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Changes in CRH and ACTH synthesis during experimental and human septic shock
Andrea Polito1, Romain Sonneville, Céline Guidoux
1Department of Intensive Care, Raymond Poincaré Hospital, Garches, France.
Plos One
|November 11, 2011
Summary
Septic shock decreases ACTH synthesis, not compensated by vasopressin (AVP) or corticotropin-releasing hormone (CRH). Increased iNOS in neurons may underlie this adrenal insufficiency in sepsis.
Area of Science:
- Neuroendocrinology
- Pathophysiology of Sepsis
Background:
- Septic shock mechanisms causing adrenal insufficiency are not fully understood.
- Investigating corticotropin-releasing hormone (CRH) and vasopressin (AVP) synthesis and adrenocorticotropic hormone (ACTH) expression in sepsis is crucial.
Purpose of the Study:
- To determine if decreased ACTH secretion in septic shock results from altered CRH or AVP synthesis.
- To conduct a neuropathological study of the human and rat antehypophyseal system during experimental sepsis.
Main Methods:
- Compared brains from 9 septic shock patients with 10 controls.
- Utilized in situ hybridization for CRH and AVP mRNA, and immunohistochemistry for ACTH, V1b receptor, CRHR1, and iNOS in parvocellular neurons.
- Replicated experiments in a fecal peritonitis-induced sepsis model in rats, comparing septic and sham-operated groups.
Main Results:
- Septic shock showed decreased ACTH expression in both humans and rats.
- AVP mRNA, V1B, and CRHR1 receptor expression remained unchanged.
- Increased inducible nitric oxide synthase (iNOS) expression was observed in parvocellular neurons during sepsis.
Conclusions:
- Septic shock is linked to reduced ACTH synthesis, uncompensated by AVP and CRH.
- Elevated iNOS expression in hypothalamic parvocellular neurons may be a key mechanism in sepsis-induced adrenal insufficiency.
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