scholarly journals Chronic exposure to tramadol induces cardiac inflammation and endothelial dysfunction in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Marwa H. Bakr ◽  
Eman Radwan ◽  
Asmaa S. Shaltout ◽  
Alshaimaa A. Farrag ◽  
Amany Refaat Mahmoud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular System ◽  
Troponin I ◽  
Cardiovascular Complications ◽  
Enos Expression ◽  
Serum Samples ◽  
Cardiac Damage ◽  
Tramadol Hydrochloride ◽  
Cardiac Inflammation ◽  
Underlying Mechanisms

AbstractTramadol is an opioid extensively used to treat moderate to severe pain; however, prolonged therapy is associated with several tissues damage. Chronic use of tramadol was linked to increased hospitalizations due to cardiovascular complications. Limited literature has described the effects of tramadol on the cardiovascular system, so we sought to investigate these actions and elucidate the underlying mechanisms. Mice received tramadol hydrochloride (40 mg/kg body weight) orally for 4 successive weeks. Oxidative stress, inflammation, and cardiac toxicity were assessed. In addition, eNOS expression was evaluated. Our results demonstrated marked histopathological alteration in heart and aortic tissues after exposure to tramadol. Tramadol upregulated the expression of oxidative stress and inflammatory markers in mice heart and aorta, whereas downregulated eNOS expression. Tramadol caused cardiac damage shown by the increase in LDH, Troponin I, and CK-MB activities in serum samples. Overall, these results highlight the risks of tramadol on the cardiovascular system.

scholarly journals Relationship Between Serum Severe Acute Respiratory Syndrome Coronavirus 2 Nucleic Acid and Organ Damage in Coronavirus 2019 Patients: A Cohort Study

2020 ◽  
Author(s):  
Dan Xu ◽  
Fuling Zhou ◽  
Wenbo Sun ◽  
Liangjun Chen ◽  
Lan Lan ◽  
...  
Keyword(s):  
Nucleic Acid ◽  
Severe Acute Respiratory Syndrome ◽  
Troponin I ◽  
Demographic Data ◽  
Organ Damage ◽  
Multiple Organ ◽  
Serum Samples ◽  
Cardiac Damage ◽  
Multiple Organs ◽  
Laboratory Biomarkers

Abstract Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread worldwide and has the ability to damage multiple organs. However, information on serum SARS-CoV-2 nucleic acid (RNAemia) in patients affected by coronavirus disease 2019 (COVID-19) is limited. Methods Patients who were admitted to Zhongnan Hospital of Wuhan University with laboratory-confirmed COVID-19 were tested for SARS-COV-2 RNA in serum from 28 January 2020 to 9 February 2020. Demographic data, laboratory and radiological findings, comorbidities, and outcomes data were collected and analyzed. Results Eighty-five patients were included in the analysis. The viral load of throat swabs was significantly higher than of serum samples. The highest detection of SARS-CoV-2 RNA in serum samples was between 11 and 15 days after symptom onset. Analysis to compare patients with and without RNAemia provided evidence that computed tomography and some laboratory biomarkers (total protein, blood urea nitrogen, lactate dehydrogenase, hypersensitive troponin I, and D-dimer) were abnormal and that the extent of these abnormalities was generally higher in patients with RNAemia than in patients without RNAemia. Organ damage (respiratory failure, cardiac damage, renal damage, and coagulopathy) was more common in patients with RNAemia than in patients without RNAemia. Patients with vs without RNAemia had shorter durations from serum testing SARS-CoV-2 RNA. The mortality rate was higher among patients with vs without RNAemia. Conclusions In this study, we provide evidence to support that SARS-CoV-2 may have an important role in multiple organ damage. Our evidence suggests that RNAemia has a significant association with higher risk of in-hospital mortality.

scholarly journals COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options

2020 ◽  
Vol 116 (10) ◽  
pp. 1666-1687 ◽  
Author(s):  
Tomasz J Guzik ◽  
Saidi A Mohiddin ◽  
Anthony Dimarco ◽  
Vimal Patel ◽  
Kostas Savvatis ◽  
...  
Keyword(s):  
Cardiovascular System ◽  
Troponin I ◽  
Inflammatory Responses ◽  
Myocardial Dysfunction ◽  
Angiotensin Receptor Blockers ◽  
Ventricular Tachyarrhythmia ◽  
Cardiac Injury ◽  
Fulminant Myocarditis ◽  
Rapid Progression ◽  
Cardiac Damage

Abstract The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and mechanistic considerations for future therapies. While COVID-19 primarily affects the lungs, causing interstitial pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the cardiovascular system. Risk of severe infection and mortality increase with advancing age and male sex. Mortality is increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer. The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). Mechanistically, SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane angiotensin-converting enzyme 2 (ACE2) —a homologue of ACE—to enter type 2 pneumocytes, macrophages, perivascular pericytes, and cardiomyocytes. This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis. Hence, patients should not discontinue their use. Moreover, renin–angiotensin–aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. Initial immune and inflammatory responses induce a severe cytokine storm [interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. Early evaluation and continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization may identify patients with cardiac injury and predict COVID-19 complications. Preventive measures (social distancing and social isolation) also increase cardiovascular risk. Cardiovascular considerations of therapies currently used, including remdesivir, chloroquine, hydroxychloroquine, tocilizumab, ribavirin, interferons, and lopinavir/ritonavir, as well as experimental therapies, such as human recombinant ACE2 (rhACE2), are discussed.

scholarly journals The effect of short-term coenzyme Q10supplementation and pre-cooling strategy on cardiac damage markers in elite swimmers

2018 ◽  
Vol 119 (4) ◽  
pp. 381-390 ◽  
Author(s):  
Ali Emami ◽  
Asghar Tofighi ◽  
Siamak Asri-Rezaei ◽  
Behnaz Bazargani-Gilani
Keyword(s):  
Oxidative Stress ◽  
Troponin I ◽  
Coenzyme Q ◽  
Myocardial Damage ◽  
Cardiac Damage ◽  
Cooling Strategy ◽  
Creatine Kinase Mb ◽  
Elite Swimmers ◽  
Two Stages ◽  
And Control

AbstractStrenuous physical exercise and hyperthermia may paradoxically induce oxidative stress and adverse effects on myocardial function. The purpose of this study was to investigate the effect of 14-d coenzyme Q10(CoQ10) supplementation and pre-cooling on serum creatine kinase-MB (CK-MB), cardiac Troponin I (cTnI), myoglobin (Mb), lactate dehydrogenase (LD), total antioxidant capacity (TAC), lipid peroxidation (LPO) and CoQ10concentration in elite swimmers. In total, thirty-six healthy males (mean age 17 (sd1) years) were randomly selected and divided into four groups of supplementation, supplementation with pre-cooling, pre-cooling and control. During an eighteen-session protocol in the morning and evening, subjects attended speed and endurance swimming training sessions for 5 km in each session. Blood sampling was done before (two stages) and after (two stages) administration of CoQ10and pre-cooling. ANCOVA and repeated measurement tests with Bonferronipost hoctest were used for the statistical analysis of the data. There was no significant statistical difference among groups for the levels of CK-MB, cTnI, Mb, LD, TAC, LPO and CoQ10at the presampling (stages 1 and 2) (P>0·05). However, pre-cooling and control groups show a significant increase in the levels of CK-MB, cTnI, Mb, LD and LPO compared with the supplementation and supplementation with pre-cooling groups in the post-sampling (stages 1 and 2) (P<0·05), except for the TAC and CoQ10. Consequently, CoQ10supplementation prevents adverse changes of myocardial damage and oxidative stress during swimming competition phase. Meanwhile, the pre-cooling strategy individually has no desired effect on the levels of CK-MB, cTnI, Mb, LD, LPO, TAC and CoQ10.

scholarly journals Cardiac Inflammation, Oxidative Stress, Nrf2 Expression, and Coagulation Events in Mice with Experimental Chronic Kidney Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Abderrahim Nemmar ◽  
Suhail Al-Salam ◽  
Sumaya Beegam ◽  
Nur Elena Zaaba ◽  
Javed Yasin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Dna Damage ◽  
Kidney Disease ◽  
Troponin I ◽  
The Body ◽  
Control Group ◽  
Cardiac Inflammation ◽  
Nrf2 Expression

Chronic kidney disease (CKD) is known to be associated with cardiovascular dysfunction. Dietary adenine intake in mice is also known to induce CKD. However, in this experimental model, the mechanisms underlying the cardiotoxicity and coagulation disturbances are not fully understood. Here, we evaluated cardiac inflammation, oxidative stress, DNA damage, and coagulation events in mice with adenine (0.2% w / w in feed for 4 weeks)-induced CKD. Control mice were fed with normal chow for the same duration. Adenine increased water intake, urine output, relative kidney weight, the plasma concentrations of urea and creatinine, and the urinary concentrations of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin. It also decreased the body weight and creatinine clearance, and caused kidney DNA damage. Renal histological analysis showed tubular dilation and damage and neutrophilic influx. Adenine induced a significant increase in systolic blood pressure and the concentrations of troponin I, tumor necrosis factor-α, and interleukin-1β in heart homogenates. It also augmented the levels of markers of lipid peroxidation measured by malondialdehyde production and 8-isoprostane, as well as the antioxidants superoxide dismutase and catalase. Immunohistochemical analysis of the hearts showed that adenine increased the expression of nuclear factor erythroid-derived 2-like 2 by cardiomyocytes. It also caused cardiac DNA damage. Moreover, compared with the control group, adenine induced a significant increase in the number of circulating platelet and shortened the thrombotic occlusion time in pial arterioles and venules in vivo, and induced a significant reduction in the prothrombin time and activated partial thromboplastin time. In conclusion, the administration of adenine in mice induced CKD-associated cardiac inflammation, oxidative stress, Nrf2 expression, and DNA damage. It also induced prothrombotic events in vivo. Therefore, this model can be satisfactorily used to study the cardiac pathophysiological events in subjects with CKD and the effect of drug treatment thereon.

scholarly journals Safety of Antitheilerial Drug Buparvaquone in Rams

2018 ◽  
Vol 46 (1) ◽  
pp. 7
Author(s):  
Nermin Isik ◽  
Ozlem Derinbay Ekici ◽  
Ceylan Ilhan ◽  
Devran Coskun
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Alkaline Phosphatase ◽  
Blood Cell ◽  
Troponin I ◽  
Oxidative Status ◽  
Cardiac Damage ◽  
Blood Samples ◽  
Heart Damage

Background: Theileriosis is a tick-borne disease caused by Theileria strains of the protozoan species. Buparvaquone is the mostly preferred drug in the treatment theileriosis, while it is safety in sheep, has not been detailed investigated. It has been hypothesized that buparvaquone may show side effects and these effects may be defined some parameters measured from blood in sheep when it is used at the recommended dose and duration. The aim of this research was to determine the effect of buparvaquone on the blood oxidative status, cardiac, hepatic and renal damage and bone marrow function markers.Materials, Methods & Results: In this study, ten adult (> 2 years) Akkaraman rams were used. Healthy rams were placed in paddocks, provided water ad libitum, and fed with appropriate rations during the experiment. Buparvaquone was administered at the dose of 2.5 mg/kg (IM) intramuscularly twice at 3-day intervals. Blood samples were obtained before (0. h, Control) and after drug administration at 0.25, 0.5, 1, 2, 3, 4 and 5 days. The blood samples were transferred to gel tubes, and the sera were removed (2000 g, 15 min). During the study, the heart rate, respiratory rate, and body temperature were measured at each sampling time. In addition, the animals were clinically observed. Plasma oxidative status markers (Malondialdehyde, total antioxidant status, catalase, glutathione peroxidase, superoxide dismutase), serum cardiac (Troponin I, creatine kinase-MBmass, lactate dehydrogenase), hepatic (Alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma glutamyltransferase, total protein, albumin, globulin) and renal (Creatinine, blood urea nitrogen) damage markers and hemogram values (white blood cell, red blood cell, platelet, hemogram, hematocrit) were measured. Buparvaquone caused statistically significantly (P < 0.05) increases in the troponin I and blood urea nitrogen levels and fluctuations in alkaline phosphatase activity, but there was no any statistically significance difference determined in the other parameters.Discussion: In this study, buparvaquone was administered two times at a dose of 2.5 mg/kg (IM) at 3-day intervals. Although the result was not statistically significant (P > 0.05), it was determined that buparvaquone gradually increased the levels of the main oxidative stress marker, MDA, by approximately 2.8 fold. CAT and GPX levels were also found to have decreased by 2.2 fold. Buparvaquone may cause lipid peroxidation by producing free radicals. Some other antiprotozoal drugs may affect the oxidative status and may increase MDA level and decrease SOD level. In this study, MDA, which is an indicator of lipid peroxidation in vivo, was used to partially detect developing lipid peroxidation. Changes in the levels of reduced GPX and CAT enzymes could be attributed to their use in mediating the hydrogen peroxide detoxification mechanisms. The absence of significant changes in the TAS levels in this study suggests that buparvaquone may partially induce oxidative stress by producing hydrogen peroxide, but no significant changes occurred in the oxidative stress level because of the high antioxidant capacity of sheep. In this study, buparvaquone caused a statistically significant increase (P < 0.05) in the level of Tn-I, which is a marker of specific cardiac damage (P < 0.05), whereas there was no statistically (P > 0.05) significant increase in CK-MBmass. Tn-I and CK-MB levels, which are used to define heart damage in humans, have been successfully used to determine heart damage in sheep. In this research study, the statistically significant increases in Tn-I but not CK-MBmass levels could be considered indicative of mild cardiac damage.

scholarly journals A Comparative study of oxidant and Anti-oxidant parameters in Chronic Renal Failure, Haemodialysis (Pre &Post) and Controls

2020 ◽  
Vol 2 (3) ◽  
pp. 78-81
Author(s):  
R. Salma Mahaboob ◽  
G. Obulesu ◽  
M. Madan Mohan Rao
Keyword(s):  
Oxidative Stress ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Kidney Function ◽  
Patient Group ◽  
Complex Disease ◽  
Cardiovascular Complications ◽  
High Morbidity ◽  
Serum Samples ◽  
Anti Oxidant

Chronic kidney disease (CKD) is featured by a progressive decline of kidney function and is mainly caused by chronic diseases such as diabetes mellitus and hypertension. CKD is a complex disease due to cardiovascular complications and high morbidity; however, there is no single treatment to improve kidney function in CKD patients. Since biological markers representing oxidative stress are significantly elevated in CKD patients, oxidative stress is receiving attention as a contributing factor to CKD pathology. Aim of our study is comparison of oxidant and anti oxidant parameters in chronic renal failure, Hemodialysis (pre and post) and control subjects. Materials and Methods: The present study was conducted on a patient group comprising of 50 patients diagnosed with CRF, 50 were pre hemodialysis, 50 were post hemodialysis (MHD). This patient group was compared to a healthy group including 100 controls. All the study participants were admitted in the department of Medicine [Nephrology department] at “Fathima Institute of Medical Sciences”, Kadapa. Andhra Pradesh. India. The obtained serum samples were used for biochemical analysis for estimating MDA, vitamin A and Glutathione Peroxidase (GPx). Conclusion: Our results reflects the primary mechanisms of oxidative stress and inflammation during hemodialysis which may cause of CVD development in hemodialysed patients.

scholarly journals Analysis of Cardiac Injury Biomarkers in COVID-19 Patients

2020 ◽  
Vol 15 (4) ◽  
Author(s):  
Salma Abdeladim ◽  
Sara Oualim ◽  
Amal Elouarradi ◽  
Ilham Bensahi ◽  
Rita Aniq Filali ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Injury ◽  
Clinical Syndrome ◽  
Cardiac Troponin I ◽  
The Novel ◽  
Cardiac Damage ◽  
The Mean ◽  
Underlying Mechanisms ◽  
Novel Coronavirus

Background: Infection with the novel coronavirus, named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), producing a clinical syndrome known as COVID-19, is a budding infectious disease that first manifested in December 2019 in China and subsequently spread worldwide. Objectives: We performed an analysis of cardiac injury markers to determine their usefulness as predictors of severity and mortality Methods: In a retrospective study, we enrolled 73 patients with confirmed diagnoses of COVID-19, from March 21, 2020, to April 24, 2020. Serial tests of cardiac injury markers, including cardiac troponin I (cTnI), N‐terminal pro‐brain natriuretic peptide (NT‐proBNP), and Lactate dehydrogenase (LDH), were considered for the analysis of potential cardiac damage. Results: Among 149 patients with confirmed COVID-19, data from 73 patients were studied. Of them, 58 (79.46%) patients were discharged, and 15 (20.54 %) patients died. The mean age was 58.50 (14.66) years. Patients were classified into mild (39 cases), severe (17 cases), and critical (17 cases) groups. The peak cardiac troponin I level (0.11 ng/mL [IQR: 0.33–0.20]), peak NT-pro BNP level (5840.35 pg/mL [IQR: 1609.39 – 10071.32]), and peak LDH level (578.65 UI/l[IQR: 313.40 – 843.90]) were significantly higher in the critical group, and the three cardiac injury parameters were significantly higher in the death group, suggesting that they are significantly associated with a higher risk of in-hospital mortality. Conclusions: The understanding of cardiovascular system injury caused by SARS-CoV-2 and its underlying mechanisms is of great importance for the early clinical management of these patients and mortality reduction.

scholarly journals Graves’ Disease and Cardiac Complications

2021 ◽  
Author(s):  
Abdulla Arslan ◽  
Hakan Altay
Keyword(s):  
Cardiovascular System ◽  
Myocardial Oxygen Consumption ◽  
Diastolic Pressure ◽  
Cardiac Contractility ◽  
Cardiovascular Complications ◽  
Cardiac Complications ◽  
Graves Disease ◽  
Autoimmune Thyroid ◽  
Diastolic Relaxation ◽  
Underlying Mechanisms

Graves’ disease is an autoimmune thyroid disease and a common cause of hyperthyroidism. Thyroid hormones have multiple adverse effect on cardiovascular system through many direct and indirect mechanisms. They increases heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption, whereas decrease systemic vascular resistance and diastolic pressure. All these hemodynamic changes in cardiovascular system can eventually lead to heart failure, tachyarrhythmias, systemic and pulmonary hypertension, if left untreated. Cardiovascular complications of Graves’ disease are frequent and important cause of increased morbidity and mortality. This chapter reviews the cardiovascular complications of Graves’ hyperthyroidism with underlying mechanisms and treatment.

SGLT1 knockdown prevents glucose fluctuation-induced apoptosis of cardiomyocytes through attenuating oxidative stress and mitochondrial dysfunction

2020 ◽  
Author(s):  
Qian Chai ◽  
Jiajing Miao ◽  
Meili Liu ◽  
Ziying Zhang ◽  
Ziang Meng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cardiovascular Complications ◽  
H9c2 Cells ◽  
Glucose Fluctuation ◽  
Sodium Glucose Cotransporter ◽  
Antioxidase Activity ◽  
H9c2 Cardiomyocytes ◽  
Underlying Mechanisms ◽  
Induced Apoptosis

Blood glucose fluctuation has been validated to be more detrimental than constant high glucose in the development of cardiovascular complications of diabetes mellitus (DM). Sodium‑glucose cotransporter 2 (SGLT2) inhibitors have been developed as antidiabetic drugs with cardiovascular benefits. However, whether inhibition of SGLT1 protects the diabetic heart remains to be elucidated. The present study investigated the role of SGLT1 in rat H9c2 cardiomyocytes subjected to glucose fluctuation and the underlying mechanisms. The results indicated that SGLT1 knockdown was able to restore cell proliferation and suppress cytotoxicity induced by glucose fluctuation. Glucose fluctuation induced oxidative stress in H9c2 cells, while these changes were reversed effectively by SGLT1 knockdown, as manifested by reduction of intracellular reactive oxygen species and increased antioxidase activity. Further study demonstrated that SGLT1 knockdown attenuated mitochondrial dysfunction in H9c2 cells exposed to glucose fluctuation, including restoration of mitochondrial membrane potential and promotion of mitochondrial fusion. In addition, SGLT1 knockdown downregulated Bax expression, upregulated Bcl-2 expression, and reduced caspase-3 activation in glucose fluctuation-induced H9c2 cells. Taken together, our study reveals that SGLT1 knockdown ameliorates glucose fluctuation-induced cardiomyocyte apoptosis, which might be ascribed to regulation of oxidative stress and mitochondrial dysfunction.

scholarly journals Analysis of Multiple Mycotoxins in the Qatari Population and Their Relation to Markers of Oxidative Stress

Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 267
Author(s):  
Belqes Al-Jaal ◽  
Aishah Latiff ◽  
Sofia Salama ◽  
Huda Mohamed Hussain ◽  
Noora Abdulaziz Al-Thani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biological Fluids ◽  
Oxidative Stress Markers ◽  
Liquid Chromatography Mass Spectrometry ◽  
Serum Samples ◽  
Stress Markers ◽  
Naturally Occurring ◽  
Markers Of Oxidative Stress ◽  
Underlying Mechanisms ◽  
Roquefortine C

Mycotoxins are naturally occurring food toxins worldwide that can cause serious health effects. The measurement of mycotoxin biomarkers in biological fluids is needed to assess individual's’ exposure. The aim of this study was to investigate the incidence of mycotoxins in the Qatari population. Serum samples from 412 adults and urinary samples from 559 adults were analyzed for the presence of mycotoxin biomarkers. Multimycotoxin approaches have been applied, using liquid chromatography mass spectrometry methods. Samples were further analyzed for the oxidative stress markers and compared with regard to the incidence of mycotoxins. The presence of mycotoxins was identified in 37% of serum samples and in less than 20% of urine samples. It was found that 88% of positive of the samples were positive for only one mycotoxin, while 12% of positive samples had two or more mycotoxins. Trichothecenes and zearalenone metabolites were most commonly detected mycotoxins, followed by aflatoxins, roquefortine C and mycophenolic acid. The presence of mycotoxins was found to positively correlate with oxidative stress markers. The obtained results illustrate the importance of mycotoxin biomonitoring studies in humans and the need to elucidate the underlying mechanisms of mycotoxin-induced toxicity.

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