{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T02:44:32Z","timestamp":1774665872709,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1996,8,1]]},"abstract":"<jats:p> The primary objective of this study was to test the hypothesis that hemorrhagic shock would stimulate alveolar liquid clearance by a catecholamine-dependent mechanism. Anesthetized rats were hemorrhaged to a mean arterial pressure of 30 mmHg for 90 min, but they were not resuscitated. Alveolar liquid clearance was measured by the concentration of labeled and unlabeled protein over 2 h in an isosmolar physiological solution of 5% albumin that had been instilled into one lung. Hemorrhaged rats developed a severe metabolic acidosis that was associated with a 5- to 10-fold rise in plasma epinephrine levels. There was a 60% increase in alveolar liquid clearance in the hemorrhaged rats compared with control rats (55 +\/- 6 vs. 34 +\/- 7%; P &lt; 0.05). Amiloride (10(-4) M) or propranolol (10(-4)M) inhibited the increase in alveolar liquid clearance. Thus the endogenous release of catecholamines associated with hemorrhagic shock markedly stimulates alveolar fluid clearance by a beta-adrenergic-mediated stimulation of active sodium transport. These data suggest a new, previously unrecognized mechanism that may protect against alveolar flooding in the acute phase of hemorrhagic shock. <\/jats:p>","DOI":"10.1152\/jappl.1996.81.2.830","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T07:33:25Z","timestamp":1513928005000},"page":"830-837","source":"Crossref","is-referenced-by-count":42,"title":["Alveolar liquid clearance is increased by endogenous catecholamines in hemorrhagic shock in rats"],"prefix":"10.1152","volume":"81","author":[{"given":"J. F.","family":"Pittet","sequence":"first","affiliation":[{"name":"Department of Anesthesia, University of California, San Francisco 94143, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T. J.","family":"Brenner","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, University of California, San Francisco 94143, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Modelska","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, University of California, San Francisco 94143, USA."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. A.","family":"Matthay","sequence":"additional","affiliation":[{"name":"Department of Anesthesia, University of California, San Francisco 94143, USA."}],"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.1996.81.2.830","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:30:14Z","timestamp":1567963814000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jappl.1996.81.2.830"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,8,1]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1996,8,1]]}},"alternative-id":["10.1152\/jappl.1996.81.2.830"],"URL":"https:\/\/doi.org\/10.1152\/jappl.1996.81.2.830","relation":{},"ISSN":["8750-7587","1522-1601"],"issn-type":[{"value":"8750-7587","type":"print"},{"value":"1522-1601","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,8,1]]}}}