Document Detail


Anesthetic preconditioning improves adenosine triphosphate synthesis and reduces reactive oxygen species formation in mitochondria after ischemia by a redox dependent mechanism.
MedLine Citation:
PMID:  12717137     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Mitochondrial changes that characterize the heart after anesthetic preconditioning (APC) or the mechanisms by which mitochondrial triggering factors lead to protection are unknown. This study hypothesized that generation of reactive oxygen species (ROS) during APC is required to initiate the mitochondrial protective effects, and that APC leads to improved mitochondrial electron transport chain function and cardiac function during reperfusion. METHODS: Isolated guinea pig hearts were subject to 30 min ischemia and 120 min reperfusion. Prior to ischemia hearts were either untreated (I/R), or treated with sevoflurane (APC), in the presence or absence of the ROS scavenger tiron (TIR), or the superoxide dismutase mimetic MnTBAP (TBAP). Intracellular ROS were measured by spectrofluorometry using the fluorescent probe dihydroethidium (DHE). In another series of experiments, using the same protocol, hearts were reperfused for only 5 min and removed for measurement of adenosine triphosphate (ATP) synthesis by luciferin-luciferase luminometry and ROS generation by dichlorohydro-fluorescein (DCF) fluorescence in isolated mitochondria. RESULTS: The APC improved cardiac function and reduced infarction. Tiron or MnTBAP abrogated the protection afforded by APC. Mitochondrial ATP synthesis was decreased by 70 +/- 3% after IR alone, by only 7 +/- 3% after APC, by 69 +/- 2% after APC+TIR, and by 71 +/- 3% after APC + TBAP. Mitochondrial ROS formation (DCF) increased by 48 +/- 3% after IR alone, by 0 +/- 2% after APC, by 43 +/- 4% after APC + TIR, and by 46 +/- 3% after APC + TBAP. ROS generation (DHE) was increased in I/R group at 5 and 120 min reperfusion. This was attenuated by APC but this protective effect was abrogated in APC + TIR and APC + TBAP groups. CONCLUSIONS: The results indicate that ROS are central both in triggering and mediating APC, and that the mitochondrion is the target for these changes.
Authors:
Enis Novalija; Leo G Kevin; Janis T Eells; Michele M Henry; David F Stowe
Related Documents :
11213237 - Adenosine and chronic ischemia of the lower limbs.
21184347 - Evaluation of the exercise workload of broadcast calisthenics for children and adolesce...
199047 - Adenosine in rat cerebral cortex: its determination, normal values, and correlation to ...
1901527 - Relations between heart rate, ischemia, and drug therapy during daily life in patients ...
8051307 - Effects of routine hyperventilation on pco2 and po2 in normal subjects: implications fo...
6941637 - Angina pectoris in the cold. effects of cold environment and cold air inhalation at exe...
Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Anesthesiology     Volume:  98     ISSN:  0003-3022     ISO Abbreviation:  Anesthesiology     Publication Date:  2003 May 
Date Detail:
Created Date:  2003-04-28     Completed Date:  2003-07-22     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  1300217     Medline TA:  Anesthesiology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1155-63     Citation Subset:  AIM; IM    
Affiliation:
Medical College of Wisconsin, Department of Anesthesiology, M4280, 8701 Watertown Plank Road, Milwaukee, Wisconsin 53226, USA. novalija@mcw.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism*
Animals
Cell Fractionation
Coronary Circulation / physiology
Guinea Pigs
Heart / drug effects,  physiology*,  physiopathology
Ischemic Preconditioning, Myocardial / methods*
Mitochondria, Heart / metabolism*,  ultrastructure
Models, Animal
Myocardial Reperfusion
Oxidation-Reduction
Reactive Oxygen Species / metabolism*
Time Factors
Ventricular Function, Left / physiology
Grant Support
ID/Acronym/Agency:
HL58691/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 56-65-5/Adenosine Triphosphate

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Midazolam stimulates vascular endothelial growth factor release in aortic smooth muscle cells: role ...
Next Document:  Role of endothelium-derived hyperpolarizing factor in phenylephrine-induced oscillatory vasomotion i...