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Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation

Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation

Published on: May 16, 2016

Myocardial expression of the endothelin system in endotoxin-treated rats.

J P Spiers¹, A Dorman, J D Allen

¹Department of Physiology, The Queen's University of Belfast, Northern Ireland. spiersj@tcd.ie

Journal of Cardiovascular Pharmacology

|August 3, 2001

Summary

Endotoxemia increases myocardial endothelin-1 (ET-1) mRNA in rats, but not its converting enzyme or receptors. This suggests ET-1

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Area of Science:

Cardiovascular Physiology
Molecular Biology
Endocrinology

Background:

Circulating endothelin (ET)-1 levels rise in endotoxemia.
Myocardial ET system expression in endotoxic shock remains poorly understood.

Purpose of the Study:

To investigate the temporal mRNA expression of the ET system in the rat myocardium during early endotoxic shock.
To elucidate the role of ET-1 in the cardiac response to endotoxemia.

Main Methods:

A rat model of early endotoxic shock induced by lipopolysaccharide (LPS).
Reverse transcription polymerase chain reaction (RT-PCR) to quantify mRNA expression of pre-pro ET (ppET)-1, ppET-2, ET-converting enzyme-1, ET(A) receptor, and ET(B) receptor.
Measurement of inducible nitric oxide synthase (iNOS) mRNA as a marker.

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Main Results:

LPS administration caused a transient increase in iNOS mRNA expression.
ppET-1 mRNA expression significantly increased approximately 12-fold at 2 hours post-LPS.
mRNA expression of ppET-2, ET-converting enzyme-1, ET(A) receptor, and ET(B) receptor remained unaltered.

Conclusions:

Myocardial ppET-1 mRNA is selectively upregulated in early endotoxic shock, potentially as an acute-phase response to hemodynamic instability.
The ET system's components, particularly ET-converting enzyme-1 and receptors, do not appear to be upregulated at the mRNA level in this early phase.
These findings highlight a specific cardiac response involving increased ET-1 production during endotoxemia.