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Effect of glucocorticoid receptor (GR) blockade on endotoxemia in rats

J Fan1, X Q Gong, J Wu

  • 1Department of Pathophysiology, Second Military Medical University, Shanghai, People's Republic of China.

Circulatory Shock
|February 1, 1994
PubMed

Insights

Glucocorticoid receptor (GR) blockade worsens endotoxemia in rats, leading to severe organ damage and circulatory issues. Reduced GR function may contribute to shock and multiple organ failure.

Area of Science:

  • Endocrinology
  • Pathophysiology
  • Pharmacology

Background:

  • Glucocorticoid receptors (GR) play a crucial role in the body's response to stress.
  • Understanding GR's function in shock is vital for clinical management.

Purpose of the Study:

  • To investigate the clinical significance of decreased glucocorticoid receptor (GR) function during stress and shock.
  • To determine the effects of GR blockade on endotoxemia-induced pathological changes in rats.

Main Methods:

  • Rats were treated with mifepristone to block GR function (50% and 80% blockade).
  • The study assessed hemodynamic, pathological, microcirculatory, and biochemical changes following endotoxemia induction.
  • Key markers included arterial blood pressure, organ pathology, leukocyte adherence, rheological changes, serum acid phosphatase (ACP), phospholipase A2 (PLA2), and lipoperoxide (LPO).

Main Results:

  • GR blockade exacerbated endotoxemia, causing a faster drop in blood pressure and more severe multi-organ damage, particularly in the lungs and intestines.
  • Increased leukocyte adherence and impaired mesenteric microcirculation were observed with GR blockade.
  • Significant elevations in serum ACP, PLA2 activity, and LPO were noted, with greater severity at 80% GR blockade compared to 50%.

Conclusions:

  • A decrease in GR function during stress and shock may contribute to the pathogenesis of shock and multiple organ failure (MOF).
  • These findings highlight the critical role of GR in mitigating endotoxemic injury.

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