Serum Levels Of Cardiac Markers Research Articles

Linagliptin and secoisolariciresinol diglucoside attenuate hyperlipidemia and cardiac hypertrophy induced by a high-methionine diet in rats via suppression of hyperhomocysteinemia-induced endoplasmic reticulum stress.

Background: Cardiac hypertrophy (CH) is one of the contributing causes of morbidity and mortality. Hyperhomocysteinemia (HHcy) is one of the diseases which may predispose hyperlipidemia and CH. Linagliptin (Lina) and secoisolariciresinol diglucoside (SDG) are known to alleviate a variety of illnesses by reducing oxidative stress and inflammation. Aim: This study aimed to study the effect of HHcy on cardiac tissues, with a special focus on endoplasmic reticulum (ER) stress as a mainstay pathophysiological pathway. In addition, our study examined the protective effect of Lina, SDG, and their combination against HHcy-induced hyperlipidemia and CH in rats. Methods: Seventy-five male Sprague-Dawley rats were randomly divided into five groups, and for 60days, the following regimen was administered: Group I: rats received distilled water; Group II: rats received methionine (MET) (2g/kg/day, p.o.); groups III and IV: rats received Lina (3mg/kg/day, p.o.) and SDG (20mg/kg/day, p.o.), respectively, followed by MET (2g/kg/day, p.o.); Group V: rats received Lina and SDG, followed by MET (2g/kg/day, p.o.). Results: Pretreatment with Lina, SDG, and their combination showed a significant decrease in serum levels of HHcy and an improved lipid profile compared to the MET group. Moreover, both drugs improved cardiac injury, as evidenced by the substantial improvement in ECG parameters, morphological features of the cardiac muscle, and reduced serum levels of cardiac markers. Additionally, Lina and SDG significantly attenuated cardiac oxidative stress, inflammation, and apoptosis. Furthermore, Lina, SDG, and their combination remarkably downregulated the enhanced expression of endoplasmic reticulum (ER) stress markers, GRP78, PERK, ATF-4, CHOP, NF-κB, and SREBP1c compared to the MET-group. Conclusion: Lina and SDG showed cardioprotective effects against HHcy-induced heart hypertrophy and hyperlipidemia in rats.

The protective effects of topiramate and spirulina against doxorubicin-induced cardiotoxicity in rats.

Doxorubicin (DOX) is a widely used chemotherapy drug that can cause significant cardiotoxicity, limiting its clinical application. This study aimed to investigate the potential protective effects of topiramate (TPM) and spirulina (SP), either alone or in combination, in preventing DOX-induced cardiotoxicity. Adult Sprague Dawley rats were divided into five groups, including a normal control group and groups receiving DOX alone, DOX with TPM, DOX with SP, or DOX with a combination of TPM and SP. Cardiotoxicity was induced by administering DOX intraperitoneally at a cumulative dose of 16 mg/kg over 4weeks. TPM and/or SP administration started 1week before DOX treatment and continued for 35 days. Body weight, serum markers of cardiac damage, oxidative stress and inflammatory parameters were assessed. Histopathological and immunohistochemical examinations were performed on cardiac tissues. Results showed that TPM and SP monotherapy led to significant improvements in serum levels of cardiac markers, decreased oxidative stress, reduced fibrosis-related growth factor levels, increased antioxidant levels, and improved histopathological features. SP demonstrated more prominent effects in comparison to TPM, and the combination of TPM and SP exhibited even more pronounced effects. In conclusion, TPM and SP, either alone or in combination, hold promise as therapeutic interventions for mitigating DOX-induced cardiotoxicity.

Biochemical, Histological, and Ultrastructural Studies of the Protective Role of Vitamin E on Cyclophosphamide-Induced Cardiotoxicity in Male Rats

Cyclophosphamide (CP) (Cytoxan or Endoxan) is an efficient anti-tumor agent, widely used for the treatment of various neoplastic diseases. The study aimed to investigate the protective role of vitamin E (vit E) in improving cardiotoxicity in rats induced by CP. Forty male Wistar rats were divided randomly into four experimental groups (each consisting of ten rats); the control group was treated with saline. The other three groups were treated with vit E, CP, and the combination of vit E and CP. Serum lipid profiles, enzyme cardiac biomarkers, and cardiac tissue antioxidants were evaluated, as well as histological and ultrastructure investigations. CP-treated rats showed a significant increase in serum levels of cardiac markers (troponin, CK, LDH, AST, and ALT), lipid profiles, a reduction in the antioxidant enzyme activities (CAT, SOD, and GPx), and an elevation in the level of lipid peroxidation (LPO). The increase in the levels of troponin, LDH, AST, ALP, and triglycerides is a predominant indicator of cardiac damage due to the toxic effect of CP. The biochemical changes parallel cardiac injuries such as myocardial infarction, myocarditis, and heart failure. Vitamin E played a pivotal role, as it attenuated most of these changes because of its ability to scavenge free radicals and reduce LPO. In addition, vit E was found to improve the histopathological alterations caused by CP where no evidence of damage was observed in the cardiac architecture, and the cardiac fibers had regained their normal structure with minimal hemorrhage. As a result of its antioxidant activity and its stabilizing impact on the cardiomyocyte membranes, vit E is recommended as a potential candidate in decreasing the damaging effects of CP.

Urolithin A prevents streptozotocin-induced diabetic cardiomyopathy in rats by activating SIRT1

This study examined the cardiac anti-cardiomyopathy (DC) protective effect of urolithin A in streptozotocin (STZ)-treated rats and investigated if this protection involves activation of SIRT1 signaling. Diabetes was induced first STZ (65 mg/kg, i.p.) before starting the experiments. Adult male rats (n = 8/group) were treated for 8 weeks as control (non-diabetic), control + urolithin A (2.5 mg/kg/i.p.), STZ, STZ + urolithin A, and STZ + urolithin A + Ex-527 (1 mg/kg/i.p.) (a SIRT1 inhibitor). With no effect on fasting glucose and insulin levels, urolithin A improved left ventricular (LV) function and structure and reduced heart weight and serum levels of cardiac markers in STZ-treated rats. Also, it prevented collagen deposition, reduced mRNA levels of Bax, cleaved caspaspe3, collagen 1A1, transforming growth factor-β1 (TGF-β1), and Smad3 but enhanced those of Bcl2 in the LVs of diabetic rats. However, urolithin A suppressed the generation of reactive oxygen species (ROS), activated the nuclear factor erythroid 2–related factor 2 (Nrf2), and increased the levels of manganese superoxide dismutase (MnSOD) and total glutathione (GSH) in the LVs of the non-diabetic and diabetic rats, In parallel, it suppressed the cardiac activity of NF-nuclear factor-kappa beta p65 (κB p65) and reduced levels of tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). Coincided with these events, urolithin A promoted higher activity, mRNA, and total/nuclear protein levels of SIRT1 and lowered the levels of acetyl-FOXO1, Nrf2, NF-κB, and p53. All these benefits of urolithin A were prevented by Ex-527. In conclusion, urolithin A protects against DC by activating SIRT signaling.

Induction Therapy for AML with 90 Mg/m² Daunorubicin Results in Higher Troponin T Serum Levels in Comparison to Treatment with 60 Mg/m² Daunorubicin

Introduction : Induction therapy for acute myeloid leukemia (AML) based on 7 days of cytarabine and 3 days of anthracycline has been standard treatment for decades. However, the optimal dose level of anthracycline is still in question. This issue is addressed by the ongoing randomized controlled DaunoDouble trial comparing 60 mg/m² versus 90 mg/m² in standard 7+3 induction for patients with newly diagnosed AML (NCT02140242). Since cardiotoxicity is considered the most dangerous side effect of anthracyclines, we compared serum levels of cardiac markers between the two study arms in the course of chemotherapy and afterwards.Methods: Serum concentrations of NT-proBNP and cardiac troponin T were measured prior to induction therapy (day 0), before (day 2) and during daunorubicin administration (days 3, 4, 5) and on day 15. The induction treatment consisted of a 7+3 induction with daunorubicin at a dose of either 60 or 90 mg/m² (Group 60 and 90). By the time of analysis, data on highly sensitive measured troponin T concentrations at day 15 was available for 116 patients.Results: With regard to NT-proBNP concentrations no significant difference between study arms was found, but NT-proBNP levels of Group 90 remained constantly higher during daunorubicin administration. Whereas there was no considerable development concerning troponin T during induction therapy, at day 15 the median troponin T concentration of all patients was 8 ng/l and as such significantly higher compared to 5 ng/l before daunorubicin administration (Wilcoxon test; Z = -3.763; p < 0.001; r = 0.38 (medium effect size)). The proportion of patients with troponin T concentrations higher than 14 ng/l, which is the 99%-percentile of the healthy population, was 9.78 percent [95% CI: 3.60 - 15.97%] before daunorubicin administration and 16.50 percent [95% CI: 9.21 - 23.80%] on day 15. Significant correlations occurred between troponin T concentrations on day 15 and pre-treatment values of troponin T (Spearman's ρ = 0.502; p < 0.001) and NT-proBNP (Spearman's ρ = 0.245; p = 0.02). Prior to daunorubicin application, the median troponin T concentration was 5 ng/l in Group 60 and 6 ng/l in Group 90, respectively. On day 15, Group 90 had significantly higher troponin levels (ctrop, Group 90, median = 10 ng/l) than Group 60 (ctrop, Group 60, median = 7ng/l; Mann-Whitney U test; U = 1332; p = 0.021; r = 0.21 (small effect size)). The proportion of patients with troponin T concentrations higher than 14 ng/l was 14.55 percent [95% CI: 4.93 - 24.16%] in Group 60 and 18.75 percent [95% CI: 7.30 - 30.20%] in Group 90.Conclusion: Prospective cardiac monitoring of a large number of patients with identical disease and treatment shows that the cardiac impairment of daunorubicin administration during AML induction therapy resulted in a significant shift to higher troponin T levels. Patients within Group 90 had significant higher troponin T concentrations on day 15 with an average increase of 3 ng/l compared to Group 60. With respect to the prognostic value of troponin T (cf. ARIC study, CHS study), a higher risk of future cardiac complications could be assumed for Group 90. Long-term follow-up is necessary to draw more precise conclusions on the clinical impact of the cardiac marker kinetics. [Display omitted] DisclosuresStoelzel:medac: Other: Travel support. Mayer:Novartis: Research Funding; Eisai: Research Funding. Hochhaus:Pfizer: Research Funding; Novartis: Research Funding; Incyte: Research Funding; BMS: Research Funding; ARIAD: Research Funding; MSD: Research Funding. Rollig:Janssen: Research Funding; Bayer: Research Funding.

Implications of cardiac markers in risk-stratification and management for COVID-19 patients

BackgroundCOVID-19 has resulted in high mortality worldwide. Information regarding cardiac markers for precise risk-stratification is limited. We aim to discover sensitive and reliable early-warning biomarkers for optimizing management and improving the prognosis of COVID-19 patients.MethodsA total of 2954 consecutive COVID-19 patients who were receiving treatment from the Wuhan Huoshenshan Hospital in China from February 4 to April 10 were included in this retrospective cohort. Serum levels of cardiac markers were collected after admission. Coronary artery disease diagnosis and survival status were recorded. Single-cell RNA-sequencing and bulk RNA-sequencing from different cohorts of non-COVID-19 were performed to analyze SARS-CoV-2 receptor expression.ResultsAmong 2954 COVID-19 patients in the analysis, the median age was 60 years (50–68 years), 1461 (49.5%) were female, and 1515 (51.3%) were severe/critical. Compared to mild/moderate (1439, 48.7%) patients, severe/critical patients showed significantly higher levels of cardiac markers within the first week after admission. In severe/critical COVID-19 patients, those with abnormal serum levels of BNP (42 [24.6%] vs 7 [1.1%]), hs-TNI (38 [48.1%] vs 6 [1.0%]), α- HBDH (55 [10.4%] vs 2 [0.2%]), CK-MB (45 [36.3%] vs 12 [0.9%]), and LDH (56 [12.5%] vs 1 [0.1%]) had a significantly higher mortality rate compared to patients with normal levels. The same trend was observed in the ICU admission rate. Severe/critical COVID-19 patients with pre-existing coronary artery disease (165/1,155 [10.9%]) had more cases of BNP (52 [46.5%] vs 119 [16.5%]), hs-TNI (24 [26.7%] vs 9.6 [%], α- HBDH (86 [55.5%] vs 443 [34.4%]), CK-MB (27 [17.4%] vs 97 [7.5%]), and LDH (65 [41.9%] vs 382 [29.7%]), when compared with those without coronary artery disease. There was enhanced SARS-CoV-2 receptor expression in coronary artery disease compared with healthy controls. From regression analysis, patients with five elevated cardiac markers were at a higher risk of death (hazards ratio 3.4 [95% CI 2.4–4.8]).ConclusionsCOVID-19 patients with pre-existing coronary artery disease represented a higher abnormal percentage of cardiac markers, accompanied by high mortality and ICU admission rate. BNP together with hs-TNI, α- HBDH, CK-MB and LDH act as a prognostic biomarker in COVID-19 patients with or without pre-existing coronary artery disease.

Implications of Cardiac Markers in Risk-Stratification and Management for COVID-19 Patients

Background: Coronavirus disease (COVID-19) has resulted in high mortality worldwide. However, information regarding cardiac markers for precise risk-stratification is limited. We aimed to discover a sensitive and reliable early-warning biomarker for optimizing management and improving COVID-19 patients’ prognosis. Methods: This single-center case series was conducted between February 4 and April 10, 2020. In total, 2,954 consecutive COVID-19 patients who were receiving treatment at Wuhan Huoshenshan Hospital in China were included in the retrospectively selected cohort. All patients were diagnosed with COVID-19 and treated at the study site. Data of serum levels of cardiac markers, coronary artery disease (CAD) diagnosis, and survival were collected after admission. Single-cell RNA-sequencing was performed to analyze severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptor expression.Findings: Median patient age was 60 years (range, 50-68 years); 1,461 (49.5%) were female, and 1,515 (51.3%) patients were in a severe/critical condition. Compared to mild/moderate patients (1,439, 48.7%), severe/critical patients showed significantly higher levels of cardiac markers within the first week after admission. Among severe/critical COVID-19 patients, those with abnormal serum levels of brain natriuretic peptide had a significantly higher mortality rate than patients with normal levels. Severe/critical COVID-19 patients with pre-existing CAD (165/1,155 [10.9%]) had more cases of abnormal brain natriuretic peptide levels than those without CAD. Enhanced SARS-CoV-2 receptor expression was observed in patients with CAD. Regression analysis revealed that patients with elevated brain natriuretic peptide levels were at a higher risk of death (hazards ratio, 1.001 [95% confidence interval, 1.0003-1.002]).Interpretation: Brain natriuretic peptide is an effective biomarker for risk assessment in COVID-19 patients with or without pre-existing CAD. The detection of BNP is widely used in clinical practice and can be easily implemented in hospitals at all levels.Funding Statement: This research was supported by grants from National Nature Science Foundation of China (Grant No. 31771334, 81970428, 91959113, 81972358, 81572893), the Key Research Plan of the National Natural Science Foundation of China (Grant No. 81820108002), the Major Research Plan of the National Natural Science Foundation of China (Grant No. 91649125, 91639204), Key Foundation of Wuhan Huoshenshan Hospital (Grant No. 2020[18]), Key Research & Development Program of Jiangsu Province (Grant Nos. BE2017733, BE2018713), Medical Innovation Project of Logistics Service (Grant No. 18JS005), Basic Research Program of Jiangsu Province (Grant No. BK20180036), and the Natural Science Foundation of the Jiangsu Higher Education Institutions of China (Grant No.18KJB180014).Declaration of Interests: The authors declare no competing interests.Ethics Approval Statement: The study design was approved by the institutional ethics board. Written informed consent was waived due to the urgency of the COVID-19 pandemic.

Exendin-4 Attenuates Remodeling in the Remote Myocardium of Rats After an Acute Myocardial Infarction by Activating β-Arrestin-2, Protein Phosphatase 2A, and Glycogen Synthase Kinase-3 and Inhibiting β-Catenin.

This study tested if the protective anti-remodeling effect of GLP-1 agonist Exendin-4 after an acute myocardial infarction (MI) in rats involves inhibition of the Wnt1/β-catenin signaling pathway. Rats were divided into sham, sham + Exendin-4 (10μg/day, i.p), MI, and MI + Exendin-4. MI was introduced to rats by permanent left anterior descending coronary artery (LAD) ligation. On day 7 post-infraction, MI rats showed LV dysfunction with higher serum levels of cardiac markers. Their remote myocardia showed increased mRNA and protein levels of collagen I/III with higher levels of reactive oxygen species (ROS) and inflammatory cytokines, as well as protein levels of Wnt1, phospho-Akt, transforming growth factor (TGF-β1), Smad, phospho-Smad3, α-SMA, caspase-3, and Bax. They also showed higher protein levels of phospho-glycogen synthase kinase-3β (p-GSK3β), as well as total, phosphorylated, and nuclear β-catenin with a concomitant decrease in the levels of cyclic adenosine monophosphate (cAMP), mRNA of manganese superoxide dismutase (MnSOD), and protein levels of Bcl-2, β-arrestin-2, and protein phosphatase-2 (PP2A). Administration of Exendin-4 to MI rats reduced the infarct size and reversed the aforementioned signaling molecules without altering protein levels of TGF-1β and Wnt1 or Akt activation. Interestingly, Exendin-4 increased mRNA levels of MnSOD, protein levels of β-arrestin-2 and PP2A, and β-catenin phosphorylation but reduced the phosphorylation of GSK3β and Smad3, and total β-catenin levels in the LV of control rats. Exendin-4 inhibits the remodeling in the remote myocardium of rats following acute MI by attenuating β-catenin activation and activating β-arrestin-2, PP2A, and GSK3β. Graphical Abstract A graphical abstract that illustrates the mechanisms by which Exendin-4 inhibits cardiac remodeling in remote myocardium of left ventricle MI-induced rats. Mechanisms are assumed to occur in the cardiomyocytes and/or other resident cells such as fibroblast. Β-catenin activation and nuclear translocation are associated with increased synthesis of inflammatory cytokines and transforming growth factor β-1 (TGF-β1). GSK3β is inhibited by phosphorylation at Ser9. Under normal conditions, β-catenin is degraded in the cytoplasm by the active GSK3β-dependent degradation complex (un-phosphorylated) which usually phosphorylates β-catenin at Ser33/37/Thr41. After MI, TGF-β1, and Wnt 1 levels are significantly increased, the overproduction of Wnt1 induces β-catenin stabilization and nuclear translocation through increasing the phosphorylation of disheveled (DVL) protein which in turn phosphorylates and inhibits GSK3β. TGF-β1 stimulates the phosphorylation of Smad-3 and subsequent nuclear translocation to activate the transcription of collage 1/III and α-smooth muscle actin (α-SMA). Besides, TGF-β1 stabilizes cytoplasmic β-catenin levels indirectly by phosphorylation of Akt at Thr308-induced inhibition of GSK3β by increasing phosphorylation of Ser9. Exendin-4, and possibly through G protein-coupled receptors (GPCRs), increases levels of cAMP and upregulates β-arrestin-2 levels. Both can result in a positive inotropic effect. Besides, β-arrestin-2 can stimulate PP2A to dephosphorylation Smad3 (inhibition) and GSK3β (activation), thus reduces fibrosis and prevents the activation of β-catenin and collagen deposition.

Myocardial injury induced by scorpion sting envenoming and evidence of oxidative stress in Egyptian children

In the present study, 45 children in Upper Egypt (less than 16 years old) were admitted to the Pediatric Intensive Care Unit for scorpion envenomation (SE). They were compared with 30 apparently healthy children of matching age and sex as controls. Out of the studied victims, 35 children (78%) showed signs of severe envenomation, while 10 victims (22%) showed signs of mild envenomation. The case fatality was 33%. The serum levels of cardiac markers, cardiac troponin T (cTnT) and I (cTnI), as well as the enzymatic activities of creatine kinase-MB (CPK-MB) and lactate dehydrogenase (LDH) were determined for both victims and controls. In addition, the serum levels of oxidative stress markers, nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH) and zinc (Zn) were measured. Electrocardiography and echocardiography were done. All the envenomed victims showed significantly higher mean values of cTnT, cTnI, CPK-MB and LDH than control group. These cardiac markers were elevated in severe cases and in non survivors in comparison with mild cases and survivors respectively. Furthermore, the serum levels of NO and MDA were significantly higher while the serum levels of SOD, GSH and Zn were significantly lower in all envenomed victims than the controls (p < 0.05 for all). There were no significant differences in the serum levels of oxidative stress markers among severe and mild cases or between survivors and non survivors victims. There were no significant correlations between the serum levels of cardiac markers and the oxidative stress markers in envenomed victims. In conclusions, oxidative stress occurs in scorpion envenomed children, but does not determine prognosis. Cardiac markers, but not the oxidative stress, remain the most important determining factor for the severity and the outcome of SE.

Trigonelline isolated from fenugreek seed protects against isoproterenol-induced myocardial injury through down-regulation of Hsp27 and αB-crystallin

ObjectiveProtective effects of trigonelline (TRG) isolated from fenugreek seed were evaluated in isoproterenol (ISO)-induced myocardial dysfunctions in adult rats and a proteomic approach was applied to understand its mechanism of action. MethodsIn a preliminary experiment, effects of TRG at 20, 40, and 80 mg/kg for 20 d were studied in ISO-induced (100 mg/kg) adult rats. As 40 mg/kg was found the most effective concentration, in the final experiment, effects of 40 mg/kg of the test drug were investigated using different indices including cardiac marker enzymes, lipid peroxidation, antioxidants, cardiac histology, and electrocardiogram. Proteomic analyses were also done in cardiac myocytes. ResultsISO administration increased serum levels of cardiac markers (creatine kinase-MB, glutamate pyruvate transaminase, and lactate dehydrogenase) and exhibited a positive reaction in the TROP-T test. It also increased the cardiac lipid peroxidation and decreased the cellular antioxidants. Proteomic data revealed nine protein spots, seven were down-regulated and two up-regulated. The overexpressions of two small stress proteins, heat shock protein (Hsp)27 and αB crystallin were confirmed by Western blot analysis. All these alterations were restored to nearly normal values in 40 mg/kg of TRG-pretreated animals, suggesting its cardioprotective effects, which were further confirmed by histologic examinations and triphenyl tetrazolium chloride staining assay. ConclusionFor the first time, our study revealed the down-regulation of Hsp27 and αB-crystallin and (CaMKII delta) isoform by TRG. As the test compound prevented the ISO-induced myocardial injury, its therapeutic use may further be explored.

Intracoronary ST-segment shift in diagnosis of early myocardial injury during percutaneous coronary intervention

Objective To evaluate role of intracoronary electrocardiogram (IcECG) in examining early myocardial damage during elective percutaneous coronary intervention (PCI). Methods Eighty-six patients of coronary heart disease with normal serum levels of creatine kinase-myoglobin (CK-MB) and cardiac troponin T (cTnT) before the procedure and undergone elective PCI were enrolled in the study.Their IcECG were recorded by a intracoronary guidewire and serum levels of CK-MB and cTnT were measured at baseline and eight and 24 hours after the procedure, respectively. The patients were divided into two group, abnormal and control, according to whether they had significant shift at ST-segment in IcECG.Cardiac events after intervention in the patients were followed-up and recorded. Myocardial damage was defined as serum level of cTnT increased to above the upper normal value after intervention. Results Significant shift at ST-segment in IcECG during PCI in 30 (35%, abnormal group) and no shift in other 56patients (65%, control group) of 86 patients with normal serum levels of cardiac markers before the procedure was observed, and all the procedure were successful Serum levels of cTuT and CK-MB significantly increased after intervention in 30 patients of abnormal group than those in control one ( P <0. 01 ). Sensitivity of intracoronary ST-segment shift was 77 percent for predicting myocardial damage, and specificity was 94 percent, with positive and negative predictive values of 90 percent and 86 percent,respectively. More cardiac events were observed at 4-week follow-up after intervention in abnormal group than those in control one (P<0. 05) and major coronary event-free survival was significantly lower in those with post-procedural ST-segment elevation in IeECG (P < 0. 05). Conclusions ST-segment shift in IcECG may be helpful for predicting myocardial damage during PCI procedure on time. Key words: Electrocardiography; Coronary disease; Angioplasty, transluminal, percutaneous coronary

Hesperidin, a flavanone glycoside, on lipid peroxidation and antioxidant status in experimental myocardial ischemic rats

Myocardial infarction continues to be a leading cause of mortality world-wide. Novel therapies are needed to treat the myocardial ischemia. This study was undertaken to evaluate the cardioprotective role of hesperidin on isoproterenol-induced myocardial ischemia in rats. Myocardial ischemia was induced by subcutaneous injection of isoproterenol hydrochloride (85 mg/kg body weight), for two consecutive days. Isoproterenol-administered rats showed elevated levels of cardiac markers (aspartate transaminase, alanine transaminase, lactate dehydrogenase, creatine kinase, creatine kinase-MB, cardiac troponins T and I) when compared with control and hesperidin treatment groups (100, 200 and 400 mg/kg body weight). The serum levels of cardiac markers were significantly reduced at the doses of 200 mg and 400 mg. All further experiments were carried out at the 200 mg dose. Lipid peroxidation markers (thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes) were elevated significantly in the plasma and heart whereas non-enzymic antioxidants (vitamin C, vitamin E and reduced glutathione) were decreased significantly. Activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferease and glutathione reductase declined significantly in the heart of ischemic rats. However, after hesperidin treatment, all the above parameters reverted to normal levels. This study demonstrated that the cardioprotective effect of hesperidin on ischemic rats could be due to its antilipidperoxidative and antioxidant properties.

Short-term effects of marathon running in master runners: no evidence of myocardial injury.

The purpose of this investigation was to analyze the short-term effects of marathon running on serum levels of cardiac markers in a group of master runners (> 60 yrs). Ten marathoners (9 male and 1 female; 63+/-4 yrs) were enrolled in the study. All of them completed the Madrid Marathon (1998). Venous blood was drawn from each subject three times during the study (48 h before the race, immediately after the race, and 24 h post-competition) for the determination of the several biochemical markers, such as total creatine kinase catalytic activity (total CK), mass concentration of creatine kinase isoenzyme MB (CK-MB mass), and cardiac troponin I (Tnl-c). The most important finding was that in each sample (pre- or post-race) serum Tnl-c was below the commonly accepted level of 0.1 ng x m(-1) indicative of myocardial injury. Although further research is needed using more complete methodology, our results suggest that marathon running does not have an acute deleterious effect on the hearts of the elderly.