OBJECTIVE: To study the changes of serum creatinine kinase(CK) and its cardiac-specific isoenzyme compound(CK-MB) levels in crush injury rats. METHODS: Crush injury was produced in SD rats, the serum levels of CK and CK-MB were studied by automated biochemical analyzer. RESULTS: The levels of plasma CK and CK-MB were much higher in crush injury rats than those of the control group. CONCLUSIONS Cardiomyocyte injury may be induced in the early stage of crush injury rats.
Animals ; Creatine Kinase/blood* ; Creatine Kinase, MB Form ; Crush Syndrome/enzymology* ; Female ; Isoenzymes/blood* ; Male ; Rats ; Rats, Sprague-Dawley

Sepsis is a common disease in critical patients, which may lead to myocardial damage, thereby aggravating the severity of the patients' condition, and causing adverse prognosis. How to detect sepsis with myocardial injury as early as possible, and use corresponding treatment measures on time are essential. Cardiac troponin I (cTnI), brain natriuretic peptide (BNP), myoglobin (Mb), MB isoenzyme of creatine kinase (CK-MB) and other traditional cardiac markers are easily affected by the complications of other critical diseases, thus the diagnostic value of those markers for myocardial injury of sepsis is reduced. In recent years, there have been some studies on heart-type fatty acid binding protein (H-FABP), microRNA (miRNA), soluble triggering receptor expressed on myeloid cell-1 (sTREM-1), high mobility group protein B1 (HMGB1), neutrophil gelatinase-associated lipocalin (NGAL), histone and other new biomarkers of myocardial injury in septic patients. This article reviewed the value of these unconventional cardiac markers in the diagnosis of sepsis-induced myocardial injury, with the hope to provide some help for clinic.
Biomarkers ; Creatine Kinase, MB Form ; Humans ; Myocardial Infarction ; Myoglobin ; Natriuretic Peptide, Brain ; Sepsis ; Troponin I

OBJECTIVETo study the changes and significance of plasma cardiotrophin-1 (CT-1) in neonates with hypoxic-ischemic encephalopathy (HIE) complicated by myocardial ischemic injury.

METHODSForty-five neonates with HIE (15 mild cases, 24 moderate cases and 6 severe cases) were enrolled and divided into two subgroups based on the presence of myocardial injury (n=19) and not (n=26). Twenty healthy neonates were used as the control group. Plasma CT-1 levels were measured using double-antibody sandwich enzyme immunoassay method. Serum creatinine kinase MB (CK-MB) and cardiac troponin I (CTnI ) levels were also measured.

RESULTSPlasma CT-1 levels in the mild HIE (169±20 pg/mL) and moderate/severe HIE subgroups (287±44 pg/mL) were significantly higher than those in the control group (30±8 pg/mL), and plasma CT-1 levels were associated with the severity of HIE (P<0.01). Plasma CT-1 levels were positively correlated with serum CK-MB and CTnI levels in neonates with HIE in the acute phase (r=0.565 and 0.621 respectively; P<0.01). Plasma CT-1 levels in neonates with myocardial injury were significantly higher than those without myocardial injury (249 ±35 pg/mL vs 177±26 pg/mL; P<0.01). Plasma CT-1 levels were significantly reduced in neonates with myocardial injury in the convalescent phase (157±19 pg/mL) compared with those in the acute phase (249±35 pg/mL; P<0.01).

CONCLUSIONSDetection of plasma CT-1 levels may be useful in the diagnosis of myocardial ischemic injury and the severity evaluation of HIE.

Creatine Kinase, MB Form ; blood ; Cytokines ; blood ; Female ; Humans ; Infant, Newborn ; Male ; Myocardial Ischemia ; blood ; Troponin I ; blood

This paper aimed to study the effect of Dalbergia cochinchinensis heartwood on plasma endogenous metabolites in rats with ligation of the left anterior descending coronary artery, and to analyze the mechanism of D. cochinchinensis heartwood in improving acute myocardial ischemic injury. The stability and consistency of the components in the D. cochinchinensis heartwood were verified by the establishment of fingerprint, and 30 male SD rats were randomly divided into a sham group, a model group, and a D. cochinchinensis heartwood(6 g·kg~(-1)) group, with 10 rats in each group. The sham group only opened the chest without ligation, while the other groups established the model of ligation. Ten days after administration, the hearts were taken for hematoxylin-eosin(HE) staining, and the content of heart injury indexes in the plasma creatine kinase isoenzyme(CK-MB) and lactate dehydrogenase(LDH), energy metabolism-related index glucose(Glu) content, and vascular endothelial function index nitric oxide(NO) was determined. The endogenous metabolites were detected by ultra-high-performance liquid chromatography-time-of-flight-mass spectrometry(UPLC-Q-TOF-MS). The results showed that the D. cochinchinensis heartwood reduced the content of CK-MB and LDH in the plasma of rats to relieve myocardial injury, reduced the content of Glu in the plasma, improved myocardial energy metabolism, increased the content of NO, cured the vascular endothelial injury, and promoted vasodilation. D. cochinchinensis heartwood improved the increase of intercellular space, myocardial inflammatory cell infiltration, and myofilament rupture caused by ligation of the left anterior descending coronary artery. The metabolomic study showed that the content of 26 metabolites in the plasma of rats in the model group increased significantly, while the content of 27 metabolites decreased significantly. Twenty metabolites were significantly adjusted after the administration of D. cochinchinensis heartwood. D. cochinchinensis heartwood can significantly adjust the metabolic abnormality in rats with ligation of the left anterior descending coronary artery, and its mechanism may be related to the regulation of cardiac energy metabolism, NO production, and inflammation. The results provide a corresponding basis for further explaining the effect of D. cochinchinensis on the acute myocardial injury.
Male ; Animals ; Rats ; Rats, Sprague-Dawley ; Dalbergia ; Myocardial Ischemia ; Metabolomics ; Heart ; Heart Injuries ; Creatine Kinase, MB Form

OBJECTIVE: To investigate the changes of creatine kinase-MB (CK-MB) and heat shock protein 60 (HSP 60) in rats without electric marks after electric injury, to identify the relationship of the CK-MB, HSP 60 and the time of electric injuries, and to evaluate the damage to cells after electric injury. METHODS: The animal model of electric injury without electric marks was established by alternating current (voltage 110 V). Automatic biochemistry analyzer was used to detect the serum CK-MB and immunohistochemical staining technology was used to analyze the tissues of myocardium and left lobe of liver. RESULTS: The amount of serum CK-MB was increased when the rats were injuried, and reached the peak at 30min. Then the amount of CK-MB began to decrease and showed a slight downward trend in 3-5 h after electric injury, and leveled off at 6 h. Immunohistochemistry staining also showed the changes of HSP 60 of rats' myocardial cells and hepatic cells regularly after electric injury. CONCLUSION The regular changes of serum CK-MB and tissular HSP 60 in rats can be used to diagnosis electric injury and assess the injury of internal organs after the electric injury without electric marks.
Animals ; Chaperonin 60/metabolism* ; Creatine Kinase, MB Form/metabolism* ; Electric Injuries/complications* ; Immunohistochemistry ; Liver/pathology* ; Myocardium/pathology* ; Rats

OBJECTIVETo study the dynamic changes of serum CK, CK-MB and myocardium histomorphology in different time periods after single bout and repeated exhausted exercise in rats.

METHODSThe animal models of myocardial injury were established by exhausted swimming. Creatine kinase (CK), creatine kinase mass (CK-MB) activities in serum were measured immediately at 3, 6, 12, 24, 48 and 96 hours after exhausted exercise, and the dynamic changes of myocardial histopathology were examined.

RESULTSThe CK, CK-MB activities were significantly increased immediately at 3, 6, 12 hours and peaked at 6 hours after single bout of exhausted exercise, meantime the degree of inflammatory cell infiltrate and strong acidophil staining were gradually increased in myocardium of rat, and the myocardial injury was most severe at 12 hours. After 1-week consecutive daily exhausted swimming, CK, CK-MB in serum were obviously increased immediately at, 3, 6, 12, 48 and 96 hours postexercise and peaked immediately and at 96 hours respectively postexercise. There were different degrees of myocardial injury in different time of recovery phase, and was most severe at 48 hours postexercise.

CONCLUSIONThe myocardial injury was induced by excessive exercise and/or exhausted exercise, and the resulting delayed-onset myocardial injury was further certified.

Animals ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; blood ; Fatigue ; blood ; Male ; Myocardium ; pathology ; Physical Exertion ; physiology ; Rats ; Rats, Wistar ; Swimming ; physiology

Acute Disease ; Carbon Monoxide Poisoning ; enzymology ; physiopathology ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; Echocardiography ; Heart ; physiopathology ; Humans ; Hyperbaric Oxygenation ; Isoenzymes ; metabolism ; Myocardium ; enzymology

Blood Pressure ; Cardiac Output ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; blood ; Female ; Heart Rate ; Humans ; Liver Transplantation ; adverse effects ; Male ; Troponin I ; blood ; Ventricular Function

OBJECTIVETo investigate (1) whether ischemic preconditioning (IPC) could protect immature rabbit hearts against ischemia-reperfusion injury and (2) the role of K(ATP) channel in the mechanism of myocardial protection. Since cardioplegia is a traditional and effective cardioprotective measure in clinic, our study is also designed to probe the compatibility between IPC and cardioplegia.

METHODSNew Zealand rabbits aged 14 - 21 days weighing 220 - 280 g were used. The animals were anesthetized and heparinized. The chest was opened and the heart was quickly removed for connection of the aorta via Langendorff's method within 30 s after excision. All hearts were perfused with Krebs-Henseleit buffer balanced with gas mixture (O(2):CO(2) = 95%:5%) at 60 cm H(2)O (perfusion pressure). IPC consisted of 5 min global ischemia plus 10 min reperfusion. Glibenclamide was used as the K(ATP) channel blocker at a concentration of 10 micro mol/L before IPC. Cardiac arrest was induced with 4 degrees C St. Thomas cardioplegic solution, at which point the heart was made globally ischemic by withholding perfusion for 45 min followed by 40 min reperfusion. Thirty immature rabbit hearts were randomly divided into four groups: CON (n = 9) was subjected to ischemia-reperfusion only; IPC (n = 9) underwent IPC and ischemia-reperfusion; Gli (n = 6) was given glibenclamide and ischemia-reperfusion; and Gli + IPC (n = 6) underwent glibenclamide, IPC and ischemia-reperfusion. Coronary flow (CF), HR, left ventricle developed pressure (LVDP), and +/- dp/dt(max) were monitored at equilibration (baseline value) and 5, 10, 20, 30 and 40 min after reperfusion. The values resulting from reperfusion were expressed as a percentage of their baseline values. Arrhythmia quantification, myocardial enzyme in the coronary effluent and myocardial energy metabolism were also determined.

RESULTSThe recovery of CF, HR, LVDP and +/- dp/dt(max) in preconditioned hearts was best among the four groups. The incidence of arrhythmia was low and less CK-MB leaked out in the IPC group. Myocardial ATP content was better preserved by IPC. Pretreatment with glibenclamide completely abolished the myocardial protection provided by IPC, but did not affect ischemia-reperfusion injury.

CONCLUSIONSWhile applying cardioplegia, IPC provides significant cardioprotective effects. Activation of K(ATP) channels is involved in the mechanism of IPC-produced cardioprotection.

Adenosine Triphosphate ; analysis ; Animals ; Creatine Kinase ; secretion ; Creatine Kinase, MB Form ; Heart Arrest, Induced ; Hemodynamics ; Ischemic Preconditioning, Myocardial ; Isoenzymes ; secretion ; Potassium Channels ; physiology ; Rabbits

Adolescent ; Alanine Transaminase ; blood ; Child ; Child, Preschool ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; blood ; Critical Illness ; Female ; Humans ; Infant ; L-Lactate Dehydrogenase ; blood ; Male ; Myocardium ; enzymology