Research Article
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Year 2015, , 429 - 438, 01.09.2015
https://doi.org/10.37212/jcnos.607125

Abstract

References

  • Alkan A, Eroglu F, Eroglu E, Ergin C, Cerci C. Alsancak G. 2006. Protective effects of N-acetylcysteine and erdosteine on hemorrhagic shock-induced acute lung injury. Eur J Emerg Med 13, 281-285. Bachofen M, Weibel ER. 1982. Structural alterations of lung parenchyma in the adult respiratory distress syndrome. Clin Chest Med 3, 35-56. Bernard GR. 1991. N-acetylcysteine in experimental and clinical acute lung injury. Am J Med 91, 54S-59S

The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study

Year 2015, , 429 - 438, 01.09.2015
https://doi.org/10.37212/jcnos.607125

Abstract

We aimed to determine the effects of delayed
fluid resuscitation on the lung oxidative stress and antioxidant vitamin levels
in a rat model of controlled hemorrhagic shock (HS).
Male Wistar rats were exposed to controlled HS via
arterial catheterization to reduce mean arterial pressure (MAP) to 40 mmHg over
10 minutes.
Two groups were constituted
according to resuscitation time: early (n=6) and delayed (n=5), respectively
resuscitated 30 or 90 minutes after HS. A control group (n=5) was subjected to
catheterization only. I
ntravenous fluid resuscitation was done with Ringer lactate
solution. After 24 hours, bronchoalveolar
lavage (BAL) was performed and
the lungs were harvested for biochemical, cytological and histopathological analyses. Lipid
peroxidation (as MDA), reduced glutathione (GSH), glutathione peroxidase
(GSH-Px) and vitamin A, vitamin C and vitamin E
levels were measured in both BAL fluid (BALF) and
lung homogenate.
Lung tissue GSH-Px and vitamin E levels are increased
in both HS groups compared to the control group. No significant differences
were found in
MDA, GSH, vitamin A and vitamin C BALF levels among
all groups, except for
GSH-Px (p=0.007). Intracellular
antioxidants, especially GSH-Px and vitamin E, increase in the lungs of rats
(in both HS groups), possibly due to increased oxidative stress and increased
physiological requirements after HS and resuscitation.

















































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































































References

  • Alkan A, Eroglu F, Eroglu E, Ergin C, Cerci C. Alsancak G. 2006. Protective effects of N-acetylcysteine and erdosteine on hemorrhagic shock-induced acute lung injury. Eur J Emerg Med 13, 281-285. Bachofen M, Weibel ER. 1982. Structural alterations of lung parenchyma in the adult respiratory distress syndrome. Clin Chest Med 3, 35-56. Bernard GR. 1991. N-acetylcysteine in experimental and clinical acute lung injury. Am J Med 91, 54S-59S
There are 1 citations in total.

Details

Primary Language English
Journal Section Original Articles
Authors

Hacı Ahmet Bircan

Publication Date September 1, 2015
Published in Issue Year 2015

Cite

APA Bircan, H. A. (2015). The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study. Journal of Cellular Neuroscience and Oxidative Stress, 7(2), 429-438. https://doi.org/10.37212/jcnos.607125
AMA Bircan HA. The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study. J Cell Neurosci Oxid Stress. September 2015;7(2):429-438. doi:10.37212/jcnos.607125
Chicago Bircan, Hacı Ahmet. “The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study”. Journal of Cellular Neuroscience and Oxidative Stress 7, no. 2 (September 2015): 429-38. https://doi.org/10.37212/jcnos.607125.
EndNote Bircan HA (September 1, 2015) The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study. Journal of Cellular Neuroscience and Oxidative Stress 7 2 429–438.
IEEE H. A. Bircan, “The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study”, J Cell Neurosci Oxid Stress, vol. 7, no. 2, pp. 429–438, 2015, doi: 10.37212/jcnos.607125.
ISNAD Bircan, Hacı Ahmet. “The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study”. Journal of Cellular Neuroscience and Oxidative Stress 7/2 (September 2015), 429-438. https://doi.org/10.37212/jcnos.607125.
JAMA Bircan HA. The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study. J Cell Neurosci Oxid Stress. 2015;7:429–438.
MLA Bircan, Hacı Ahmet. “The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study”. Journal of Cellular Neuroscience and Oxidative Stress, vol. 7, no. 2, 2015, pp. 429-38, doi:10.37212/jcnos.607125.
Vancouver Bircan HA. The Effects of Delayed Fluid Resuscitation on Lung Oxidative Stress and Antioxidant Vitamin Levels in Controlled Hemorrhagic Shock: An Experimental Study. J Cell Neurosci Oxid Stress. 2015;7(2):429-38.