Creatine Phosphokinase Isoenzyme Research Articles

English

The prevalence of cardiovascular changes markedly increases with deterioration of patient's renal function and can stack up 65 to 70% in end-stage renal disease. A rapid fall in renal function is often associated with uncontrolled congestive heart failure. Beyond their lipid-lowering effect, statins have been shown to protect the heart in different diseases. Liraglutide is a glucagon-like peptide-1 (GLP-1) analogue, used to control diabetes. It improves cardiac dysfunction in non-diabetics, but underlying mechanisms remain to some extent, unclear. Fifty two male Sprague-Dawley rats weighing 200 to 250 g were grouped into negative control, positive control, liraglutide treated group (0.3 mg/kg), atorvastatin treated group (10 mg/kg), liraglutide and atorvastatin treated group (0.3 and 10 mg/kg, respectively), liraglutide and atorvastatin treated group (0.15 and 5 mg/kg, respectively). Combination of both drugs significantly reduce creatine phosphokinase isoenzyme (CK-MB) in both doses (p<0.008, p <0.002) and lactate dehydrognase (LDH) (p<0.04, p<0.01). Liraglutide alone or in combination with atorvastatin in both doses (p<0.02, p<0.01 and p<0.01) significantly increased superoxide dismutase (SOD). Atorvastatin alone (p<0.02) or in combination with liraglutide in both doses (p<0.001, p<0.001) induced a significant decrease of malondialdehyde (MDA). Atorvastatin alone (p<0.01) or in combination with liraglutide in both doses induced a significant amelioration of nitric oxide (NO) and cholesterol (p<0.01 and p<0.02). Significant improvements in blood urea nitrogen (BUN) and glucose profile were seen with all tested drugs either single or in combination. Combined implementation of both drugs improves histopathological changes of cardiac muscle fibres. Liraglutide has promising effects on cardiovascular changes in adenine induced chronic nephropathy through modulation of LDH, CK-MB and improvement of NO and SOD. Also, it can mitigate fibrosis and cardiac tissue changes. Its effects markedly increase in conjunction with atorvastatin. Combined administration of liraglutide and atorvastatin in a high dose has a reliable effect on improving outcome in biochemical and histopthological cardiac muscle fibers changes. Key word: Atorvastatin, liraglutide, adenine, renal failure.

Correlation Between Hyperhomocysteinemia and Outcomes of Patients With Acute Myocardial Infarction.

Overwhelming clinical and epidemiological studies have identified elevated plasma total homocysteine (Hcy) as new important risk factor for atherosclerotic vascular disease. But the relationship between outcome and hyperhomocysteinemia in patients with acute myocardial infarction (AMI) has been rarely reported. This study aimed to evaluate the association between hyperhomocysteinemia and short-term outcomes of patients with AMI. Eight hundred five patients were divided into high Hcy level group (group H: N = 457) and low Hcy level group (group L: N = 348) according to the plasma Hcy levels of 15 mmol/L. The comparisons were made between 2 groups in the following aspects: sex, hypertension, diabetes, hyperlipidemia, the time for symptom from onset to percutaneous coronary intervention, homoccyteine, creatine phosphokinase isoenzyme (creatine kinase myocardial band), and the incidence of 30-day adverse events. The incidences of heart failure, cardiac rupture, death, and the total adverse cardiovascular events were statistically significantly higher in group H than in group L. But the incidence of postoperative angina pectoris and reinfarction was similar between groups. The results of logistic regression showed that the incidence of 30-day adverse events was closely related to the age and the level of Hcy. An elevated plasma total Hcy level in patients with AMI experienced pemutaneous coronary intervention may be related to the short-term outcomes. An elevated high plasma Hcy level also seems to be an independent predictor of 30-day cardiovascular events in patients with AMI.

Application of temporary balloon occlusion of the abdominal aorta in the treatment of complete placenta previa complicated with placenta accreta

Objective: To investigate the value of temporary balloon occlusion of the abdominal aorta in the treatment of complete placenta previa with placenta accreta. Methods: From January 2015 to February 2016, 24 cases of complete placenta previa with placenta accreta were treated with temporary balloon occlusion of the abdominal aorta(the study group)before cesarean, and 24 cases of complete placenta previa with placenta accreta did not receive balloon occlusion(the control group). The operation time, intraoperative blood loss, intraoperative blood transfusion volume, the perioperative hemoglobin level, the hysterectomy rate and the related complications were compared retrospectively.Also, the hospitalization time, the blood coagulation parameters after operation, including activated partial thromboplastin time(APTT), fibrinogen(FIB), D-Dimer and reperfusion injury parameters including creatine phosphokinase(CK), creatine phosphokinase isoenzyme(CK-MB), lactate dehydrogenase(LDH)and serum creatinine were compared between the 2 groups. Results: The blood loss[750 ml(400- 2 000 ml)vs 2 000 ml(1 500- 2 375 ml); Z=-3.214, P=0.001]and blood transfusion volume[200 ml(0-800 ml)vs 800 ml(0-1 200 ml); Z=- 2.173, P=0.030]in the study group were lower than in the control group. The hemoglobin difference between before and after operation in the study group was lower than the control group[(12.8±13.4)g/L vs(22.9±20.1)g/L; t=-2.041, P=0.047]. In the study group, there were still bleeding in 13 cases after releasing the balloon, 5 of them received uterine artery embolization, 5 cases received uterine artery ligation, and 3 cases received uterine packing. One case had venous thrombosis in the right lower limb. Two cases(8%,2/24)in the control group had hysterectomy, while none in the study group, there was no statistical significance(P= 0.489). Conclusions: Temporary balloon occlusion of the abdominal aorta can effectively reduce blood loss and blood transfusion in the treatment of complete placenta previa with placenta accreta, but there is still the risk of continuing bleeding after releasing the balloon. Other methods of hemostasis might be needed.

Urocortin attenuates myocardial fibrosis in diabetic rats via the Akt/GSK-3β signaling pathway

ABSTRACTObjective: Urocortin, a novel identified corticotropin-releasing factor-related endocrinal peptide, has been shown to play an essential role in cardioprotection. Until recently, whether urocortin can protect the heart against diabetic cardiomyopathy (DCM) remained unclear. Herein, we evaluated the cardioprotective effect of urocortin on cardiac dysfunction, inflammation, and fibrosis and demonstrated the potential mechanism in a diabetic rat model. Methods: Diabetic rats were randomly divided into 4 groups: diabetic control group, urocortin, urocortin + astressin (a selective CRF receptor 2 antagonist) and urocortin + triciribine (an Akt pathway blocker). Cardiac catheterization was performed to evaluate cardiac function. The levels of creatine phosphokinase isoenzyme (CK-MB), plasma brain natriuretic peptide (BNP), myocardial collagen volume fraction (CVF) and left ventricular mass index (LVWI) were measured. Inflammatory factors (transforming growth factor beta 1, TGF-β1; connective tissue growth factor, CTGF) and activation of signaling proteins (Akt, GSK-3β) were also detected using western blot. Results: DCM was successfully induced by the injection of streptozotocin (STZ) as evidenced by abnormal heart mass and cardiac function as well as the imbalance of extracellular matrix homeostasis. Rats in the DCM group showed increased mRNA and protein levels of LVWI, BNP, CK-MB, CVF, TGF-β1 and CTGF compared to the control group, which were accompanied with diminished phosphorylation of Akt and GSK-3β. Interestingly, myocardial dysfunction, cardiac fibrosis, and inflammation were suppressed by urocortin in the heart of diabetic rats. Moreover, inhibition of phosphorylation of Akt and GSK-3β was also reversed by urocortin. These effects of urocortin were suppressed by astressin. In addition, triciribine partially reduced the effects of urocortin on myocardial dysfunction, inflammation, and cardiac fibrosis. Conclusions: These results suggest that urocortin exhibits a therapeutic benefit in the treatment of DCM by attenuating fibrosis and inflammation. Furthermore, inhibition of the Akt/GSK-3β signaling pathway may be partially responsible for these effects.

Impact of Acute Bronchiolitis on Cardiac Functions and Serum microRNA-122 and 499

Bronchiolitis is an acute inflammatory injury of the bronchioles that is usually caused by a viral infection, most commonly Respiratory Syncytial Virus (RSV). This study aimed to verify the direct injurious effect of acute bronchiolitis on the myocardium and serum level of microRNA-122 and 499 (miR-122 and miR-499) of infected infants. Serum lactate dehydrogenase (LDH), creatine phosphokinase-isoenzyme MB (CK-MB) and cardiac troponin I (cTp I) were significantly elevated in mild to moderate group as well as severe group except cTp I which showed non-significant elevation in mild to moderate group, compared to control group. Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR) was carried out to evaluate the serum level of miR-122 and miR-499. Sharp elevation in serum miR-122 was observed in severe cases, while miR-499 was statistically non-significant as compared to both normal and mild to moderate groups. The flow velocities across the pulmonary, tricuspid and mitral valves were recorded using standard echocardiographic techniques. Echocardiographic data showed significant reduction in pulmonary At/Et ratio in severe bronchiolitis group, compared to both normal and mild to moderate groups, respectively. Parallel reduction was also observed in tricuspid and mitral E/A ratios, compared to both normal and mild to moderate groups, respectively. Severe bronchiolitis causes cardiac dysfunction due to hypoxia, cardiac strain and pulmonary hypertension in addition to up-regulation of serum miRNA-122.

Lycopene modulates cholinergic dysfunction, Bcl-2/Bax balance, and antioxidant enzymes gene transcripts in monosodium glutamate (E621) induced neurotoxicity in a rat model.

The effect of monosodium glutamate (MSG) on brain tissue and the relative ability of lycopene to avert these neurotoxic effects were investigated. Thirty-two male Wistar rats were distributed into 4 groups: group I, untreated (placebo); group II, injected with MSG (5 mg·kg(-1)) s.c.; group III, gastrogavaged with lycopene (10 mg·kg(-1)) p.o.; and group IV received MSG with lycopene with the same mentioned doses for 30 days. The results showed that MSG induced elevation in lipid peroxidation marker and perturbation in the antioxidant homeostasis and increased the levels of brain and serum cholinesterase (ChE), total creatine phosphokinase (CPK), creatine phosphokinase isoenzymes BB (CPK-BB), and lactate dehydrogenase (LDH). Glutathione S-transferase (GST), superoxide dismutase (SOD), and catalase (CAT) activities and gene expression were increased and glutathione content was reduced in the MSG-challenged rats, and these effects were ameliorated by lycopene. Furthermore, MSG induced apoptosis in brain tissues reflected in upregulation of pro-apoptotic Bax while lycopene upregulated the anti-apoptotic Bcl-2. Our results indicate that lycopene appears to be highly effective in relieving the toxic effects of MSG by inhibiting lipid peroxidation and inducing modifications in the activity of cholinesterase and antioxidant pathways. Interestingly, lycopene protects brain tissue by inhibiting apoptosis signaling induced by MSG.

Changes in Creatine Phosphokinase Isoenzymes Following Resistance Exercise at Different Intensities

Creatine phosphokinase (CK) isoenzymes are found in various tissues, such as skeletal muscle (CK-MM), cardiac muscle (CK-MB), and the brain (CK-BB). Elevated CK isoenzymes indicate damage or injury to specific tissue. Changes in CK isoenzymes in response to resistance exercise at different intensities have not been clearly examined. PURPOSE: To determine the changes in CK isoenzymes following resistance exercise at different intensities. METHODS: Ten healthy recreationally resistance-trained (at least 3–6 days per week for a minimum of one year) men participated in the study. The participants performed a lower body resistance exercise, composed of leg press and unilateral knee extension, at two different intensities (low: 50% of 1-RM and high: 80% of 1-RM) in random order. The volume of two intensities was similar. Serum samples were collected at baseline and 3-hr, 24-hr, and 48-hr post exercise for each intensity to determine CK-MM, CK-MB, and CK-BB using electrophoresis. A 2 X 4 ANOVA with repeated measures was used to examine the mean differences in intensity and time on dependent variables. The Bonferroni pairwise comparisons were conducted to locate the significant mean differences. If a significant interaction was found, the follow-up simple effects test was conducted. A p-value < .05 was set for the statistical significance. RESULTS: There was no significant main effect for intensity or time on CK-MM, CK-MB, or CK-BB. However, the significant interaction between intensity and time indicated that CK-MM was significantly higher (93.00±4.03 vs. 86.39±4.15%, p = 0.002), while CK-MB was significantly lower (7.13±4.22 vs. 12.37±3.30%, p = 0.006), at 48-hr following the high-intensity exercise trial as compared with the same time point of low intensity exercise trial. CONCLUSION: Elevated CK-MM observed several days after high intensity resistance exercise indicates that exercise-induced skeletal muscle damage is dependent on the intensity. Interestingly, high intensity resistance exercise may positively influence cardiac muscle damage by reducing CK-MB.

Urocortin ameliorates diabetic cardiomyopathy in rats via the Akt/GSK-3β signaling pathway.

Urocortin has been shown to exert powerful protective effects on various cardiovascular disease models. However, the role and mechanism of urocortin in protecting against diabetic cardiomyopathy (DCM) has not yet been elucidated. In the present study, the effects of urocortin on cardiac dysfunction, fibrosis, inflammation and the interrelated signaling pathways were investigated in a diabetic rat model. Diabetes mellitus (DM) was induced in the rats by intraperitoneal injection of streptozotocin. The diabetic rats were randomly divided into four groups: Diabetic control, urocortin, urocortin + astressin treatment and urocortin + triciribine treatment groups. All the experiments were conducted at 16 weeks following the induction of DM. The levels of glycosylated hemoglobin (HbA1c), creatine phosphokinase isoenzyme (CK-MB) and plasma brain natriuretic peptide (BNP), as well as the myocardial collagen volume fraction (CVF) and left ventricular mass index (LVWI), were measured. In addition, levels of inflammatory factors, including transforming growth factor (TGF)-β1, connective tissue growth factor (CTGF) and interrelated proteins, such as Akt and glycogen synthase kinase (GSK)-3β, were detected by biochemical analyses. In the diabetic group, the levels of BNP and CK-MB, as well as the mRNA and protein expression levels of TGF-β1 and CTGF, and the LVWI and CVF, were higher compared with the rats in the control group (P<0.05). This was accompanied by decreased Akt and GSK-3β phosphorylation (P<0.05). Notably, urocortin attenuated myocardial dysfunction, cardiac fibrosis and inflammation in the hearts of the diabetic rats. However, urocortin exhibited no effect on the level of HbA1c. In addition, the inhibited phosphorylation of Akt and GSK-3β was restored with urocortin administration. However, all the effects of urocortin were eliminated with treatment of the corticotropin releasing factor receptor 2 antagonist, astressin. Triciribine, an Akt inhibitor, partially eliminated the effects of urocortin on myocardial dysfunction, inflammation and cardiac fibrosis in the hearts of the diabetic rats. These results indicated that urocortin may exhibit great therapeutic potential in the treatment of DCM by attenuating fibrosis and inflammation. Furthermore, the Akt/GSK-3β signaling pathway may be partially involved in mediating these effects.

Serum dosage of CPK-MB in dogs with ST deviation by chemiluminescence

Abstract: Although frequently in humans, hypoxic and ischemic heart diseases are poorly documented in dogs, with only few reports of acute myocardial infarction (AMI) in this species. Some electrocardiographic findings might suggest myocardium hypoxia/ischemia, like ST segment elevation or depression, but there are no studies showing whether deviations in ST segment are associated to myocardial injury and serum increase of creatine phosphokinase (CPK-MB). In order to investigate possible myocardial cells injury in poor perfusion conditions, 38 dogs were studied, 20 with normal electrocardiogram and 18 with ST segment elevation or depression, recorded in lead II, at a paper speed of 50 mm/sec and N sensibility (1mV=1cm). Serum measurement of creatine phosphokinase isoenzyme MB (CPK-MB) in normal dogs (group 1) determined control values (in ng/mL), which were compared to those obtained from dogs with deviation (group 2), which allowed confirmation or not of myocardial injury. CPK-MB mean values obtained from dogs in groups 1 and 2 were 0.540ng/ml (SD±0.890)ng/mL and 0.440ng/mL (SD±1.106), respectively. At a significance level of 5%, the relation of CPK-MB with age, mass and total creatine phosphokinase (CPK-T) was not significant in groups 1 and 2. CPK-MB showed no difference, at 5% level, between groups 1 and 2. In conclusion, it is possible to use the human chemiluminescent immunometric assay kit in canine species and that hypoxia/ischemia revealed by ST segment deviation does not mean significant myocardium injury.

Search of substances with the cardioprotective activity in the series of derivatives of halogenides 1-alkyl- and carboxyalkyl-4-ylideneamino-1,2,4-triazole

In spite of achievements in the sphere of highly effective drugs creation for treating cardiovascular diseases the problem is still urgent since mortality is high because of these diseases, and it takes the 2-nd – 3-d place among the population of industrially developed countries. In the Research and Production Association “Pharmatron” a new approach concerning creation of new effective anti-anginal drugs has been developed; it is a chemical modification of position 1 and 4 of 1,2,4-triazole molecule by introduction of the structural fragments of the most active medicines and structures imitating sites of adrenergic receptors. Bromides of 1-(alkyl) carboxyalkyl-4-ylideneamino-1,2,4-triazole have been synthesized at the Pharmaceutical Chemistry department of Zaporizhzhia State Medical University under the supervision of professor I.A.Mazur. The cardioprotective activity of 12 compounds – derivatives of 1-carboxyalkyl-4-ylideneamino-1,2,4-triazole bromides and 1-alkyl-4-ylidenamino-1,2,4-triazole bromides has been investigated. The experiments were conducted in 510 white outbred male rats weighing 120-130 g from the mouse bank of the Institute of Pharmacology and Toxicology of the AMS of Ukraine. Determination of acute toxicity of the compounds investigated was conducted according to Kerber method. It has been found that LD50 of these compounds when introduced intraabdominally to rats is within 29.5-295 mg/kg. It allows to refer the compounds under research to the III and IV classes of toxicity (moderate or low toxic). The model of acute myocardial infarction in rats was used for studying the cardioprotective activity of the compounds, the infarction was modeled by staged introduction of isadrin and pituitrin. It has been found that intraabdominal introduction of 8 compounds of 12 ones in the dose of 1/100 LD50 to rats with myocardial infarction leads to decrease of hyperenzymemia of cardiospecific isoenzymes of creatine phosphokinase (MB CPK) and lactate dehydrogenase (LDH-1), which play the role of biochemical markers of the myocardium damage, and decrease of electrophysiological marker ΣΔST during electrocardiography. The structural fragments of the molecule, which play a determinative role in manifestation of the cardioprotective effect of such series as β-phenylethyl, carboxy propyl, octyl in position 1 and the presence of amino- and n-methoxybensilidenamino-groups in position 4, have been revealed. It has been determined that compound MT significantly exceeds the therapeutical efficacy of metoprolol by decrease of MB CPK and LDH-1 activity in the blood serum of rats with myocardial infarction, as well as decrease of ECG ST amplitude.

Clinical, biochemical and genetic analysis of the mitochondrial disorders presenting with cardiac damage

Mitochondrial disease is a group of energy metabolic disorders, characterized by involvement of multisystem with high energy requirements. Encephalomyopathies are common clinical findings of the mitochondrial diseases. However, mitochondrial cardiac damage is not rare. In this study, the clinical, biological, and genetic analyses were performed in three patients with mitochondrial cardiac damage, in order to understand the characteristics of mitochondrial diseases. Three girls presented with arrhythmia and cardiac enlargement from the age of 3, 4 and 8 years respectively. They were admitted into the Peking University First Hospital. Infection, autoimmune diseases, aminoacidopathies, organic acidurias, mitochondrial-fatty acid oxidation defects, and lysosomal storage disease were excluded by routine laboratory examinations and metabolic analysis for blood amino acids, acylcarnitines, urinary organic acids, and lysosome activity assay. Peripheral leukocytes mitochondrial respiratory chain enzyme I to V activities were measured by spectrophotometry. The entire sequence of the mitochondrial DNA was analyzed. In two patients (case 1 and case 3), hypertrophic cardiomyopathy and grade I to grade II of cardiac function were found. One patient (case 2) was diagnosed with arrhythmia and grade I of cardiac function. Increased creatine phosphokinase and creatine kinase isoenzyme MB were observed. Mitochondrial respiratory chain complex deficiencies were indentified in the three patients. Patient 1 had combined deficiencies of complex III and V. The activity of complex I+III was 18.7 nmol/(min·mg mitochondrial protein) (control 84.4 ± 28.5). The activity of complex V was 20.4 nmol/(min·mg mitochondrial protein) (control 103.7 ± 29.2). In her mitochondrial gene, A14693G on tRNA(Glu) and T16519C on D-loop were found. Patient 2 had an isolated complex I deficiency. The activity was 22.0 nmol/(min·mg mitochondrial protein) (control 44.0 ± 5.4). A16183C, T16189C and G15043A mutations on D-loop were found. Patient 3 had a combined deficiency of complex IV and V. The activity of complex IV was 21.0 nmol/(min·mg mitochondrial protein) (control 54.1 ± 12.3). The activity of complex V was 23.2 nmol/(min·mg mitochondrial protein) (control 103.7 ± 29.2). C253T and C16187T mutations on D-loop were detected. Haplotype analysis showed that three patients belong to H2a2a. Improvement was observed after the treatment with L-carnitine, coenzyme Q10, vitamin C and E. At present, the patients are 7, 5 and 8 years old. Although excise intolerance still persists, they had a good general condition with normal school life. The mitochondrial diseases with cardiac damage show cardiomyopathy, arrhythmia and exercise intolerance. Many kinds of mitochondrial respiratory chain deficiency were observed. A14693G in mitochondrial tRNA(Glu) gene is probably one of the causes in China.

Dilated Cardiomyopathy in Becker Muscular Dystrophy: A Case Report

BACKGROUND: Becker Muscular Dystrophy (BMD) is a rare X-linked muscular dystrophy, with an incidence of 3 in 100,000 live male births. The most common cardiac presentation is cardiomyopathy (occurs in 50% of cases) and conduction disorders. CASE: This is a case of a 27 year-old male who was diagnosed with BMD during his childhood. He developed gradual progressive muscle weakness with decrease in basal functional capacity. Dilated cardiomyopathy was observed based on clinical and echocardiographic findings. He was later admitted due to ventricular tachycardia. Upon admission, the chest x-ray showed cardiomegaly. Laboratory examination showed markedly elevated creatine phosphokinase (CPK) isoenzymes. Two- dimensional echocardiography showed generalized hypokinesia with severely depressed systolic function; and dilated left ventricular cavity and left atrium. The hospital course of the patient is herein described.

Evaluation of Creatine Phosphokinase Isoenzyme Activity in Acute Myocardial Infarction

Evaluation of Creatine Phosphokinase Isoenzyme Activity in Acute Myocardial Infarction

Fluorescent Determination of Creatine Phosphokinase Isoenzymes by Using Stream-Switching System

Fluorescent Determination of Creatine Phosphokinase Isoenzymes by Using Stream-Switching System

Antioxidant and antiapoptotic effects of proanthocyanidin and ginkgo biloba extract against doxorubicin‐induced cardiac injury in rats

Grape seed proanthocyanidins (GSPE) and ginkgo biloba extract (EGb761) are considered to have protective effects against several diseases. The cardiotoxicity of doxorubicin (DOX) has been reported to be associated with oxidative damage. This study was conducted to evaluate the cardioprotective effects of GSPE and EGb761 against DOX-induced heart injury in rats. DOX was administered as a single i.p. dose (20 mg kg(-1)) to adult male rats. DOX-intoxicated rats were orally administered GSPE (200 mg kg(-1) day(-1)) or EGb761 (100 mg kg(-1) day(-1)) for 15 consecutive days, starting 10 days prior DOX injection. DOX-induced cardiotoxicity was evidenced by a significant increase in serum aspartate transaminase (AST), creatine phosphokinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), total cholesterol (TC) and triglyceride (TG) activities and levels. Increased oxidative damage was expressed by the depletion of cardiac reduced glutathione (GSH), elevation of cardiac total antioxidant (TAO) level and accumulation of the lipid peroxidation product, malondialdehyde (MDA). Significant rises in cardiac tumour necrosis factor-alpha (TNF-α) and caspase-3 levels were noticed in DOX-intoxicated rats. These changes were ameliorated in the GSPE and EGb761-treated groups. Histopathological analysis confirmed the cardioprotective effects of GSPE and EGb761. In conclusion, GSPE and EGb761 mediate their protective effect against DOX-induced cardiac injury through antioxidant, anti-inflammatory and antiapoptotic mechanisms.

Metformin Attenuates Doxorubicin‐induced Cardiotoxicity In Rats

The clinical use of doxorubicin (DOX), a potent chemotherapeutic agent, is limited by its cardiotoxic side effects that are attributed to free radical generation. Recent studies have established that metformin (MET), an oral antidiabetic drug, possesses an antioxidant activity. However, whether it can protect against DOX‐induced cardiotoxicity has not been reported before. The goal of the present study was to assess the extent to which MET can prevent cardiotoxicity induced by DOX. Results of our study in a rat model of DOX‐induced cardiotoxicity show that DOX treatment caused significant increases in serum levels of lactate dehydrogenase (LDH) and creatine phosphokinase isoenzyme MB (CK‐MB), indicators of cardiac injury. In addition, DOX therapy decreased cardiac glutathione, an endogenous antioxidant; CoA‐SH, an activator in mitochondrial energy providing systems. These biochemical changes were associated with myocardial histopathological and ultrastructural deteriorations. Co‐treatment with MET eliminated all DOX‐induced increases of LDH and CK‐MB and prevented GSH, CoA‐SH and ATP depletions. MET therapy also prevented all the myocardial histopathological and ultrastructural deteriorations. These findings demonstrate, that MET successfully prevents DOX‐induced cardiotoxicity.

The role of CPK isoenzymes in predicting extrauterine early pregnancy

To evaluate the ability of Creatine phosphokinase (CPK) levels and CPK-MB proportion to differentiate between extra and intrauterine of very early gestations with unknown location. The study is case-control. CPK levels and CPK-MB proportion in 51 women with extrauterine pregnancies were compared to those in 28 women with early intrauterine pregnancies. No significant difference was found between women with extrauterine pregnancies and early intrauterine pregnancies in the levels of CPK (80.9 ± 62.1 vs. 74.9 ± 51.5; p = 0.66) and CPK-MB proportion (16.2 ± 10.1% vs. 15.1 ± 11.1%; p = 0.86). CPK and CPK-MB proportion determinations do not contribute to the clinical differentiation between early intra and extrauterine pregnancies.

筋ジストロフイー症及び類縁疾患におけるlactate dehydrogenase isoenzymeとcreatine phosphokinase isoenzymeの検討

筋ジストロフイー症及び類縁疾患におけるlactate dehydrogenase isoenzymeとcreatine phosphokinase isoenzymeの検討

Tranexamic Acid Reduces Blood Loss After Off-Pump Coronary Surgery

Bleeding and the need for allogeneic transfusions are still problems after off-pump coronary artery bypass grafting (OPCAB) surgery. We therefore evaluated the effects of an antifibrinolytic, tranexamic acid, on postoperative bleeding and transfusion requirements in patients undergoing OPCAB surgery. Two hundred thirty-one consecutive patients scheduled for elective OPCAB were enrolled in the study. Using a double-blind method, the patients were randomly assigned to receive either tranexamic acid (bolus 1 g before surgical incision followed by an infusion of 400 mg/h during surgery; n = 116) or a placebo (infusion equivalent volume of saline solution; n = 115). The primary outcome was 24-hour postoperative chest tube drainage. Allogeneic transfusion, mortality, major morbidities, and resource utilization were also recorded. In comparison with the placebo group, the patients receiving tranexamic acid had a significant reduction in chest tube drainage at 6 hours (270 ± 118 mL vs 416 ± 179 mL, P < 0.001) and 24 hours (654 ± 224 mL vs 891 ± 295 mL, P < 0.001). There was also a significant reduction in allogeneic red blood cell transfusions (47 vs 31.9%, P = 0.019) and fresh frozen plasma (29.6% vs 17.2%, P = 0.027) transfusions. There were no differences in mortality, morbidity, and resource utilization between the 2 groups. Tranexamic acid reduces postoperative chest tube drainage and the requirement for allogeneic transfusion in off-pump coronary surgery.

Sesamol Attenuates Isoproterenol-induced Acute Myocardial Infarction via Inhibition of Matrix Metalloproteinase-2 and -9 Expression in Rats

Background/Aims: The protective role of sesamol and its possible action against isoproterenol-induced myocardial injury and infarction is unknown. We tested the hypothesis that sesamol’s protection against myocardial infarction is associated with the inhibition of matrix metalloproteinase (MMP)-2 and MMP-9. Methods: Four groups of experimental rats were subcutaneously injected with sesamol (0, 1, 3, or 10 mg/kg) and then, 2 h later, intraperitoneally injected with isoproterenol (100 mg/kg 24 h apart on 2 consecutive days) to induce myocardial infarction. Control rats were treated with saline only. Blood pressure (BP), heart rate (HR), and electrocardiography (ECG) wave durations, serum creatine phosphokinase isoenzymes (CKMB), lactate dehydrogenase (LDH), myocardial histology, MMP-2, and MMP-9 were assessed 24 h after the last dose of isoproterenol was given. Results: BP was lower, and HR, ECG wave durations, CKMB, LDH, myocardial injury, MMP-2, and MMP-9 levels were higher in experimental rats than in control rats. BP was significantly higher, and all the other parameters were significantly lower in the rats treated with sesamol than in those treated with isoproterenol only. Conclusions: Sesamol effectively prevented myocardial infarction, at least in part, by controlling proteolytic activities and the expression of MMP-2 and -9 in isoproterenol-treated rats.