Prevention of "irreversible" hemorrhagic shock by the preservation of cellular integrity.
The clinically encountered state of hypovolemic shock results from a series of metabolic and cardiovascular responses to tissue hypoperfusion. Recent advances have increased our understanding of the consequences of tissue hypoxia, and identified at the cellular level those changes which cause the damage to be "irreversible", or refractory to treatment. To be successful, therapeutic interventions should be designed to 1) limit, if not reverse, the subcellular alterations in membrane stability and mitochondrial function which herald the transition from compensated to decompensated shock, and 2) re-hydrate the individual to restore normal circulatory dynamics and to prevent further cellular damage. It is proposed that calcium channel blocking agents and/or high energy phosphate compounds may delay the positive feedbacks which cause irreversible tissue damage, and thus may be useful initial interventions in the treatment of hypovolemic shock.
D000255:Adenosine Triphosphate / Q000378:metabolism / Q000627:therapeutic use; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D005246:Feedback; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D007473:Ion Channels / Q000378:metabolism; D008954:Models, Biological; D012771:Shock, Hemorrhagic / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control*
D002121:Calcium Channel Blockers; D007473:Ion Channels; D000255:Adenosine Triphosphate; D002118:Calcium