Journals / Hacettepe Üniversitesi Eczacılık Fakültesi Dergisi / 2005 / Sayı: 1

Ischemia-Reperfusion Injury and Ischemic Preconditioning in the Lungs

Akciğerlerde İskemi-Reperfüzyon Hasarı ve İskemik Önkoşullama

Pages
35–49
Publication Date
2005-01-01
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)

In this review, I/R injury, IP and its possible mechanisms in the lung were evaluated.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Ischemia-reperfusion I/R is defined as the condition of inadequate blood supply to a tissue or organ for a limited time which is followed by the restoration of blood flow.
📊
Key Findings & Data:In recent years, multiple clinical strategies are suggested to prevent I/R injury such as complement inhibition, surfactant therapy, nitric oxide inhalation.
💡
Conclusion & Impact:In this review, I/R injury, IP and its possible mechanisms in the lung were evaluated.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Akciğer · iskemi-reperfüzyon · iskemik önkoşullama

Abstract

Ischemia-reperfusion I/R is defined as the condition of inadequate blood supply to a tissue or organ for a limited time which is followed by the restoration of blood flow. I/R- induced lung injury is a common situation occurring in lung transplantation. In recent years, multiple clinical strategies are suggested to prevent I/R injury such as complement inhibition, surfactant therapy, nitric oxide inhalation. In 1986, Murry and coworkers was the first to demonstrate that ischemic preconditioning was a protective mechanism against I/R injury in the hearth. A short period of ischemia-reperfusion protects against detrimental effects of subsequent prolonged ischemia; this endogenous mechanism of protection has been termed as ischemic preconditioning IP . After its demonstration in myocardium, several studies have addressed that IP may also occur in brain, skeletal muscle, liver, kidney and the lung. In this review, I/R injury, IP and its possible mechanisms in the lung were evaluated.

Özet

İskemi-reperfüzyon İ/R , doku veya organa giden kan akımında bir süre azalma ve sonrasında yeniden kanlanma olarak tanımlanmaktadır. İ/R ile indüklenen akciğer hasarı akciğer tranplantasyonunda sık karşılaşılan bir durumdur. Son yıllarda klinikte akciğer İ/R hasarını engellemeye yönelik kompleman inhibisyonu, sürfaktan tedavisi, nitrik oksit inhalasyonu gibi farklı yaklaşımlar kullanılmaktadır. 1986 yılında Murry ve arkadaşları tarafından miyokardda İ/R hasarına karşı güçlü endojen koruma oluşturan bir mekanizma iskemik önkoşullama gösterilmiştir. İskemik önkoşullama, doku veya hücrelerin iskemi ve reperfüzyona kısa süreli maruz kalmasını takiben daha uzun süreli iskemi ile oluşan doku hasarında belirgin bir azalmadır. Kalpte gösterilmesinden sonra beyin, omurilik, iskelet kası, karaciğer, böbrek, akciğer, gibi pek çok farklı dokuda önkoşullama oluşturulabileceği gösterilmiştir. Bu derlemede akciğerlerde İ/R hasarı, iskemik önkoşullama ve olası etki mekanizmaları değerlendirilmiştir.

🔖

Cite This Article

KANDİLCİ, H. B., GÜMÜŞEL, B. (2005). Ischemia-Reperfusion Injury and Ischemic Preconditioning in the Lungs. Hacettepe Üniversitesi Eczacılık Fakültesi Dergisi, Sayı: 1, 35–49. https://ajindex.com/articles/762461

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Siemionow M, Arslan E.: Ischemia/reperfusion injury: A review in relation to free tissue transfers. Microsurgery, 24, 468-475 (2004).
  2. Maxwell, S.R.J., Lip, G.Y.H.: Reperfusion injury: a review of the pathophysiology,clinical manifestations and therapeutic options. Int. J. Cardiol., 58, 95-117 (1997)
  3. Carden, D.L., Granger, D.N.: Pathophysiology of ischemia-reperfusion injury. J. Pathol., 190, 255-66 (2000).
  4. Collard, C.D., Gelman, S.: Pathophysiology, Clinical Manifestations, and Prevention of Ischemia-Reperfusion Injury. Anesthesiology, 94, 1133-1138 (2001).
  5. Nakamura, T., Vollmar, B., Winning, J., Ueda M., Menger, M.D., Schäfers, H.-J.: Hepa- rin and the nonanticoagulant N-acetyl heparin attenuate capillary no-reflow after nor- mothermic ischemia of the lung. Ann. Thorac. Surg., 72, 1183-1189 (2001).
  6. Crestani, B., Cornillet, P., Dehoux, M., Rolland, C., Guenounou, M., Aubier, M.: Al- veolar type II epithelial cells produce interleukin-6 in vitro and in vivo: regulation by alveolar macrophage secretory products. J. Clin. Invest., 94, 731-740 (1994).
  7. Levinson, R.M., Shure, D., Moser, K.M.: Reperfusion pulmonary edema after pulmo- nary artery thromboendarterectomy. Am. Rev. Respir. Dis., 134, 1241-1245 (1986).
  8. Vural, K.M., Öz, M.C.: Endothelial adhesivity, pulmonary hemodynamics and ni- tric oxide synthesis in ischemia-reperfusion. Eur. J. Cardiothorac. Surg., 18, 348-352 (2000).
  9. Krishnadasan B, Naidu BV, Byrne K,et al.: The role of proinflammatory cytokines in lung ischemia-reperfusion injury. J. Thorac. Cardiovasc Surg., 125, 261-272 (2003).
  10. Connaughton, P.J., Bahuth, J.J., Lewis, F.J.: Lung ischemia up to six hours; influence of topical cooling in situ on subsequent pulmonary function. Dis. Chest., 41, 404-408 (1962). McCord JM.: Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med., 312, 159-163 (1985). McCord JM.: Oxygen-derived free radicals in postischemic tissue injury. N Engl J Med., 312, 159-163 (1985).
  11. Al-Mehdi AB, Shuman H, and Fisher AB.: Intracellular generation of reactive oxygen species during nonhypoxic lung ischemia. Am J Physiol 272, L294-300 (1997). Kelly RF.: Current strategies in lung preservation. J Lab Clin Med., 136, 427-440 (2000).
  12. Zhao, G., Al-Mehdi, A.B., Fisher, A.B.: Anoxia-reoxygenation versus ischemia in iso- lated rat lungs. Am. J. Physiol., 273, L1112-1117 (1997).
  13. Date H, Matsumura A, Manchester JK, Obo H, Lima O, Cooper JM, Sundaresan S, Lowry OH, and Cooper JD.: Evaluation of lung metabolism during succe