ACUTE DEFENSE-MECHANISMS AGAINST HEMORRHAGE FROM MECHANICAL GILL INJURY IN RAINBOW-TROUT

By cutting gill filaments in anesthetized rainbow trout (Oncorhynchus mykiss), observing the bleeding through a stereomicroscope, and using blockers of various known endogenous filament artery vasoconstrictors, we have here attempted to characterize hemostatic mechanisms in gills . The immediate hemostatic response to a cut in a gill filament artery was a local vasoconstriction, stopping the hemorrhage within similar to 20 s. In heparinized fish, the hemorrhage recommenced after similar to 8 min, suggesting that the vasoconstriction soon subsides and bloo d clotting becomes responsible for the hemostasis. Antagonists of acet ylcholine, adenosine, and serotonin receptors were unable to block the hemostatic vasoconstriction. Also, tetrodotoxin was without effect, i ndicating a nonnervous origin. By contrast, indomethacin significantly affected the measured bleeding times, suggesting that eicosanoids pla y a significant role in this process (possibly by stimulating vasocons triction and/or by inducing local thrombocyte aggregation). By possess ing several hundred virtually identical filaments with readily observa ble vasculature, the fish gill appears to be a good experimental model for studying hemostatic mechanisms.