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Akut Atak, Stabil KOAH ve Kor Pulmonale Hastalarında ADMA, Arjinin ve NO Düzeylerinin Belirlenmesi

Investigation of ADMA, Arginine and NO Levels of Patients with Acute Attack, Stable COPD and Cor Pulmonale

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  • Selçuk Tıp Dergisi

Publication Year:

  • 2010

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Abstract (2. Language): 
The aim of our study was to determine serum asymmetric dimethylarginine (ADMA), nitric oxide (NO) and arginine levels in patients with acute attack, stable and cor pulmonale Chronic Obstuctive Pulmonary disease (COPD). Twenty five acute attack of COPD, twenty five stable of COPD, twenty five cor pulmonale subjects partipicated in this study. To be selected patients had to have no other diseases. The control group was formed by twenty five appearentely healthy people. ADMA and arginine levels were measured by high performance liquid chromatoghraphy with fluorecence detection. Serum nitrite/nitrate concentrations were determined using a commercial colorimetric assay. Patients of acute (p<0.01), stable (p<0.05) and cor pulmonale (p<0.001) of COPD had statistically significant higher values of ADMA compared to control group. There was no difference between stable, attack and control groups for arginine values. Cor pulmonale group had statistically significant lower values arginine compared to control (p<0.05) and attack groups (p<0.01). Our study shows that ADMA level is increased in the acute attack, stable and cor pulmonale of COPD patients. ADMA may play an important role in the progression of pulmonary hypertension in COPD patients. ADMA may therefore represent a novel therapeutic target for the treatment and prevention of pulmonary hypertension and cor pulmonale in COPD patients.
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Abstract (Original Language): 
Bu çalışmada atak, stabil ve kor pulmonale grubu kronik obstrüktif akciğer hastalığı (KOAH) olanlarda asimetrik dimetilarjinin (ADMA), nitrik oksit (NO) ve arjinin düzeylerindeki değişiklikleri belirlemeyi amaçladık. Çalışmamıza 25 akut atak KOAH, 25 stabil KOAH, 25 kor pulmonale hastası dahil edildi. Hastaların KOAH ve kor pulmonale dışında ek bir hastalığı yoktu. Kontrol grubu 25 sağlıklı kişiden oluşturuldu. ADMA ve Arjinin düzeyleri yüksek basınçlı likit kromatografi yöntemiyle floresans dedektörde ölçüldü. Serum nitrit/nitrat konsantrasyonları kolorimetrik metotla ölçüldü. Akut atak,(p<0.01) stabil (p<0.05) ve kor pulmonale (p<0.001) grubu KOAH hastalarında ADMA seviyeleri kontrol grubundan istatistiksel olarak anlamlı yüksek bulundu. Serum arjinin düzeylerinde stabil, atak ve kontrol grupları arasında anlamlı bir değişiklik gözlenmedi. Serum arjinin düzeyleri kor pulmonale grubunda kontrol (p<0.05) ve atak grubuna (p<0.01) oranla istatistiksel olarak anlamlı düşük bulundu. Bizim çalışmamız ADMA seviyelerinin atak, stabil ve kor pulmonale KOAH hastalarında arttığını göstermiştir. Sonuçlarımız artmış ADMA oranının KOAH temelinde gelişen pulmoner hipertansiyonun gelişiminde önemli rolü olabileceğini göstermektedir. Bu hastalarda gelişen pulmoner hipertansiyon ve kor pulmonalenin önlenmesi ve tedavisinde ADMA önemli bir hedef olabilir
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  • Turkish

REFERENCES

References: 

1- Kocabaş A. Kronik Obstrüktif Akciğer Hastalığı. Umut S, Erdinç E (Editörler).
Turgut yayıncılık; 2000;1-24.
2- O’Byrne PM, Postma DS. The Many Faces of Airway Inflammation. Asthma
and Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med
1999; 159: 41–66.
3- National Heart, Lung and Blood Instutute. Morbidity and mortality: chartbook
cardiovascular, lung and blood diseases. Bethesda, MD: US Departement,
of health and Human Services, Public Health Services, : National Instutute
of Health: 2003.
4- Numanoğlu N. Solunum Sistemi ve Hastalıkları, Antıp Yayınları 2001; 436-
41.
5- Marletta MA. Nitric oxide synthase: aspects, concerning structure and
catalysis. Cell 1994;78:927-30.
6- Stamler JS, Singel DJ, Loscalzo J. Biochemistry of nitric oxide and its
redox-activated forms. Science 1992; 26: 1898-902.
7- Naseem KM. The Role of Nitric Oxide İn Cardiovascular Disease Molecular
Aspects of Medicine 2005; 26:33-65.
8- Clarke S. Protein methylation. Curr Opin Cell Biol 1993;5:977–83.
9- McBride AE, Silver PA. State of the Arg: protein methylation at arginine
comes of age. Cell 2001;106:5–8.
10- Krause CD, Yang ZH, Kim YS, et al. Protein arginine methyltransferases:
Evolution and assessment of their pharmacological and therapeutic
potential. Pharmacol Ther 2006.
11- Vallance P, Leiper J. Cardiovascular Biology of the Asymmetric
Dimethylarginine: Dimethylarginine Dimethylaminohydrolase Pathway.
Arterioscler Thromb Vasc Biol 2004;24:1023-30.
12- Millat LJ, Whitley J, Leiper JM, et al. Evidence for Dysregulation of
Dimethylarginine Dimethylaminohydrolase I in Chronic Hypoxia-Ýnduced
Pulmonary Hypertension. Circulation 2003;108:1493-8.
13- Chen BM, Xia LW, Zhao RQ. Determination of NG, NG dimethylarginine in
human plasma by high performance liquit chromatography. J Chromatogr B
1997; 692: 467-71.
14- Pullamsetti S, Kiss L, Ghofrani HA, et al. Increased levels and reduced
catabolism asymmetric dimethylarginines in pulmonary hypertension. The
FASEB Journal 2005;19: 1175-7.
15- Gorenflo M, Zheng C, Werle E, et al. Plasma levels of asymmetric dimethylL-Arginine in Patients with Congenital Heart Disease and pulmonary
hypertension. Pharmacology 2001;37:489-92.
16- Arrigoni FI, Vallance P, Haworth SG, Leiper JM. Metabolism of asymmetric
dimethylarginines is regulated in the lung developmentally and with
pulmonary hypertension induced by hypobaric hypoxia. Circulation
2003;107;1195-201.
17- Anemon A, Backman V, Snygg J, et al. Accumulation of an endogenous
inhibitor of nitric oxide synthase during graded hemorragic shock. Circ
Shock 1994;44(3):111-4.
18- Yıldırım AO, Bulau P, Zakrzewicz D, et al. Increased Protein Arginine
Methylation in Chronic Hypoxia: Role of Protein Arginine Methyltransferases.
Am J Respir Cell Mol Biol 2006; 35: 436-43.
19- Dong Y, Thompson LP. Differential Expression of Endothelial Nitric Oxide
Synthase in Coronary and Cardiac Tissue in Hypoxic Fetal Guinea Pig
Hearts. J Soc Gynecol Investig 2006;13;483-90.
20- Eskiocak S, Tütüncüler F, Başaran UN, et al. The effect of melatonin on
protein oxidation and nitric oxide in the brain tissue of hypoxic neonatal rats.
Brain Dev 2007 ; 29: 19-24.
21- Fesler P, Pagnamenta A, Rondelet B, et al. Effects of sildenafil on hypoxic
pulmonary vascular function in dogs. J Appl Physiol 2006;101:1085-90.
22- Sandimo MM, Hernandez A. Pulmonary arteriole remodeling in hypoxic
broilers expressing different amounts of endothelial nitric oxide synthase.
Poult Sci 2006;85:899-901.
23- Maziak W, Loukides S, Culpitt S, et al. Exhaled Nitric Oxide Chronic
Obstructive Pulmonary Disease. Am. J. Respir. Crit. Med 1998;157:998-
1002.
24- Bae SW, Stühlinger MC, Yoo HS, et al. Plasma Asymmetric
Dimethylarginine Concentrations in Newly Diagnosed Patients With Acute
Myocardial Infarction or Unstable Angina Pectoris During Two Weeks of
Medical Treatment. Am J Cardiol 2005;95:729–33.
25- Saitoh M, Osanai T, Kamada T, et al. High Plasma Level of asymmetric
dimethylarginine in patients with acutely exacerbated congestive heart
failure: role in reduction of plasma nitric oxide level. Heart Vessels 2003;18:
177-82.

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