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Does the PAF antagonist CV-6209 prevent PAF-induced cardiac depression and oxyradical release in anesthetized dogs?
Does the PAF antagonist CV-6209 prevent PAF-induced cardiac depression and oxyradical release in anesthetized dogs?
The PAF antagonist CV-6209 completely prevents PAF-induced cardiac depression and oxidative stress in a canine model, suggesting a role for oxyradicals in PAF-mediated cardiovascular effects.
The effects of platelet-activating factor (PAF) on cardiac function and contractility and its mechanism of action are not fully understood. The authors investigated the effects of PAF in the absence or presence of a potent PAF antagonist CV-6209 on the cardiac function and contractility; lipid peroxidation product malondialdehyde (MDA), an indirect measure of oxygen free radicals; serum creatine kinase (CK); blood lactate; and pH in anesthetized dogs. CV-6209 (1 mg/kg, IV) did not produce significant changes in the various parameters studied. PAF (1 microgram/kg, IV) produced decreases in the cardiac function (cardiac index, left ventricular work index) and indices of cardiac contractility [(+) and (-) dp/dt, dp/dt at CPIP, (dp/dt)/IP, dp/dt at CPIP/IP, Vmax] and increases in the systemic and pulmonary vascular resistance. It also produced increases in cardiac MDA, serum CK, blood lactate, and H+ and decreases in blood pH and HCO3-. CV-6209 completely prevented the PAF-induced changes in the hemodynamic and biochemical parameters. These results suggest that PAF-induced cardiac depression may be due to PAF-induced release of oxyradicals from neutrophils and that PAF antagonist may be useful in counteracting the deleterious effects of PAF on the cardiovascular system.
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Gupta et al. (1994) studied this question.
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