. The expression of AQP-1 in scald group was markedly increased from PSH 2 to PSH 48. The expression of myocardial AQP-1 mRNA in scald group was markedly higher from PSH 2 to PSH 48 than that in normal control group (P values all below 0.01), and it peaked at PSH 12 [(6.2 ± 0.7)%]. The serum content of cTnI in scald group was obviously higher from PSH 2 to PSH 48 than that in normal control group (P values all below 0.01), and it peaked at PSH 12 [(5.83 ± 0.51) µg/L]. There were statistically positive correlations between AQP-1 mRNA expression and myocardial water ratio (r = 0.849, P < 0.01), AQP-1 mRNA expression and the serum content of cTnI (r = 0.973, P < 0.01) in scald group.

CONCLUSIONSAQP-1 may play a key role in the development of myocardial edema in rats with scald.

Animals ; Aquaporin 1 ; metabolism ; Burns ; metabolism ; pathology ; Cardiomyopathies ; metabolism ; Disease Models, Animal ; Edema ; metabolism ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Wistar ; Troponin I ; blood

OBJECTIVETo study possible correlation between matrix metalloproteinases (MMPs) activities and myocardial injury after asphyxia in neonatal Wistar rats.

METHODSixty neonatal Wistar rats (7 to 10 days old) were randomly divided into four groups: control group (group D); asphyxia groups A, B and C (1 day, 7 days, 14 days after asphyxia), every group had 15 rats. In the asphyxia groups, animal model was produced by normobaric asphyxia. Groups A, B and C were sacrificed on days 1, 7 and 14 days after asphyxia, and group D rats were sacrificed on the 7 th day. Then the heart blood was taken to tested the serum cTnI. The myocardial MMPs-3 and 9 activity was measured by using immunohistochemical assay. Histological sections of the hearts were stained with hematoxylin-eosin and myocardial histopathological scores were determined under an optical microscope. The amount of myocardial collagen was measured by means of chloramines T.

RESULTScTnI was significantly higher in group A (0.3680 +/- 0.40 ng/ml) than group D (0.0783 +/- 0.06 ng/ml) (P < 0.05), and was lower in group B (0.1889 +/- 0.15 ng/ml) but still significantly different from that of group D (P < 0.05), and declined to the normal level in group C (0.1338 +/- 0.07 ng/ml), but the difference between groups C and D was not significant (P > 0.05). Myocardial tissue MMPs-3 activity was transiently high in group A (0.1847 +/- 0.04), higher in group B (0.2780 +/- 0.05) as compared to group D (0.1213 +/- 0.03) (P < 0.05 for all). The activity of MMPs-3 increased earlier than that of MMPs-9. The amount of myocardial collagen of group B (38.94 +/- 0.67) and C (40.69 +/- 0.75) was significantly greater than that of group D (P < 0.05). Myoardial tissue MMPs-3 and MMPs-9 positively correlated with myocardial histopathological scores (r = 0.669, 0.667, P < 0.05) and myocardial collagen (r = 0.482, 0.679, P < 0.05).

CONCLUSIONSIn rats with asphyxia, there was an excess activation of myocardial MMPs-3 and MMPs-9 activities and secondary to which, the quantity of myocardial collagen increased. The injuries of myocardium may be closely associated with myocardial tissue MMPs. MMPs may be used to evaluate the severity of myocardial interstitial damage.

Animals ; Asphyxia ; metabolism ; pathology ; Collagen ; metabolism ; Disease Models, Animal ; Matrix Metalloproteinase 3 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Wistar ; Troponin I ; blood