scholarly journals Levosimendan inhibits release of reactive oxygen species in polymorphonuclear leukocytes in vitro and in patients with acute heart failure and septic shock: a prospective observational study

Critical Care ◽  
2011 ◽  
Vol 15 (4) ◽  
pp. R166 ◽  
Author(s):  
Julia Hasslacher ◽  
Klaudija Bijuklic ◽  
Cristina Bertocchi ◽  
Jordan Kountchev ◽  
Romuald Bellmann ◽  
...  
Keyword(s):  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Septic Shock ◽  
Observational Study ◽  
Acute Heart Failure ◽  
Polymorphonuclear Leukocytes ◽  
Prospective Observational Study ◽  
Reactive Oxygen ◽  
Oxygen Species

The Influence of Some Immunosuppressive Drugs on the Metabolic Activity of Human Phagocytes and Lymphocytes in vitro

1998 ◽  
Vol 11 (3) ◽  
pp. 155-162 ◽  
Author(s):  
M. Dušková ◽  
L. Dušek ◽  
M. Čìž ◽  
A. Lojek ◽  
H. Slavíková
Keyword(s):  
Reactive Oxygen Species ◽  
Cyclosporine A ◽  
Polymorphonuclear Leukocytes ◽  
Thymidine Incorporation ◽  
Reactive Oxygen ◽  
Blast Transformation ◽  
Oxygen Species ◽  
Fk 506 ◽  
Control Value

The effect of azathioprine, cyclosporine A and FK 506 on the production of reactive oxygen species by polymorphonuclear leukocytes (Iuminol-dependent chemiluminescence) and on the blast transformation of lymphocytes ([3H]thymidine incorporation) was studied in dose-response experiments under in vitro conditions. Although there were no significant effects of immunosuppressives on non-stimulated blast transformation, FK 506 and cyclosporine A significantly inhibited the blast transformation stimulated by concanavaline A and protein A and the effects made it possible to build 2nd-order polynomial dose-response models. Azathioprine was found to be a relatively weak inhibitor of [3H]thymidine incorporation in lymphocytes (76% of control value). Spontaneous production of reactive oxygen species by polymorphonuclear leukocytes was significantly inhibited, particularly by FK 506 (1–100 ng.ml−1) in comparison to the control value, while there was no effect of the immunosuppressives on this system activated either by starch grains or zymosan. Only the highest applied concentrations of azathioprine (100 ng.ml−1) and cyclosporine A (1000 ng.ml−1) led to a significant decline in spontaneous phagocytosis. The direct effect of immunosuppressives on activated production of reactive oxygen species by neutrophiles was not proved.

scholarly journals HUBUNGAN KADAR ASAM URAT DENGAN KEJADIAN GAGAL JANTUNG AKUT PADA PASIEN HIPERTENSI

e-CliniC ◽  
2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Rezuanto Pualillin ◽  
Starry H. Rampengan ◽  
Frans Wantania
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Uric Acid ◽  
Acute Heart Failure ◽  
Heart Muscle ◽  
Odds Ratio ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Probability Sampling

Abstract: Long period of hypertension causes enlargement of the heart muscle, which leads to heart failure. Increased uric acid will causes endothelial dysfunction nas a result of the over production of reactive oxygen species (ROS), decrease the amount of nitric oxide (NO), increased rennin production, and the occurrence of inflammatory reactions. This speeds up the deterioration of the heart muscle, causing acute phase of heart failure. This study aimed to determine the relationship between uric acid levels and the incidence of acute heart failure in hypertensive patients in the emergency department and hypertension clinic of Prof. Dr R.D Kandou Hospital in Manado. This was an analytical observation by using the cross-sectional design. By using a non-probability sampling method we found 40 people as samples who had been diagnosed with heart failure due to hypertension. There were 15 samples that had experienced acute heart failure and 25 samples did not. Logistic Regression Test results stated that there was no significant effect of uric acid level with the incidence of acute heart failure (p = 0.188), with the value of the odds ratio of 1.198. Conclusion: There was no correlation between the levels of uric acid with the incidence of acute heart failure in patients with hypertension.Keywords: uricacid, hypertension, acute heart failureAbstrak: Hipertensi yang lama menyebabkan terjadinya pembesaran otot jantung sehingga berdampak pada terjadinya gagal jantung. Peningkatan asam urat juga menyebabkan disfungsi endotel akibat produksi reactive oxygen species (ROS) yang berlebihan, penurunan jumlah nitric oxide(NO), produksi renin meningkat, dan terjadinya reaksi inflamasi. Hal ini mempercepat perburukan otot jantung sehingga terjadi fase akut gagal jantung. Untuk mengetahui hubunganantara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensidi instalasi rawat daruratdan poliklinik hipertensi RSUP Prof. Dr. R.D Kandou Manado. Jenis Penelitian ini adalah observasi analitik dengan menggunakan rancangan penelitian potong lintang. Dengan menggunakan metode non-probability sampling didapatkan 40 orang sebagai sampel yang telah didiagnosis menderita gagal jantung akibat hipertensi dimana 15 sampel yang mengalami episode akut dan 25 sampel yang tidak mengalami gagal jantung akut. Hasil Uji Regresi Logistik menyatakan bahwa tidak ada pengaruh yang signifikan antara kadar asam urat dengan kejadian gagal jantung akut (p=0,188), dengan nilai odds ratio sebesar 1,198. Simpulan: Tidak terdapat hubungan antara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensi.Abstract: Long period of hypertension causes enlargement of the heart muscle, which leads to heart failure. Increased uric acid will causes endothelial dysfunction nas a result of the over production of reactive oxygen species (ROS), decrease the amount of nitric oxide (NO), increased rennin production, and the occurrence of inflammatory reactions. This speeds up the deterioration of the heart muscle, causing acute phase of heart failure. This study aimed to determine the relationship between uric acid levels and the incidence of acute heart failure in hypertensive patients in the emergency department and hypertension clinic of Prof. Dr R.D Kandou Hospital in Manado. This was an analytical observation by using the cross-sectional design. By using a non-probability sampling method we found 40 people as samples who had been diagnosed with heart failure due to hypertension. There were 15 samples that had experienced acute heart failure and 25 samples did not. Logistic Regression Test results stated that there was no significant effect of uric acid level with the incidence of acute heart failure (p = 0.188), with the value of the odds ratio of 1.198. Conclusion: There was no correlation between the levels of uric acid with the incidence of acute heart failure in patients with hypertension.Keywords: uricacid, hypertension, acute heart failureAbstrak: Hipertensi yang lama menyebabkan terjadinya pembesaran otot jantung sehingga berdampak pada terjadinya gagal jantung. Peningkatan asam urat juga menyebabkan disfungsi endotel akibat produksi reactive oxygen species (ROS) yang berlebihan, penurunan jumlah nitric oxide(NO), produksi renin meningkat, dan terjadinya reaksi inflamasi. Hal ini mempercepat perburukan otot jantung sehingga terjadi fase akut gagal jantung. Untuk mengetahui hubunganantara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensidi instalasi rawat daruratdan poliklinik hipertensi RSUP Prof. Dr. R.D Kandou Manado. Jenis Penelitian ini adalah observasi analitik dengan menggunakan rancangan penelitian potong lintang. Dengan menggunakan metode non-probability sampling didapatkan 40 orang sebagai sampel yang telah didiagnosis menderita gagal jantung akibat hipertensi dimana 15 sampel yang mengalami episode akut dan 25 sampel yang tidak mengalami gagal jantung akut. Hasil Uji Regresi Logistik menyatakan bahwa tidak ada pengaruh yang signifikan antara kadar asam urat dengan kejadian gagal jantung akut (p=0,188), dengan nilai odds ratio sebesar 1,198. Simpulan: Tidak terdapat hubungan antara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensi.Kata kunci: asam urat, hipertensi, gagal jantung akut: asam urat, hipertensi, gagal jantung akut

scholarly journals Dual SGLT-1 and SGLT-2 inhibition improves left atrial dysfunction in HFpEF

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
David Bode ◽  
Lukas Semmler ◽  
Paulina Wakula ◽  
Niklas Hegemann ◽  
Uwe Primessnig ◽  
...  
Keyword(s):  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Left Atrial ◽  
Buffer Capacity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Co Morbidity

Abstract Background Sodium–glucose linked transporter type 2 (SGLT-2) inhibition has been shown to reduce cardiovascular mortality in heart failure independently of glycemic control and prevents the onset of atrial arrhythmias, a common co-morbidity in heart failure with preserved ejection fraction (HFpEF). The mechanism behind these effects is not fully understood, and it remains unclear if they could be further enhanced by additional SGLT-1 inhibition. We investigated the effects of chronic treatment with the dual SGLT-1&2 inhibitor sotagliflozin on left atrial (LA) remodeling and cellular arrhythmogenesis (i.e. atrial cardiomyopathy) in a metabolic syndrome-related rat model of HFpEF. Methods 17 week-old ZSF-1 obese rats, a metabolic syndrome-related model of HFpEF, and wild type rats (Wistar Kyoto), were fed 30 mg/kg/d sotagliflozin for 6 weeks. At 23 weeks, LA were imaged in-vivo by echocardiography. In-vitro, Ca2+ transients (CaT; electrically stimulated, caffeine-induced) and spontaneous Ca2+ release were recorded by ratiometric microscopy using Ca2+-sensitive fluorescent dyes (Fura-2) during various experimental protocols. Mitochondrial structure (dye: Mitotracker), Ca2+ buffer capacity (dye: Rhod-2), mitochondrial depolarization (dye: TMRE) and production of reactive oxygen species (dye: H2DCF) were visualized by confocal microscopy. Statistical analysis was performed with 2-way analysis of variance followed by post-hoc Bonferroni and student’s t-test, as applicable. Results Sotagliflozin ameliorated LA enlargement in HFpEF in-vivo. In-vitro, LA cardiomyocytes in HFpEF showed an increased incidence and amplitude of arrhythmic spontaneous Ca2+ release events (SCaEs). Sotagliflozin significantly reduced the magnitude of SCaEs, while their frequency was unaffected. Sotagliflozin lowered diastolic [Ca2+] of CaT at baseline and in response to glucose influx, possibly related to a ~ 50% increase of sodium sodium–calcium exchanger (NCX) forward-mode activity. Sotagliflozin prevented mitochondrial swelling and enhanced mitochondrial Ca2+ buffer capacity in HFpEF. Sotagliflozin improved mitochondrial fission and reactive oxygen species (ROS) production during glucose starvation and averted Ca2+ accumulation upon glycolytic inhibition. Conclusion The SGLT-1&2 inhibitor sotagliflozin ameliorated LA remodeling in metabolic HFpEF. It also improved distinct features of Ca2+-mediated cellular arrhythmogenesis in-vitro (i.e. magnitude of SCaEs, mitochondrial Ca2+ buffer capacity, diastolic Ca2+ accumulation, NCX activity). The safety and efficacy of combined SGLT-1&2 inhibition for the treatment and/or prevention of atrial cardiomyopathy associated arrhythmias should be further evaluated in clinical trials.

Surgery-Derived Reactive Oxygen Species Produced by Polymorphonuclear Leukocytes Promote Tumor Recurrence: Studies in an In Vitro Model

2007 ◽  
Vol 140 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Wilhelmina M.U. van Grevenstein ◽  
Arend G.J. Aalbers ◽  
Sander ten Raa ◽  
Wim Sluiter ◽  
Leo J. Hofland ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Polymorphonuclear Leukocytes ◽  
Tumor Recurrence ◽  
In Vitro Model ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Vitro Model

scholarly journals Navigating Calcium and Reactive Oxygen Species by Natural Flavones for the Treatment of Heart Failure

2021 ◽  
Vol 12 ◽  
Author(s):  
Tianhao Yu ◽  
Danhua Huang ◽  
Haokun Wu ◽  
Haibin Chen ◽  
Sen Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Cellular Level ◽  
Calcium Signal ◽  
Oxygen Species ◽  
Therapeutic Implications ◽  
Artery Disease

Heart failure (HF), the leading cause of death among men and women world-wide, causes great health and economic burdens. HF can be triggered by many factors, such as coronary artery disease, heart attack, cardiomyopathy, hypertension, obesity, etc., all of which have close relations with calcium signal and the level of reactive oxygen species (ROS). Calcium is an essential second messenger in signaling pathways, playing a pivotal role in regulating the life and death of cardiomyocytes via the calcium-apoptosis link mediated by the cellular level of calcium. Meanwhile, calcium can also control the rate of energy production in mitochondria that are the major resources of ROS whose overproduction can lead to cell death. More importantly, there are bidirectional interactions between calcium and ROS, and such interactions may have therapeutic implications in treating HF through finely tuning the balance between these two by certain drugs. Many naturally derived products, e.g., flavones and isoflavones, have been shown to possess activities in regulating calcium and ROS simultaneously, thereby leading to a balanced microenvironment in heart tissues to exert therapeutic efficacies in HF. In this mini review, we aimed to provide an updated knowledge of the interplay between calcium and ROS in the development of HF. In addition, we summarized the recent studies (in vitro, in vivo and in clinical trials) using natural isolated flavones and isoflavones in treating HF. Critical challenges are also discussed. The information collected may help to evoke multidisciplinary efforts in developing novel agents for the potential prevention and treatment of HF.

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