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Our previous data showed membrane hyperpolarization of arteriolar smooth muscle cells (ASMCs) caused by adenosine triphosphate (ATP)-sensitive potassium channels (K(ATP)) 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.

Mitochondrial Injury Underlies Hyporeactivity of Arterial Smooth Muscle in Severe Shock