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Am J Physiol. 1998 Aug;275(2):R460-5. doi: 10.1152/ajpregu.1998.275.2.R460.

Acute defense mechanisms against hemorrhage from mechanical gill injury in rainbow trout.

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Department of Zoophysiology, University of Göteborg, S-413 90 Göteborg, Sweden.


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 approximately 20 s. In heparinized fish, the hemorrhage recommenced after approximately 8 min, suggesting that the vasoconstriction soon subsides and blood clotting becomes responsible for the hemostasis. Antagonists of acetylcholine, adenosine, and serotonin receptors were unable to block the hemostatic vasoconstriction. Also, tetrodotoxin was without effect, indicating a nonnervous origin. By contrast, indomethacin significantly affected the measured bleeding times, suggesting that eicosanoids play a significant role in this process (possibly by stimulating vasoconstriction and/or by inducing local thrombocyte aggregation). By possessing several hundred virtually identical filaments with readily observable vasculature, the fish gill appears to be a good experimental model for studying hemostatic mechanisms.

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