Journals / Türk Anestezi ve Reanimasyon Dergisi / 2009 / Cilt: 37 - Sayı: 4

The effect of N-acetylcysteine on oxidative stress in induced hemorrhagic shock model in rats

Ratlarda oluşturulan hemorajik şok modelinde N-asetilsistein’in oksidatif stres üzerine olan etkisi

Pages
208–216
Publication Date
2022-11-05
DOI
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AI Summary & Key Takeaways

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

It is concluded that in order to clarify this issue different hemorrhagic shock models where MAP values are maintained at lower levels are needed.

📌 3 Key Takeaways

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Objective & Hypothesis:Aim: It was brought forward that reactive oxygen species (ROS) released by the activation of the immuno-inflamatory mediators in the late period of the hemorrhagic shock lead to multiple organ failure.
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Key Findings & Data:Blood samples were withdrawn within 15 minutes from mechanically ventilated rats in which hemorrhagic shock model was induced.
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Conclusion & Impact:It is concluded that in order to clarify this issue different hemorrhagic shock models where MAP values are maintained at lower levels are needed.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Aim: It was brought forward that reactive oxygen species (ROS) released by the activation of the immuno-inflamatory mediators in the late period of the hemorrhagic shock lead to multiple organ failure. For this reason in our study investigation of the effects of n-acetylcysteine (NAC); one of the antioxidant agents with approved free radical collecting property was aimed. Material and Methods: Sixteen adult Winstar rats were randomly divided into two groups. Blood samples were withdrawn within 15 minutes from mechanically ventilated rats in which hemorrhagic shock model was induced. After 60 minutes of hemorrhagic shock, autologous blood and crystalloid infusions were given until the mean arterial pressure reached to 80-90 mmHg in Group I. In the Group 2, N-acetylcysteine 150 mg/kg IV were given concomitantly with autologous blood and crystalloid infusions. After the end of one hour period, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) levels in blood samples obtained before and after the hemorrhagic shock were measured. Results: When changes in MDA, SOD and CAT values relative to baseline and intergroup comparisons of these changes occurring in these parameters were considered, any statistically significant difference was not detected.Conclusion: It was observed that in moderate hemorrhagic shock model where MAP was kept between 50 and 55 mmHg, any increase in ROS was not detected ,and NAC did not have any protective effect in this experimental model. It is concluded that in order to clarify this issue different hemorrhagic shock models where MAP values are maintained at lower levels are needed.

Özet

Amaç: İmmuno-inflamatuvar mediyatörlerin aktive olmasıyla açığa çıkan serbest oksijen radikallerinin (SOR) hemorajik şokun geç döneminde multipl organ yetmezliğine neden olduğu ileri sürülmektedir. Çalışmamızda; serbest radikal toplayıcı özellikleri olan antioksidan ajanlardan biri olarak kabul edilen N-asetilsistein (NAS)’in etkinliğinin araştırılması amaçlandı. Gereç ve Yöntem: On altı adet Winstar türü erişkin erkek rat rasgele 2 gruba ayrıldı. Mekanik ventilasyon desteği altındaki ratların tümünden 15 dk.’lık bir süre içinde hemorajik şok modeli oluşturuldu. Altmış dk.’lık hemorajik şok dönemi sonrasında ortalama arteryel basınç 80-90 mmHg oluncaya dek I. Gruptaki ratlara otolog kan transfüzyonu ve kristalloid infüzyonu yapılırken, II. Gruptaki ratlara otolog kan transfüzyonu ve kristalloid infüzyonu ile aynı anda 150 mg kg-1 dozunda N-asetilsistein IV olarak verildi. Bir saatlik sürenin sonunda şok dönemi öncesinde ve sonrasında alınan tüm kanlardan malondialdehit (MDA), superoksit dismutaz (SOD) ve katalaz (KAT) tetkikleri yapıldı.Bulgular: SOD, KAT ve MDA analizlerinin başlangıca göre olan değişimleri ve bu değişimlerin gruplar arasındaki karşılaştırmaları yapıldığında istatistiksel olarak anlamlı bir fark bulunmadı.Sonuç: OAB’ın 50-55 mmHg arasında tutulduğu kompansatuvar hemorajik şok modelinde SOR’da yükselme saptanmadığı ve bu deneysel modelde NAS’ın koruyucu etkinliğinin olmadığı görüldü. Konunun açıklığa kavuşabilmesi için; OAB’ın daha düşük düzeylerde tutulduğu hemorajik şok modelleriyle araştırılmasına gereksinim olduğu kanısına varıldı.

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Cite This Article

SOLAK, İ., SEZER, E., DEMİRAĞ, K., ERİŞ, O., MORAL, A. R., ÇANKAYALI, İ. (2022). The effect of N-acetylcysteine on oxidative stress in induced hemorrhagic shock model in rats. Türk Anestezi ve Reanimasyon Dergisi, Cilt: 37 - Sayı: 4, 208–216. https://ajindex.com/articles/619954

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References (15)

  1. Izumi M, McDonald MC, Sharpe MA, Chatterjee PK, Thiemermann C. Superoxide dismutase mimetics with catalase activity reduces the organ injury in hemorrhagic shock. Shock 2002;18(3):230-5
  2. Kentner R, Safar P, Behringer W, et al. Early antioxidant therapy with tempol during hemorrhagis shock increases survival in rats. The Journal of Trauma Injury, Infection and Critical Care 2002;53(5):968-77
  3. Hoye TH, Davoren JE, Wipf P, Fink MP, Kagan VE. Targeting Mitochondria. Accounts of Chemical Research 2008;41(1):87-97
  4. Gutierrez G, Reines HD, and Wulf-Gutierrez ME. Clinical Review: Hemorrhagic shock. Crit Care 2004;8:373-81
  5. Mauriz JL, Martin Renedo J, Barrio JP, Culebras JM, Gonzalez P. Experimental models on hemorragic shock. Nutr Hosp 2007;22(2):190-8. (Abstract
  6. Bahrami S, Zimmermann K, Szelenyi Z et al. Small volume fluid resuscitation with hypertonic saline prevents inflammation but not mortality in a rat model of hemorrhagic shock. Shock 2006;25(3):283-9
  7. Jarrar D, Wang P, Cioffi WG, Bland KI, Chaudry IH. Critical role of oxygen radicals in the initiation of hepatic depression after trauma hemorrhage. The Journal of Trauma ® Injury, Infection and Critical Care 2000;49(5):879-85
  8. Peitzman AB, Harbrecht BG, Udekwu AO, Billiar TR, Kelly E, Simmons RL. Hemorrhagic shock. HYPERLINK “http://www.sciencedirect.com/science/journal/00113840” Current Problems in Surgery 1995;32(11):925-1002
  9. Duranteau J, Harrois A. Hemorrhagic shock. Rev Pract 2006;56(8):849-57
  10. Bumbasirevic V, Jovanovic B, Palibrk I et al. Hemorrhagic shock Acta Chir Iugosl 2007;54(1):63-70. (Abstract
  11. Portella AOV, Montero EFS, Poli de Figueiredo LF et al. Effects of N-Acetylcysteine in hepatic ischemi reperfusion injury during hemorrhagic shock. Tranplantation Proceedings 2004;36:846-8
  12. Eser O, Kalkan E, Buyukbas S, Avunduk MC, Aslan A, Kocabas V. The effect of aprotinin on brain ischemic-reperfusion injury after hemorrhagic shock in rats: An experimental study. The Journal of Trauma ® Injury, Infection and Critical Care 2007;63(2):373-8
  13. Powers KA, Kapus A, Khadaroo RG et al. Twenty-five percent albumin prevents lung injury following shock/resuscitation. Crit Care Med 2001;31(9):2355-63
  14. Powers KA, Zurawska J, Szaszi K, Khadaroo RG, Kapus A, Rotstein OD. Hypertonic resuscitation of hemorrhagic shock prevents alveolar macrophage activation by preventing systemic oxidative stres due to gut ischemia/ reperfusion. Surgery 2005;137(1):67-74
  15. Alkan A, Ero