{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:49:12Z","timestamp":1787017752851,"version":"build-2736575974"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1986,12,1]]},"abstract":"<jats:p>We altered the concentration of plasma proteins in human blood in vitro by adding solutions with [Na+], [K+], and [Cl-] resembling those in normal blood plasma, either protein-free or with a high concentration of human albumin. After equilibrating the samples with a gas containing 5% CO2-12% O2\u201383% N2 at 37 degrees C, we measured pH, PCO2, and PO2; in separated plasma, we determined the concentrations of total plasma proteins and albumin and of the completely dissociated electrolytes (strong cations Na+, K+, Mg2+ and anions Cl-, citrate3-). With PCO2 nearly constant (mean = 35.5 Torr; coefficient of variation = 0.02), lowering plasma protein concentration produced a metabolic alkalosis, whereas increasing plasma albumin concentration gave rise to a metabolic acidosis. These acid-base disturbances occurred independently of a minor variation in the balance between the sums of strong cations and anions. We quantified the dependence of several acid-base variables in plasma on albumin (or total protein) concentration. Normal plasma proteins are weak nonvolatile acids. Although their concentration is not regulated as part of acid-base homeostasis, hypoproteinemia and hyperalbuminemia per se produce alkalosis and acidosis, respectively.<\/jats:p>","DOI":"10.1152\/jappl.1986.61.6.2260","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T06:13:14Z","timestamp":1513836794000},"page":"2260-2265","source":"Crossref","is-referenced-by-count":104,"title":["Acid-base effects of altering plasma protein concentration in human blood in vitro"],"prefix":"10.1152","volume":"61","author":[{"given":"T. H.","family":"Rossing","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Maffeo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V.","family":"Fencl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","container-title":["Journal of Applied Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/jappl.1986.61.6.2260","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T11:00:29Z","timestamp":1567940429000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jappl.1986.61.6.2260"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1986,12,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1986,12,1]]}},"alternative-id":["10.1152\/jappl.1986.61.6.2260"],"URL":"https:\/\/doi.org\/10.1152\/jappl.1986.61.6.2260","relation":{},"ISSN":["8750-7587","1522-1601"],"issn-type":[{"value":"8750-7587","type":"print"},{"value":"1522-1601","type":"electronic"}],"subject":[],"published":{"date-parts":[[1986,12,1]]}}}