Journals / Ulusal Travma ve Acil Cerrahi Dergisi / 2013 / Cilt: 19 - Sayı: 6

Multipl travmayı takiben enflamatuvar yanıt, apopitozis ve bakteriyel translokasyonda torasik travmanın rolü

The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas

Pages
491–499
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)

Our results indicate that thoracic trauma plays a major role in post-traumatic bacterial translocation, inflammation, and apoptosis following multiple traumas.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:BACKGROUND: Blunt chest trauma and its complications are commonly encountered in emergency medicine.
📊
Key Findings & Data:Rats underwent a standardized blunt thoracic and/or head trauma and were sacrificed 24 or 48 hours after the trauma.
💡
Conclusion & Impact:Our results indicate that thoracic trauma plays a major role in post-traumatic bacterial translocation, inflammation, and apoptosis following multiple traumas.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

BACKGROUND: Blunt chest trauma and its complications are commonly encountered in emergency medicine. Herein, we used a rat model to investigate the role of thoracic trauma in inflammation, apoptosis and bacterial translocation following multiple traumas. METHODS: Ninety Wistar rats were divided equally into nine groups. Rats underwent a standardized blunt thoracic and/or head trauma and were sacrificed 24 or 48 hours after the trauma. Specimens from various organs and blood samples were collected and quantitatively cultured for aerobic organisms. Interleukins, TNF-α, and MCP-1 levels were assessed in the sera and markers of apop- tosis were detected in the lungs. RESULTS: Levels of interleukins, TNF-α and MCP-1 in all of the groups undergoing trauma were significantly higher than those of the control group (p=0.001). Levels of apoptotic cells in the groups undergoing head and thoracic trauma (HTT) were significantly higher than those of the control group (p=0.009). Light microscopic evaluation indicated that damage in the HTT groups was signifi- cantly higher than that in the control group. The incidence of bacterial translocation was also significantly higher in the HTT groups (p=0.003). CONCLUSION: Multiple inflammatory mediators are activated in multiple traumas (including blunt thoracic trauma), which allow bacterial translocation and apoptotic processes to occur. Our results indicate that thoracic trauma plays a major role in post-traumatic bacterial translocation, inflammation, and apoptosis following multiple traumas.

Özet

AMAÇ: Künt göğüs travması ve komplikasyonları acil servislerde karşılaşılan en yaygın klinik problemlerden biridir. Postkontüzyon pnömoninin pa- togenezi, akut akciğer hasarı, akut solunum yetersizliği sendromu ve diğer etkili faktörler ile enflamatuvar yanıt arasındaki ilişkisi konusunda araştır- malara ihtiyaç duyulmaktadır. Bu çalışmamızda çoklu travma modelinde enflamasyon, apopitozis ve bakteriyel translokasyonun gelişimini araştırdık. GEREÇ VE YÖNTEM: Doksan adet Wistar cinsi sıçanı dokuz gruba ayırdık; 24 ve 48. saat torasik travma (TT), 24 ve 48. saat kafa travması (HT), 24 ve 48. saat kafa ve toraks travması (HTT), 0.24 ve 48 saat kontrol grupları. Sıçanlara standart künt toraks ve/veya kafa travması uygulandı ve travma sonrası 24. ve 48. saatte sakrifiye edildi. Farklı organlardan alınan çoklu örnekler ve kan örnekleri toplandı ve aerobik organizmalar için kantitatif kültür yapıldı. Serumda interlökinler, MCP-1 seviyeleri ve akciğerde apopitozis değerlendirildi. BULGULAR: Kontrol grubu ile karşılaştırıldığında tüm travma gruplarında interlökin, TNF-α, MCP-1 sevileri anlamlı olarak yüksekti (p=0.001). Kontrol grubu ile karşılaştırıldığında HTT grubunda apopitotik hücreler anlamlı olarak fazlaydı (p=0.009). Tüm grupların ışık mikroskopik değerlen- dirmesinde kontrol grubuna göre HTT grubunda belirgin artış vardı. Bakteriyel translokasyon HTT grubunda anlamlı biçimde yüksekti (p=0.003). TARTIŞMA: Künt toraks travmasının olduğu çoklu travmalarda çok sayıda enflamauvar mediatör artmakta ve bakteriyel translokasyon ve apopitotik proçesi etkilemektedirler. Travma ile ilişkili enflamasyon ve enfeksiyonlar arasındaki ilişkinin anlaşılmasının komplike hastaları tedavi yaklaşımlarında etkili olacağına inanıyoruz.

🔖

Cite This Article

AYAN, E., KÖKSEL, M. O., POLAT, A., TAME, L., ERSÖZ, G., DEMİR, M., YILDIRIM, H. Y., AKDAĞ, A., ÖZDÜLGER, A., ERDEN, S. (2013). Multipl travmayı takiben enflamatuvar yanıt, apopitozis ve bakteriyel translokasyonda torasik travmanın rolü. Ulusal Travma ve Acil Cerrahi Dergisi, Cilt: 19 - Sayı: 6, 491–499. https://ajindex.com/articles/324118

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Laudi S, Donaubauer B, Busch T, Kerner T, Bercker S, Bail H, et al. Low incidence of multiple organ failure after major trauma. Injury 2007;38:1052-8
  2. Lazarus HM, Fox J, Burke JP, Lloyd JF, Snow GL, Mehta RR, et al. Trau- ma patient hospital-associated infections: risks and outcomes. J Trauma 2005;59:188-94
  3. Raghavendran K, Davidson BA, Woytash JA, Helinski JD, Marschke CJ, Manderscheid PA, et al. The evolution of isolated bilateral lung contusion from blunt chest trauma in rats: cellular and cytokine responses. Shock 2005;24:132-8
  4. Raghavendran K, Davidson BA, Helinski JD, Marschke CJ, Manders- cheid P, Woytash JA, et al. A rat model for isolated bilateral lung contu- sion from blunt chest trauma. Anesth Analg 2005;101:1482-9
  5. Liener UC, Knöferl MW, Sträter J, Barth TF, Pauser EM, Nüssler AK, et al. Induction of apoptosis following blunt chest trauma. Shock 2003;20:511-6
  6. Wang ND, Stevens MH, Doty DB, Hammond EH. Blunt chest trau- ma: an experimental model for heart and lung contusion. J Trauma 2003;54:744-8
  7. Lichtman SM. Bacterial [correction of baterial] translocation in humans. J Pediatr Gastroenterol Nutr 2001;33:1-10
  8. Brathwaite CE, Ross SE, Nagele R, Mure AJ, O’Malley KF, García-Perez FA. Bacterial translocation occurs in humans after traumatic injury: evi- dence using immunofluorescence. J Trauma 1993;34:586-90
  9. Peitzman AB, Udekwu AO, Ochoa J, Smith S. Bacterial translocation in trauma patients. J Trauma 1991;31:1083-67
  10. Moore FA, Moore EE, Poggetti RS, Read RA. Postinjury shock and early bacteremia. A lethal combination. Arch Surg 1992;127:893-8
  11. Foda MA, Marmarou A. A new model of diffuse brain injury in rats. Part II: Morphological characterization. J Neurosurg 1994;80:301-13
  12. Baron EJ, Peterson LR, Finegold SM. Hospital epidemiology. In: Baron EJ, Peterson LR, Finegold SM, editors. Bailey and Scott’s diagnostic mi- crobiology. 9th ed. St. Louis: Mosby - Year Book; 1994. p. 284-95
  13. Steffen EK, Berg RD, Deitch EA. Comparison of translocation rates of various indigenous bacteria from the gastrointestinal tract to the mesen- teric lymph node. J Infect Dis 1988;157:1032-8
  14. Koksel O, Cinel I, Tamer L, Cinel L, Ozdulger A, Kanik A, et al. N-ace- tylcysteine inhibits peroxynitrite-mediated damage in oleic acid-induced lung injury. Pulm Pharmacol Ther 2004;17:263-70
  15. Turina M, Hoth JJ, Turpen RM, Scott MJ, Cheadle WG. Alveolar inter- leukin-10 regulates neutrophil apoptosis in severely traumatized pati