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Related Experiment Videos

Insulin effectiveness in hypovolemic dogs

R A Swerlick, N A Drucker, S McCoy

    The Journal of Trauma
    |December 1, 1981
    PubMed
    Summary
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    Exogenous insulin accelerated blood glucose decline in hypovolemic dogs, but did not increase glucose uptake. Insulin administration may inhibit hepatic glucose release during hypovolemic shock.

    Area of Science:

    • Physiology
    • Endocrinology
    • Metabolic Research

    Background:

    • Prolonged hypovolemia can impair homeostasis and alter glucose metabolism.
    • The role of exogenous insulin in glucose assimilation during hypovolemic shock is not fully understood.
    • Understanding insulin's effects is crucial for managing metabolic disturbances in critical care settings.

    Purpose of the Study:

    • To investigate whether exogenous insulin enhances blood glucose assimilation after prolonged hypovolemia.
    • To determine the impact of insulin on glucose uptake and hepatic glucose release during waning homeostasis.

    Main Methods:

    • Mongrel dogs were subjected to prolonged hypovolemia (mean arterial blood pressure of 50 mm Hg).
    • Insulin (2 units) or saline was administered at the onset of physiological deterioration.

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  • Measurements included plasma glucose, insulin, femoral blood flow, and hematocrit.

    • Main Results:

    • Insulin administration led to a significantly faster decline in blood glucose compared to controls.
    • No significant difference in hindlimb glucose uptake was observed between groups.
    • Insulin accentuated hemoconcentration and may have inhibited hepatic glucose release.

    Conclusions:

    • Exogenous insulin accelerates blood glucose decline in late-stage hypovolemic shock.
    • Insulin does not enhance peripheral glucose uptake under these conditions.
    • The findings suggest insulin may suppress hepatic glucose production, challenging existing theories of insulin resistance in shock.