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Related Experiment Videos

Calcium entry blockers: potential applications in shock.

M L Hess, L J Greenfield

    Advances in Shock Research
    |January 1, 1983
    PubMed
    Summary
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    Intracellular calcium overload contributes to cell death in shock. Calcium channel blockers may offer a therapeutic strategy for managing shock by preventing this calcium imbalance.

    Area of Science:

    • Cardiovascular Physiology
    • Cellular Biology
    • Pathophysiology

    Background:

    • Myocardial and vascular smooth muscle cells rely on calcium homeostasis to prevent cell death and necrosis.
    • Conditions like hypoxia, low-flow states, and reperfusion injury can lead to intracellular calcium overload.
    • The shock syndrome, encompassing cardiogenic, septic, and hemorrhagic shock, presents scenarios conducive to calcium overload.

    Purpose of the Study:

    • To discuss the pathophysiologic sequence of the shock syndrome.
    • To illustrate the potential role of intracellular calcium overload in shock progression.
    • To review existing data on slow calcium channel blockers in shock and propose future research.

    Main Methods:

    • Review of pathophysiologic mechanisms in various shock states.

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  • Analysis of the role of intracellular calcium in cellular damage.
  • Examination of data concerning slow calcium channel blockers in shock models.

    • Main Results:

    • Intracellular calcium overload is a common pathway in diverse shock etiologies, leading to cell death.
    • Shock syndromes share a potential for intracellular calcium overload.
    • Slow calcium channel blockers have been studied in shock, suggesting a basis for further investigation.

    Conclusions:

    • Intracellular calcium overload is a critical factor in the pathophysiology of shock.
    • Calcium channel blockers represent a promising therapeutic avenue for shock management.
    • Further studies are warranted to explore the efficacy of calcium entry blockers in treating shock.