Prevention of Trauma/Hemorrhagic Shock-Induced Mortality,Apoptosis, Inflammation and Mitochondrial Dysfunction

2013 ◽  
Author(s):  
David J. Tweardy
Keyword(s):  
Hemorrhagic Shock ◽  
Mitochondrial Dysfunction

scholarly journals Inhaled carbon monoxide or nebulized sodium nitrite protect against hemorrhagic shock-induced mitochondrial dysfunction

Critical Care ◽  
2013 ◽  
Vol 17 (S2) ◽  
Author(s):  
H Gomez ◽  
D Escobar ◽  
B Ataya ◽  
L Gordon ◽  
O Ogundele ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Hemorrhagic Shock ◽  
Mitochondrial Dysfunction ◽  
Sodium Nitrite

Polydatin, a natural polyphenol, protects arterial smooth muscle cells against mitochondrial dysfunction and lysosomal destabilization following hemorrhagic shock

2012 ◽  
Vol 302 (7) ◽  
pp. R805-R814 ◽  
Author(s):  
Xingmin Wang ◽  
Rui Song ◽  
Hui Ning Bian ◽  
Ulf T. Brunk ◽  
Ming Zhao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Hemorrhagic Shock ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Permeability Transition ◽  
Hydrolytic Enzymes ◽  
Permeability Transition ◽  
Muscle Cells ◽  
Lysosomal Stability ◽  
Severe Shock

The main objective of this study was to investigate the activity of polydatin on mitochondrial dysfunction and lysosomal stability of arteriolar smooth muscle cells (ASMCs) in severe shock. The experimental animals (rats) were divided into five groups: control, hemorrhagic shock, shock + CsA, shock + Res, and shock + PD (exposed to cyclosporin A, resveratrol, or polydatin following induction of hemorrhagic shock, respectively). The calcein-Co2+ technique revealed opening of ASMC mitochondrial permeability transition pores (mPTP) after shock with resulting mitochondrial swelling, decreased mitochondrial membrane potential (ΔΨm), and reduced intracellular ATP levels. These alterations were all inhibited by exposure to PD, which was significantly more effective than CsA and Res. PD also preserved lysosomal stability, suppressed activation of KATP channels, ASMC hyperpolarization, and reduced vasoresponsiveness to norepinephrine that normally follows severe shock. The results demonstrate that exposure to PD after initiation of severe shock effectively preserves ASMC mitochondrial integrity and has a significant therapeutic effect in severe shock. The effects may partially result from lysosomal stabilization against shock-induced oxidative stress and depressed relocation of hydrolytic enzymes and redox-active lysosomal iron that, in turn, may induce mPTP opening.

scholarly journals Mitochondrial dysfunction in rat splenocytes following hemorrhagic shock

2017 ◽  
Vol 1863 (10) ◽  
pp. 2526-2533 ◽  
Author(s):  
Marie Warren ◽  
Kumar Subramani ◽  
Richard Schwartz ◽  
Raghavan Raju
Keyword(s):  
Hemorrhagic Shock ◽  
Mitochondrial Dysfunction
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