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Circulating endothelin in cardiac operations: influence of blood pressure and endotoxin
H te Velthuis1, P G Jansen, H M Oudemans-van Straaten
1Centre for Cardiopulmanary Surgery and Amsterdam, Vrije Universiteit Hospital, Amsterdam, Netherlands.
Insights
Cardiopulmonary bypass (CPB) onset causes a rapid rise in endothelin, linked to blood pressure changes. Endotoxin levels correlate with a slower endothelin increase during CPB.
Area of Science:
- Cardiovascular Physiology
- Neuropeptide Signaling
Background:
- Endothelin plays a key role in regulating cardiovascular and renal functions.
- Endothelin also acts as a neuromodulator in the body.
Purpose of the Study:
- To investigate the release patterns of circulating endothelin.
- To identify potential stimuli for endothelin release during coronary artery bypass grafting (CABG).
Main Methods:
- Prospective study involving 15 male patients undergoing CABG.
- Monitoring of circulating endothelin concentrations and related physiological parameters.
Main Results:
- A significant increase in endothelin concentrations was observed immediately after initiating cardiopulmonary bypass (CPB).
- A secondary, smaller increase in endothelin occurred during CPB.
- The initial rise in endothelin correlated with changes in arterial pressure (r = -0.57; p < 0.03).
- The sustained increase in endothelin during CPB correlated with endotoxin levels (r = 0.60; p < 0.02).
Conclusions:
- Arterial pressure changes at CPB onset likely trigger a rapid, baroreceptor-mediated increase in endothelin.
- Elevated endotoxin levels during CPB are associated with a slower rise in endothelin.
- Potential mechanisms include endothelin-induced vasoconstriction facilitating endotoxin transmigration or endotoxin stimulating endothelial endothelin secretion.
Background:
Endothelin is involved in the control of cardiovascular and renal functions and acts as a neuromodulator.
Methods:
In a prospective study among 15 male patients who underwent coronary artery bypass grafting, we investigated the release pattern and possible stimuli of circulating endothelin.
Results:
We detected a steep increase in endothelin concentrations after the onset of cardiopulmonary bypass (CPB), and a second minor increase during CPB. The steep increase in endothelin concentrations correlated with the change in arterial pressures at the onset of CPB (r = -0.57; p < 0.03). The slow increase in endothelin concentrations during CPB, however, correlated with mean endotoxin levels during and after CPB (r = 0.60; p < 0.02).
Conclusions:
The change in arterial pressure at the onset of CPB seems to induce a steep and fast increase in circulating endothelin level, which is probably mediated through the baroreceptors. The slow increase in endothelin level during CPB is associated with increased circulating endotoxin concentration. It may be that either endothelin-mediated vasoconstriction induces endotoxin transmigration from the intestine or endotoxin stimulates secretion from endothelial cells.