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Lowering hematocrit from 14.2 \u00b1 0.4% (mean \u00b1 SE; N = 31) to 5.2 \u00b1 0.1% ( N = 31) had no significant impact on arterial or venous CO<jats:sub>2<\/jats:sub>tensions (Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>and Pv<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>, respectively) over the subsequent 2 h. Pco<jats:sub>2<\/jats:sub>was maintained despite the reduction in red cell number and a significant 32% increase in cardiac output (V\u0307<jats:sub>b<\/jats:sub>), both of which have been found to cause Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>increases in teleost fish. By contrast, treatment of anemic dogfish with the CA inhibitors benzolamide (1.3 mg\/kg) or F3500 (50 mg\/kg), to selectively inhibit extracellular CA, elicited rapid and significant increases in Pa<jats:sub>CO<jats:sub>2<\/jats:sub><\/jats:sub>of 0.68 \u00b1 0.17 Torr ( N = 6) and 0.53 \u00b1 0.11 Torr ( N = 7), respectively, by 30 min after treatment. These findings provide a functional context in which extracellular CA in dogfish contributes substantially to CO<jats:sub>2<\/jats:sub>excretion. Additionally, the apparent lack of effect of V\u0307<jats:sub>b<\/jats:sub>changes on Pco<jats:sub>2<\/jats:sub>suggests that, in contrast to teleost fish, CO<jats:sub>2<\/jats:sub>excretion in dogfish does not behave as a diffusion-limited system.<\/jats:p>","DOI":"10.1152\/ajpregu.00219.2003","type":"journal-article","created":{"date-parts":[[2004,3,2]],"date-time":"2004-03-02T01:51:13Z","timestamp":1078192273000},"page":"R1138-R1148","source":"Crossref","is-referenced-by-count":15,"title":["Branchial membrane-associated carbonic anhydrase activity maintains CO<sub>2<\/sub>excretion in severely anemic dogfish"],"prefix":"10.1152","volume":"286","author":[{"given":"K. M.","family":"Gilmour","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. 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