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Platelet-activating factor: evidence against a role in hypoxic pulmonary vasoconstriction
D G McCormack1, P J Barnes, T W Evans
1Department of Thoracic Medicine, National Heart and Lung Institute, London, ON, Canada.
Critical Care Medicine
|December 1, 1990
Summary
Platelet-activating factor (PAF) increases pulmonary vascular resistance in pigs, but does not appear to mediate hypoxic pulmonary vasoconstriction (HPV). The PAF antagonist WEB 2086 blocked PAF
Area of Science:
- Physiology
- Pharmacology
Background:
- The mechanism of hypoxic pulmonary vasoconstriction (HPV) is not fully understood.
- Platelet-activating factor (PAF) has been implicated in HPV, but its role in intact animals requires further investigation.
Purpose of the Study:
- To evaluate the effect of the PAF antagonist WEB 2086 on HPV in an intact pig model.
- To determine if PAF mediates HPV in pigs.
Main Methods:
- Pigs were anesthetized and mechanically ventilated, with hemodynamic variables monitored.
- Pulmonary vascular resistance (PVR) was measured after intravenous PAF administration and during hypoxic ventilation.
- The effect of WEB 2086 on PAF-induced PVR increases and HPV was assessed.
Main Results:
- Intravenous PAF dose-dependently increased PVR in pigs, an effect completely blocked by WEB 2086.
- Indomethacin partially attenuated the PAF-induced increase in PVR.
- WEB 2086 did not significantly alter the PVR increase during hypoxic ventilation, indicating it did not block HPV.
Conclusions:
- Intravenous PAF increases PVR in pigs via a mechanism partially mediated by cyclooxygenase products.
- PAF does not appear to play a significant role in mediating HPV in pigs.
- WEB 2086 effectively blocks PAF-induced PVR increases but does not inhibit HPV in this species.