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Indomethacin enhances histamine-induced pulmonary hemodynamic changes
Prostaglandins
|February 1, 1990
Summary
Histamine causes pulmonary hemodynamic changes. Inhibiting prostaglandins with indomethacin amplified these changes, indicating prostaglandins normally oppose histamine-induced pulmonary vasoconstriction.
Area of Science:
- Physiology
- Pharmacology
Background:
- Histamine is known to induce changes in pulmonary hemodynamics.
- Prostaglandins play a role in regulating vascular tone.
- The specific role of prostaglandins in histamine-induced pulmonary responses requires further elucidation.
Purpose of the Study:
- To investigate the role of prostaglandins in mediating histamine-induced pulmonary hemodynamic alterations in pigs.
- To determine if inhibiting prostaglandin synthesis affects the pulmonary vascular response to histamine.
Main Methods:
- Anesthetized pigs were administered intravenous histamine.
- Pulmonary artery pressure, pulmonary arterial wedge pressure, left ventricular end diastolic pressure, and cardiac output were measured.
- Pulmonary arterial resistance and pulmonary venous resistance were calculated.
- Responses were compared with and without pre-treatment with indomethacin, a cyclo-oxygenase inhibitor.
Main Results:
- Histamine administration led to changes in pulmonary hemodynamics.
- Pre-treatment with indomethacin resulted in a 2-fold greater increase in pulmonary arterial and venous resistance in response to histamine.
- The increases in resistance were more prolonged after indomethacin pre-treatment.
Conclusions:
- Prostaglandins released from pulmonary endothelial cells normally act as vasodilators, opposing histamine-induced pulmonary vasoconstriction.
- Inhibition of prostaglandin synthesis potentiates histamine-induced pulmonary vasoconstriction and increases pulmonary resistance.