Abstract
Platelet activating factor (PAF) was first derived from rabbit basophiles that had been sensitized with a specific IgE-antibody. Subsequent studies have shown this compound to have a unique structure, [1-o-alkyl-2-acetyl-sn-glycero-3-phosphocholine]. PAF is a potent mediator of anaphylaxis and inflammation, as well as the ability to aggregate platelets.
The present investigation was conducted to explore the effect of PAF on various drug-induced contractile responses in rabbit pulmonary artery and descending aorta strips.
Seventeen Japanese albino rabbits, weighing about 3kg, were sacrificed. Rabbit pulmonary artery and descending aorta were removed, cut spirally, set up in bioassay glass jackets and superfused with Krebs-Henseleit solution at 37°C, saturated with oxygen and carbon dioxide. Contraction of tissues was detected by an isotonic transducer and displayed on a polyrecorder.
1) Norepinephrine-induced contractile responses in rabbit pulmonary artery and descending aorta strips were potentiated significantly by continuous infusion of PAF at a low concentration (5×10-5-5×10pg/ml) and the degree of potentiation became more marked by increasing the dose of PAF.
2) Angiotensin II-induced contractile responses in rabbit pulmonary artery and descending aorta strips were potentiated significantly by continuous infusion of PAF at a low concentration (5×10-5-5×10pg/ml) and the degree of potentiation became more marked by increasing the dose of PAF.
3) Prostaglandin F2α-induced contractile responses in rabbit pulmonary artery and descending aorta strips were potentiated significantly by continuous infusion of PAF at a low concentration(5×10-5-5×10pg/ml)and the degree of potentiation became more marked by increasing the dose of PAF.
The above results may suggest that PAF plays a very important role in the regulatory mechanism of pulmonary circulation and systemic circulation.
