Abstract
The effect of vitamin E (VE) on arachidonate-induced respiratory distress and sudden death in rats was examined. Fourteen VE deficient rats (VEDR), 11 normal control rats (NCR) and 12 VE supplemented rats (VESR) were injected with sodium arachidonate into the central vein. VEDR developed various arrhythmias, respiratory distress, apnea, hypotension, and 11 out of 14 VEDR (79%) died shortly after the injection. Many of these rats demonstrated obstruction of the small pulmonary vasculature with platelet aggregates. On the other hand, NCR and VESR developed much attenuated respiratory insufficiency and 5 out of 11 (45%) and 2 out of 12 (17%) died respectively. Twenty-six VEDR, 16 NCR and 25 VESR were used for an in vitro study of the platelet and vessel wall. VEDR demonstrated increases in platelet counts and aggregation as compared with NCR and VESR. Lipid peroxide in platelets, plasma and the aorta was significantly increased in VEDR. Prostacyclin-like activity in the aorta was not different among VEDR, NCR and VESR. The above results indicate that the pronounced respiratory distress, high mortality rate and pulmonary microembolism with platelet aggregates in VEDR may be attributed to the increase in platelet number and aggregability. The increased platelet aggregability was suggested to be the result of increased prostaglandin biosynthesis in platelets. The increased lipid peroxidation in vessel wall and plasma might also contribute to the enhanced respiratory distress. The respiratory distress and mortality as well as in vitro laboratory results were not different between NCR and VESR. This study indicates that vitamin E supplementation does not protect against the development of respiratory distress and sudden death induced by arachidonic acid over the normal control rats.
