Asset Details
Do you wish to reserve the book?
Mitochondrial Injury Underlies Hyporeactivity of Arterial Smooth Muscle in Severe Shock
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Mitochondrial Injury Underlies Hyporeactivity of Arterial Smooth Muscle in Severe Shock
Do you wish to request the book?
Mitochondrial Injury Underlies Hyporeactivity of Arterial Smooth Muscle in Severe Shock
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Mitochondrial Injury Underlies Hyporeactivity of Arterial Smooth Muscle in Severe Shock
2011
Overview
Background
Our previous data showed membrane hyperpolarization of arteriolar smooth muscle cells (ASMCs) caused by adenosine triphosphate (ATP)-sensitive potassium channels (KATP) activation contributed to vascular hyporeactivity in shock. Despite supply of oxygen and nutrients, vascular hyporeactivity to vasoconstrictor agents still remains, which may result from low ATP level. The study was designed to investigate shock-induced mitochondrial changes of rat ASMCs in the genesis and treatment of hypotension in severe shock
Methods
The animals were divided into four groups: controls, hemorrhagic shock, CsA+shock (preadministration of cyclosporin A before bleeding), and ATR+CsA+shock (preadministration of atractyloside, followed by CsA and bleeding). ASMCs were isolated and the ultrastructure and function of ASMC mitochondria and the vasoresponsiveness to norepinephrine (NE) was measured on microcirculatory preparations.
Results
Ultrastructurally, the hemorrhagic shock group showed swollen
mitochondria with poorly defined cristae. In this group, the number
of ASMCs with low mitochondrial membrane potential (Δψm) was
increased by 49.7%, and the intracellular ATP level was reduced by 82.1%, which led to activation of KATP plasma membrane channels with resultant ASMC hyperpolarization and low vasoreactivity. These changes were reduced in the CsA+shock group. When mitochondrial damage was aggravated by ATR in the ATR+CsA+shock group, the CsA did not protect. Compared to the shock group, vasoresponsiveness to NE was much improved in the CsA+shock group.
Conclusion
Mitochondrial ASMC dysfunction is involved in the genesis of reduced vasoreactivity in severe shock. Mitochondrial protection may therefore be a new approach in the treatment of shock-induced hypotension.
American Journal of Hypertension, advance online publication 9 September 2010; doi:10.1038/ajh.2010.184
Publisher
Oxford University Press,Nature Publishing Group
Subject
Adenosine Triphosphate - analysis
/ Animals
/ Arterial hypertension. Arterial hypotension
/ Arterioles - physiopathology
/ Biological and medical sciences
/ Fundamental and applied biological sciences. Psychology
/ Membrane Potential, Mitochondrial
/ Mitochondria - ultrastructure
/ Muscle, Smooth, Vascular - physiopathology
/ Potassium Channels - physiology
/ Rats
