HUBUNGAN 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.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

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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 ◽

10.1186/cc10307 ◽

2011 ◽

Vol 15 (4) ◽

pp. R166 ◽

Cited By ~ 41

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

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Nitric Oxide/Reactive Oxygen Species Generation and Nitroso/Redox Imbalance in Heart Failure: From Molecular Mechanisms to Therapeutic Implications

Antioxidants and Redox Signaling ◽

10.1089/ars.2010.3198 ◽

2011 ◽

Vol 14 (2) ◽

pp. 289-331 ◽

Cited By ~ 57

Author(s):

Chiara Nediani ◽

Laura Raimondi ◽

Elisabetta Borchi ◽

Elisabetta Cerbai

Keyword(s):

Nitric Oxide ◽

Heart Failure ◽

Reactive Oxygen Species ◽

Molecular Mechanisms ◽

Reactive Oxygen Species Generation ◽

Reactive Oxygen ◽

Oxygen Species ◽

Therapeutic Implications ◽

Redox Imbalance

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Faculty Opinions recommendation of Sources of vascular nitric oxide and reactive oxygen species and their regulation

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.734520172.793578224 ◽

2020 ◽

Author(s):

Paschalis-Thomas Doulias

Keyword(s):

Nitric Oxide ◽

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Oxygen Species

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The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

Current Cardiology Reviews ◽

10.2174/1573403x16666201014142446 ◽

2020 ◽

Vol 16 ◽

Author(s):

Andrey Krylatov ◽

Leonid Maslov ◽

Sergey Y. Tsibulnikov ◽

Nikita Voronkov ◽

Alla Boshchenko ◽

...

Keyword(s):

Nitric Oxide ◽

Reactive Oxygen Species ◽

Hydrogen Sulfide ◽

Ischemia Reperfusion ◽

Reactive Oxygen ◽

Ischemia And Reperfusion ◽

Oxygen Species ◽

Ischemia And Reperfusion Injury ◽

Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

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Plasmonic Enhancement of Nitric Oxide Generation

Nanoscale ◽

10.1039/d1nr02126e ◽

2021 ◽

Author(s):

Rachael Knoblauch ◽

Chris Geddes

Keyword(s):

Nitric Oxide ◽

Reactive Oxygen Species ◽

Reactive Nitrogen Species ◽

Reactive Oxygen ◽

Reactive Nitrogen ◽

Oxygen Species ◽

Nitrogen Species ◽

Plasmonic Enhancement ◽

Cancer Treatments

While the utility of reactive oxygen species in photodynamic therapies for both cancer treatments and antimicrobial applications has received much attention, the inherent potential of reactive nitrogen species (RNS) including...

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Reactive Oxygen Species-Dependent Nitric Oxide Production in Reciprocal Interactions of Glioma and Microglial Cells

Journal of Cellular Physiology ◽

10.1002/jcp.24659 ◽

2014 ◽

Vol 229 (12) ◽

pp. 2015-2026 ◽

Cited By ~ 21

Author(s):

Shing-Chuan Shen ◽

Ming-Shun Wu ◽

Hui-Yi Lin ◽

Liang-Yo Yang ◽

Yi-Hsuan Chen ◽

...

Keyword(s):

Nitric Oxide ◽

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Microglial Cells ◽

Nitric Oxide Production ◽

Oxygen Species ◽

Reciprocal Interactions ◽

Oxide Production

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The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

Medicinski pregled ◽

10.2298/mpns1012827r ◽

2010 ◽

Vol 63 (11-12) ◽

pp. 827-832 ◽

Cited By ~ 7

Author(s):

Tatjana Radosavljevic ◽

Dusan Mladenovic ◽

Danijela Vucevic ◽

Rada Jesic-Vukicevic

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Reactive Oxygen Species ◽

Liver Injury ◽

Kupffer Cells ◽

Reactive Oxygen ◽

Oxygen Species ◽

Severe Liver ◽

Hepatocellular Necrosis

Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito?chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu?cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion radicals through the enzyme nicotinamide adenine dinucleotide phosphate oxidase. Hydrogen peroxide, which is influenced by the neutrophil-derived enzyme myeloperoxidase, generates hypochlorus acid as a potent oxidant. Role of peroxynitrite in paracetamol-induced oxidative stress. Superoxide can react with nitric oxide to form peroxynitrite, as a potent oxidant. Nitrotyrosine is formed by the reaction of tyrosine with peroxynitrite in paracetamol hepatotoxicity. Conclusion. Overdose of paracetamol may produce severe liver injury with hepatocellular necrosis. The most important mechanisms of cell injury are metabolic activation of paracetamol, glutathione depletion, alkylation of proteins, especially mitochondrial proteins, and formation of reactive oxygen/nitrogen species.

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