Increased thromboxane level in experimental spinal cord injury.
An increased accumulation of tissue thromboxane A2 occurred shortly after spinal cord injury. Prostacyclin formation was not affected. The magnitude of the increase in thromboxane and the extent of post-traumatic vascular damage as determined by extravasation of 125I-labeled human serum albumin were both dependent on the degree of injury. These findings raise the possibility that activation of arachidonic acid metabolism with a preponderance in thromboxane formation may contribute to microvascular injury in experimental spinal cord contusion.
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis*; D000818:Animals; D001808:Blood Vessels / Q000473:pathology; D004487:Edema / Q000473:pathology; D011464:Epoprostenol / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D013116:Spinal Cord / Q000032:analysis* / Q000098:blood supply; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000473:pathology; D013928:Thromboxane A2 / Q000096:biosynthesis; D013929:Thromboxane B2 / Q000032:analysis*
D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol