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Angiotensin-converting enzyme (ACE) in sepsis
Circulatory Shock
|January 1, 1983
Summary
Sepsis significantly depletes serum angiotensin-converting enzyme (ACE) activity in baboons, correlating with decreased blood pressure. This suggests sepsis-induced endothelial dysfunction may impair bradykinin inactivation.
Area of Science:
- Physiology
- Biochemistry
Background:
- Angiotensin-converting enzyme (ACE) is crucial for blood pressure regulation and peptide inactivation.
- Sepsis can lead to endothelial cell dysfunction.
- Previous studies indicated reduced serum ACE in septic patients with Adult Respiratory Distress Syndrome (ARDS).
Purpose of the Study:
- To investigate the effect of induced sepsis on serum ACE activity in a baboon model.
- To explore the relationship between serum ACE levels and hemodynamic changes during sepsis.
Main Methods:
- Seven baboons were induced into sepsis using live E. coli infusion.
- Serum ACE activity was measured over time.
- Mean arterial pressure and PaO2 were monitored.
Main Results:
- Serum ACE activity significantly declined from a control value of 41.5 +/- 4.2 to 25.8 +/- 2.2 U/L at 8 hours post-sepsis induction (P < 0.05).
- The decrease in serum ACE correlated with a 65 +/- 11 torr decline in mean arterial pressure.
- No significant change in PaO2 was observed.
Conclusions:
- Sepsis causes a marked depletion of serum ACE activity.
- This depletion correlates with decreased mean arterial pressure in septic baboons.
- Reduced serum ACE may indicate impaired bradykinin inactivation due to endothelial dysfunction in sepsis.