{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,20]],"date-time":"2026-02-20T23:05:52Z","timestamp":1771628752804,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1976,4,1]]},"abstract":"<jats:p> Regulation of CSF HCO3-in respiratory acidosis was studied in light of the \u201cdual contribution theory,\u201d which proposed that there were two sources for the CSF HCO3-increase: 1) HCO3-by diffusion from plasma and 2) HCO3-generated in the CNS and catalyzed by the local carbonic anhydrase (J. Appl. Physiol. 38: 504\u2013512, 1975). In anesthetized dogs with an increase in Paco2 of 30 mmHg for 4 h the plasma HCO3 increased 2 meq\/1 and CSF 6 meq\/1. In combined respiratory and metabolic acidosis, plasma HCO3-did not increase but CSF HCO3-increased 6 meq\/1. In combined acidosis and intraventricular injections of acetazolamide no increase in plasma or CSF HCO3-occurred. In combined respiratory acidosis and metabolic alkalosis and intraventricular acetazolamide, plasma HCO3-increased 15 meq\/1 but CSF HCO3-increased 6 meq\/1. Brain and CSF ammonia increased linearly and selectively with the increase in the relative contribution of CNS HCO3-increase. Therefore regulation of CSF HCO3-in respiratory acidosis depends on both components of the dual contribution theory, where each component can provide the total CSF HCO3-increase under appropriate experimental conditions. The control mechanism may be sensitive to changes in [H+] on the brain side of the blood-brain barrier. <\/jats:p>","DOI":"10.1152\/jappl.1976.40.4.559","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T22:18:33Z","timestamp":1514153913000},"page":"559-567","source":"Crossref","is-referenced-by-count":42,"title":["Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis"],"prefix":"10.1152","volume":"40","author":[{"given":"F. M.","family":"Hasan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.","family":"Kazemi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["Journal of Applied Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jappl.1976.40.4.559","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,9]],"date-time":"2019-09-09T00:01:56Z","timestamp":1567987316000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jappl.1976.40.4.559"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1976,4,1]]},"references-count":0,"journal-issue":{"issue":"4","published-print":{"date-parts":[[1976,4,1]]}},"alternative-id":["10.1152\/jappl.1976.40.4.559"],"URL":"https:\/\/doi.org\/10.1152\/jappl.1976.40.4.559","relation":{},"ISSN":["8750-7587","1522-1601"],"issn-type":[{"value":"8750-7587","type":"print"},{"value":"1522-1601","type":"electronic"}],"subject":[],"published":{"date-parts":[[1976,4,1]]}}}