Study on SOD, MDA and IL-6 in a rat model of acute pulmonary edema
Author:
  • Article
  • | |
  • Metrics
  • |
  • Reference [14]
  • | | | |
  • Comments
    Abstract:

    Objective To investigate Interleukin 6(IL-6),superoxide dismutase (SOD),malondialdehyde (MDA) in lung tissues of a rat acute pulmonary edema model induced by acute hypoxia. Methods 50 adult Wistar rats were randomly divided into group A (normal),B (acute pulmonary edema,hypoxia for 24 h),C (acute pulmonary edema,hypoxia for 48h),D(acute pulmonary edema,hypoxia for 72 h) and E (dexamethasone treatment,hypoxia for 72h). The model of acute pulmonary edema was established by intraperitoneal injection with 6% ammonium chloride. In group E, dexamethasone (6mg/kg) was injected in tail vein following intraperitoneal injection of 6% ammonium chloride. The rats were killed 24(group B), 48 (C) and 72 hours(D&E) later. Plasma was isolated and lungs were removed. MDA,SOD in lung tissues and IL-6 in plasma were analyzed by ELISA. Results The wet weight of lung tissues were significantly increased in group B, C and D compared to group A(P<0.05). The lung tissues of group A had no obvious congestion and edema,and the morphology of lung tissues was normal(P>0.05). Pulmonary edema,interstitial spaces and alveolar filled fluid can be seen in group B,C,D and transparent membrane formed within alveoli. The lung tissue congestion and edema in group D were the most obvious(P<0.05). The above changes obviously improved in group E. Compared with group A,MDA,IL-6 increased and SOD decreased in lung tissues of group C and D. Compared with group D, MDA was decreased and SOD was increased in lung tissues of group E and IL-6 was also decreased significantly in plasma(P<0.05). Conclusion The occurrence of acute pulmonary edema related to oxidative stress and decreased antioxidant capacity. Increased free radical is an important mechanism of pulmonary edema. SOD,MDA and IL-6 in the lung tissue may be indexes for the prognosis.

    Reference
    [1] Smith WS,Matthay MA. Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema[J]. Chest,1997,111:1326-33.
    [2] Theodore J,Robin ED. Pathogenesis of neurogenic pulmonary oedema[J]. Lancet,1975,18(2):749-751.
    [3] Minnear FL,Kite C,Hill LA,et al. Endothelial injury and pulmonary congestion characterize neurogenic pulmonary edema in rabbits[J]. J Appl Physiol,1987,63(1):335-341.
    [4] Hamdy O,Maekawa H,Shimada Y. Role of central nervous system nitric oxide in the development of neurogenic pulmonary edema in rats[J]. Crit Care Med,2001,29(6):1222-1228.
    [5] Lionte C,Sorodoc L,Laba Y. Respiratory syndromes in acute poisoning[J]. Rev Med Chir Soc Med Natiasi,2004,108(3):544-548.
    [6] Bur A,Wagner A,Roggla M,et al. Fatal pulmonary edema after nitric acid inhalation[J].Resuscitation,1997,35(1):33-36
    [8] Prys-Roberts C. Principles of treatment of poisoning by higher oxides of nitrogen[J]. Br J Anaesth,1967,39(5):432-439.
    [9] Parsons PE. Respiratory failure as a result of drugs,overdoses,and poisonings[J]. Clin Chest Med,1994.15(1):93-102.
    [10] Theodore J,Robin ED. Pathogenesis of neurogenic pulmonary oedema[J]. Lancet,1975,18; 2(7938):749-751.
    [11] 缪捷飞. 益气活血方对大鼠胸部照射肺组织SOD活性、MDA及HP含量的影响[J]. 南通大学学报:医学版,2010,30(4):255-257.
    [12] Drobinski G,Eugine M. Exploration Hemodynamique Cardiovasculaire[M]. 1982; Masson,Paris.
    [13] Elsayed NM, Gorbunov NV, Mayorga MA,et al.Significant pulmonary response to a brief high-level, nose-only nitrogen dioxide exposure:an interspecies dosimetry perspective[J].Toxicol Appl Pharmacol.2002,184(6):1-10.
    [14] 马钧. 急性呼吸窘迫综合征患者糖皮质激素合理使用方案及受体机制[J]. 中国危蕈病急救医学.2003,15(3):680-682.
    [15] 徐仁宝.大剂基激素作用的受体机制以及危重病人激素治疗的新策略[J].外科理论与实践,2000,5(2):76-78.
    Related
    Cited by
    Comments
    Comments
    分享到微博
    Submit
Get Citation
Share
Article Metrics
  • Abstract:1977
  • PDF: 1475
  • HTML: 0
  • Cited by: 0
History
  • Revised:June 01,2016
  • Online: November 18,2016
Article QR Code