Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016:2016:7463407.
doi: 10.1155/2016/7463407. Epub 2015 Dec 7.

The Responses of Tissues from the Brain, Heart, Kidney, and Liver to Resuscitation following Prolonged Cardiac Arrest by Examining Mitochondrial Respiration in Rats

Junhwan Kim  1 , José Paul Perales Villarroel  1 , Wei Zhang  1 , Tai Yin  1 , Koichiro Shinozaki  1 , Angela Hong  2 , Joshua W Lampe  1 , Lance B Becker  1
Affiliations

The Responses of Tissues from the Brain, Heart, Kidney, and Liver to Resuscitation following Prolonged Cardiac Arrest by Examining Mitochondrial Respiration in Rats

Junhwan Kim et al. Oxid Med Cell Longev. 2016.

Abstract

Cardiac arrest induces whole-body ischemia, which causes damage to multiple organs. Understanding how each organ responds to ischemia/reperfusion is important to develop better resuscitation strategies. Because direct measurement of organ function is not practicable in most animal models, we attempt to use mitochondrial respiration to test efficacy of resuscitation on the brain, heart, kidney, and liver following prolonged cardiac arrest. Male Sprague-Dawley rats are subjected to asphyxia-induced cardiac arrest for 30 min or 45 min, or 30 min cardiac arrest followed by 60 min cardiopulmonary bypass resuscitation. Mitochondria are isolated from brain, heart, kidney, and liver tissues and examined for respiration activity. Following cardiac arrest, a time-dependent decrease in state-3 respiration is observed in mitochondria from all four tissues. Following 60 min resuscitation, the respiration activity of brain mitochondria varies greatly in different animals. The activity after resuscitation remains the same in heart mitochondria and significantly increases in kidney and liver mitochondria. The result shows that inhibition of state-3 respiration is a good marker to evaluate the efficacy of resuscitation for each organ. The resulting state-3 respiration of brain and heart mitochondria following resuscitation reenforces the need for developing better strategies to resuscitate these critical organs following prolonged cardiac arrest.

PubMed Disclaimer

Figures

Scheme 1
Scheme 1
Diagram showing surgical procedure of asphyxial CA and CPB resuscitation. 1. Capnograph. 2. Oxygen saturation and hematocrit (Critline). 3. Pump. 4. Temperature, PO2, and system pressure of arterial return. 5. Rectal temperature. 6. Arterial and central venous blood pressure, ABG. 7. ECG. 8. Esophageal temperature. 9. Pulse oximetry.
Figure 1
Figure 1
Heart rate (HR), mean arterial pressure (MAP), and pulse pressure (PP) following 30 mim CA and 60 min CPB resuscitation.
Figure 2
Figure 2
The decrease rates in state-3 respiration of heart, liver, brain, and kidney mitochondria following CA.
Figure 3
Figure 3
Changes in state-3 respiration activity of mitochondria following 30 min CA or 30 min CA and 60 min CPB resuscitation from brain, heart, kidney, and liver (∗against  control; ‡against  CA30).
Figure 4
Figure 4
Dot plot of state-3 respiration against isolation yield of brain mitochondria following 30 min CA and 60 min CPB resuscitation.
See this image and copyright information in PMC

References

    1. Roberts B. W., Kilgannon J. H., Chansky M. E., et al. Multiple organ dysfunction after return of spontaneous circulation in postcardiac arrest syndrome. Critical Care Medicine. 2013;41(6):1492–1501. doi: 10.1097/ccm.0b013e31828a39e9. - DOI - PubMed
    1. Li H., Zhang L., Yang Z., et al. Even four minutes of poor quality of CPR compromises outcome in a porcine model of prolonged cardiac arrest. BioMed Research International. 2013;2013:6. doi: 10.1155/2013/171862.171862 - DOI - PMC - PubMed
    1. Jiang H., Meng F., Li W., Tong L., Qiao H., Sun X. Splenectomy ameliorates acute multiple organ damage induced by liver warm ischemia reperfusion in rats. Surgery. 2007;141(1):32–40. doi: 10.1016/j.surg.2006.03.024. - DOI - PubMed
    1. Czerski L. W., Szweda P. A., Szweda L. I. Dissociation of cytochrome c from the inner mitochondrial membrane during cardiac ischemia. Journal of Biological Chemistry. 2003;278(36):34499–34504. doi: 10.1074/jbc.m302021200. - DOI - PubMed
    1. Chen Q., Moghaddas S., Hoppel C. L., Lesnefsky E. J. Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria. American Journal of Physiology—Cell Physiology. 2008;294(2):C460–C466. doi: 10.1152/ajpcell.00211.2007. - DOI - PubMed

Publication types

LinkOut - more resources