Journals / Ulusal Travma Dergisi / 2003 / Cilt: 9 - Sayı: 3

The role of supplementation or inhibition of nitric oxide production in burn injury to reduce ischemic damage

Yanıkta nitrik oksit üretiminin desteklenmesi veya azaltılmasının iskemik hasarı azaltmadaki rolü

Pages
169–175
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Inhibition of NO production is found more useful after thermal injury in rats.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background: To determine the role of nitric oxide (NO) which is vasodilator agent and inflammatory cytokine, in burn injury.
📊
Key Findings & Data:Methods: Rats were divided into 5 groups, and a 30 % burn was inflicted.
💡
Conclusion & Impact:Inhibition of NO production is found more useful after thermal injury in rats.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Hastalık modelleri · hayvan · İskemi

Abstract

Background: To determine the role of nitric oxide (NO) which is vasodilator agent and inflammatory cytokine, in burn injury. Methods: Rats were divided into 5 groups, and a 30 % burn was inflicted. In addition to sham control and burn control groups, other 3 groups were given L-Arginin, and L-nitro-L-Arginine methylester (L-NAME), and both. Neutrophil and heametocrit percentage in blood, NO, TNF-alfa and malondialdehit (MDA) levels in plasma and neutrophil infiltration in the lung were evaluated at 24 hours after thermal injury. Results: The inhibition of NO production with L-NAME treatment significantly decreased these parameters when compared to burned control group. MDA was decreased significantly in all groups which were given drugs. Conclusion: The induction and inhibition of NO production both reduced lipid peroxidation but induction increased the mortality, plasma TNF-alfa and neutrophil in the blood. Inhibition of NO production is found more useful after thermal injury in rats.

Özet

Amaç: Vazoregülatör ajan ve enflamatuar sitokinlerden biri olan nitrik oksit’in (NO) etkisi yanık modelinde araştırıldı. Gereç ve yöntem: Çalışmada sıçanlar 5 gruba ayrıldı ve üzerinde % 30 oranında III. derecede yanık oluşturuldu. Grup 1: yanıksız, grup 2; yanıklı kontrol grubu, ve yanıklı tedavi gruplarında grup 3; L-Arginin, grup 4; L-nitro-L-Arginine methylester (L-NAME) ve grup 5; her iki ilaç aynı dozlarda verildi. Yanıktan 24 saat sonra kanda nötrofil ve akciğer nötrofil infiltrasyonu sayımı ve hematokrit, plazmada TNF-alfa, NO ve Malondialdehit (MDA) düzeyleri ölçüldü. Bulgular: Sadece L-NAME verilerek NO üretimi engellenen grupta plazma TNF-alfa, MDA, kan ve akciğer nötrofil değerlerinde grup 2’ye göre anlamlı düşüş görüldü. Tedavi gruplarında plazma MDA düzeylerinde anlamlı azalma görüldü. Sonuçlar: Yanıktan sonra kanda seviyesi artan NO miktarının hem indüklenerek arttırılması hem de üretiminin engellenmesi ile lipid peroksidasyonun azalabileceğini ortaya koymuş ancak indüklenmesi mortalite ile birlikte plazma TNF-alfa ve nötrofil sayısını arttırmıştır. NO üretiminin engellenmesinin daha yararlı olduğu görülmüştür.

🔖

Cite This Article

ZİLAN, A., ÇETİNKALE, O., KIRAN, B., ÜNLÜÇERÇİ, Y. M. Y., OLGAÇ, N. V., DENİZ, G., BEKPINAR, S. (2003). The role of supplementation or inhibition of nitric oxide production in burn injury to reduce ischemic damage. Ulusal Travma Dergisi, Cilt: 9 - Sayı: 3, 169–175. https://ajindex.com/articles/324961

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (17)

  1. Becker WK, Shippee RL, Mc Manus AT, et al. Kinetics of nitrogen oxide following experimental thermal injury in rats. J Trauma. 1993; 34: 855 - 862
  2. Soejima K, Schmalstieg, Traber LD, et al. Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury. Burn. 2001; 27: 809 - 813
  3. Cordeiro PG, Mastorakos DP, Hu QY, et al. The pro- tective effect of L-arginine on ischemia reperfusion injury in rat skin flap. Plast Reconstr Surg. 1997: 100; 1227 - 1233
  4. Shridan RL, Tompkins RG. Etiology and prevention of multysystem organ failure. In: Hendon DN. ed. Total Burn Care, Chapter 29, London, WB Saunders 1996: 302-312
  5. Sozumi T. The role of nitric oxide in vascular perme- ability after a thermal injury. Ann Plast Surg. 1997; 39: 272-277
  6. Gamelli RL, George M, Sharp-Pucci M, et al. Burn- induced nitric oxide release in humans. J Trauma. 1995; 39: 869-878
  7. Preiser JC, Reper P, Vlasselaer D, et al. Nitric Oxide production is increased in patients after burn injury. J Trauma. 1996; 40: 368-371
  8. Nakae H, Endo S, Inada K. et al. Are nitrite/nitrate (NOx) levels elevated by inhalation injury? Burns. 2000; 26: 515-519
  9. Cordeiro PG, Santamaria E, Hu QY. Use of a nitric oxide precursor to protect pig myocutaneous flaps from ischemia-reperfusion injury. Plast Reconstr Surg. 1998: 102; 2040-2051
  10. Oshima H. The influence of skin flap ischemia on serum nitric oxide concentrations. Microsurgery. 1996; 17: 191-197
  11. Walker HL.,Mason AD. A standard animal burn. J Trauma. 1968; 8:1049-1051
  12. Bender Med Systems Diagnostics GmbH, Rennweg 95b A-1030 Vienna, Austria Europe. Cat No: BMS 622
  13. Yoshioka T, Kawaka K, Shimada T, et al. Lipid peroxi- dation in maternal and cord blood and protective mechanisms against achieved oxygen toxicity in the blood. Am J Obstet Gynecol. 1979; 135: 372-376
  14. Grisham MB, Johnson GG, Gautreaux MD, et al. Measurement of nitrate and nitrite in entrocellular flu- ids: A window to systemic nitric oxide metabolism. Methods. 1995; 7: 84-90
  15. Lovett JE, Fink BF, Bernard A, et al. Analysis of nitric oxide activity in prevention of reperfusion injury Ann Plast Surg. 2001; 46: 269- 274
  16. Lindblom L, Cassuto J, Yregard L, et al. Importance of nitric oxide in the regulation of burn oedema, protein- uria and urine output. Burn. 2000: 26; 13-18
  17. Tsai HJ, Shang HF, Yeh CL, et al. Effects of arginine supplementation on antioxidant enzyme activity and macrophage response in burned mice. Bur