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Heparin-protamine complexes cause pulmonary hypertension in goats
T Horiguchi1, K Enzan, H Mitsuhata
1Department of Anesthesia, Akita Kumiai Hospital, Japan.
Anesthesiology
|October 1, 1995
Summary
Heparin-protamine complexes cause pulmonary hypertension by releasing thromboxane. Inhibiting thromboxane synthesis or cyclooxygenase blocks this response, identifying thromboxane A2 as a key mediator.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Protamine reversal of heparin anticoagulation can trigger thromboxane release and pulmonary vasoconstriction.
- Heparin-protamine (H-P) complexes are suspected mediators of these adverse effects.
Purpose of the Study:
- To determine if H-P complexes cause thromboxane release and pulmonary hypertension.
- To investigate the role of thromboxane A2 in the pulmonary hypertensive response to H-P complexes.
Main Methods:
- H-P and non-H-P complexes were isolated from human plasma using chromatography.
- Hemodynamic and airway pressure changes, along with thromboxane B2 levels, were measured after complex injection in goats.
- The effect of cyclooxygenase and thromboxane synthetase inhibitors on these responses was assessed.
Main Results:
- H-P complexes significantly increased pulmonary arterial pressure, airway pressure, and thromboxane B2 levels.
- Non-H-P complexes did not induce significant hemodynamic changes.
- Indomethacin completely blocked, and OKY-046 partially blocked, the pulmonary hypertension and thromboxane B2 increase.
Conclusions:
- H-P complexes are a primary cause of pulmonary hypertension following protamine reversal of heparin.
- Thromboxane A2 is a key mediator of the pulmonary hypertensive response induced by H-P complexes in goats.