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Protamine-induced pulmonary venoconstriction in heparinized pigs
T S Hakim1, A Picone, C E Oleary
1Department of Surgery, State University of New York Health Science Center, Syracuse 13210, USA.
Anesthesia and Analgesia
|July 1, 1995
Summary
Protamine administration causes acute pulmonary vasoconstriction, primarily in the venous system. Nitric oxide (NO) does not appear to play a significant role in this protamine-induced pulmonary vascular resistance increase.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Heparin reversal with protamine can lead to acute pulmonary vasoconstriction.
- The precise location of this vasoconstriction remains undetermined.
Purpose of the Study:
- To pinpoint the site of protamine-induced pulmonary vasoconstriction.
- To investigate the role of nitric oxide (NO) in this response.
Main Methods:
- Anesthetized pigs were instrumented to monitor pulmonary arterial, systemic arterial, and central venous pressures.
- Pulmonary capillary pressure and left atrial pressure were estimated.
- Hemodynamic measurements were taken at baseline, after heparin, and at peak protamine response.
Main Results:
- Protamine significantly increased pulmonary vascular resistance (PVR) from 2.7 to 8.0 mm Hg.L-1.min-1.
- This increase was mainly due to elevated venous resistance, with a smaller rise in arterial resistance.
- Inhibition of nitric oxide (NO) synthesis did not alter the protamine-induced PVR increase.
Conclusions:
- Protamine-induced pulmonary vasoconstriction occurs predominantly in the venous vasculature.
- Nitric oxide does not seem to mediate the acute increase in pulmonary vascular resistance following protamine administration.