More recently, Knapp et al studied the effects of fish oil on platelet-vascular interactions as measured by urinary prostaglandin metabolites in patients with advanced atherosclerotic peripheral vascular disease. When fish oil containing 10 g of EPA was administered daily for 4 weeks, elevated levels of urinary TXB2-M fell by almost 60% with only small amounts of TXB3-M appearing in the urine. However, when the dose of EPA was decreased to 1 g/day, the urinary TXB2-M rapidly returned to baseline levels, which suggested that rather large amounts of fish oil are required to inhibit platelet-vascular interactions in these patients with extensive atherosclerotic vascular disease.
The PGI2-M was also elevated in the urine of these patients at the beginning of the study, most likely due to increased vascular production of prostacyclin as a response to an atherosclerosis-induced increase in platelet reactivity. After fish oil was administered, PGI2-M fell toward normal, and increased amounts of PGI3-M appeared in the urine. Plasma levels of BTG were initially elevated in the patients but fell toward normal by the third week of treatment. read
Recently, the effect of fish oil on experimental vascular injury in several species of animals has been examined. Dietary cod liver oil inhibited intimal proliferation in saphenous veins interposed in the arterial circulation of dogs fed a hypercholesterolemic diet. In another study, swine fed fish oil underwent balloon catheter endarterectomy of the carotid artery. The amount of vasoconstriction and deposition of radiolabeled platelets at the injury site was significantly reduced in the treated animals. Earlier studies conducted on dogs and cats suggested a beneficial effect of fish oil on the inhibition of coronary artery thrombosis induced by electric stimulation or in the volume of cerebral infarction after cerebral artery ligation.