{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T16:57:48Z","timestamp":1789145868653,"version":"build-2803163510"},"reference-count":51,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2017,5,30]],"date-time":"2017-05-30T00:00:00Z","timestamp":1496102400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Respir Care"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>\n                      ARDS is characterized by decreased functional residual capacity (FRC), heterogeneous lung injury, and severe hypoxemia. Tidal ventilation is preferentially distributed to ventilated alveoli. Aerosolized prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      exploits this pathophysiology by inducing local vasodilation, thereby increasing ventilation-perfusion matching and reducing hypoxemia. Therefore, aerosolized prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      efficacy may depend upon FRC. Both P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      and compliance of the respiratory system (C\n                      <jats:sub>RS<\/jats:sub>\n                      ) are indirect signifiers of FRC and thus may partly determine the response to aerosolized prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      We reviewed the records of 208 ARDS subjects who received aerosolized prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      and had arterial blood gases done before and after the initiation of therapy, without other ventilator manipulations. Subjects were grouped according to baseline P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      (lowest: &lt; 60, intermediate: 60\u201390, highest: &gt; 90 mm Hg) and C\n                      <jats:sub>RS<\/jats:sub>\n                      (&lt; 20, 20\u201329, 30\u201339, and \u2265 40 mL\/cm H\n                      <jats:sub>2<\/jats:sub>\n                      O) and by other factors, such as sepsis. Comparisons were analyzed by paired\n                      <jats:italic toggle=\"yes\">t<\/jats:italic>\n                      tests, or Kruskal-Wallis and Dunn post-tests. Multivariate logistic regression modeling was done to determine which of 18 clinically relevant factors were most predictive for responding to aerosolized prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      . \u03b1 was set at .05.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Mean P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      increased by 33 mm Hg (42%) upon initiation of prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      , with a responder rate of 62%. P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      increased significantly in all oxygenation groups. The highest baseline P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      group had the greatest improvement and responder rate (51 \u00b1 63 mm Hg, and 82%). In addition, those with sepsis had a smaller improvement in P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      compared with those without sepsis (18 \u00b1 35 vs 40 \u00b1 55 mm Hg,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = .002). Both P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      and responder rate increased as C\n                      <jats:sub>RS<\/jats:sub>\n                      improved, but between-group improvements were not as consistent. In the final model, the only factors that predicted a positive response to aerosolized prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      were baseline P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      (odds ratio 1.10 [1.004\u20131.205],\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = .042) and C\n                      <jats:sub>RS<\/jats:sub>\n                      (odds ratio 1.04 [1.01\u20131.08],\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = .02).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      Aerosolized prostaglandin I\n                      <jats:sub>2<\/jats:sub>\n                      improves oxygenation in approximately 60% of ARDS cases. A favorable response was most strongly associated with baseline P\n                      <jats:sub>\n                        aO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      \/F\n                      <jats:sub>\n                        IO\n                        <jats:sub>2<\/jats:sub>\n                      <\/jats:sub>\n                      and C\n                      <jats:sub>RS<\/jats:sub>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.4187\/respcare.05268","type":"journal-article","created":{"date-parts":[[2017,5,30]],"date-time":"2017-05-30T20:20:17Z","timestamp":1496175617000},"page":"1014-1022","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":25,"title":["Severity of Hypoxemia and Other Factors That Influence the Response to Aerosolized Prostacyclin in ARDS"],"prefix":"10.1177","volume":"62","author":[{"given":"Richard H","family":"Kallet","sequence":"first","affiliation":[{"name":"Respiratory Care Services, Department of Anesthesia and Perioperative Care"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory","family":"Burns","sequence":"additional","affiliation":[{"name":"Respiratory Care Services, Department of Anesthesia and Perioperative Care"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanjing","family":"Zhuo","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Institute, University of California, San Francisco, California."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly","family":"Ho","sequence":"additional","affiliation":[{"name":"Respiratory Care Services, Department of Anesthesia and Perioperative Care"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin S","family":"Phillips","sequence":"additional","affiliation":[{"name":"Respiratory Care Services, Department of Anesthesia and Perioperative Care"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lance P","family":"Pangilinan","sequence":"additional","affiliation":[{"name":"Respiratory Care Services, Department of Anesthesia and Perioperative Care"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vivian","family":"Yip","sequence":"additional","affiliation":[{"name":"Respiratory Care Services, Department of Anesthesia and Perioperative Care"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonio","family":"Gomez","sequence":"additional","affiliation":[{"name":"Department of Pulmonary and Critical Care Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael S","family":"Lipnick","sequence":"additional","affiliation":[{"name":"Department of Anesthesia and Perioperative Care, University of California, San Francisco at Zuckerberg San Francisco General Hospital and Trauma Center, San Francisco, California."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2017,5,30]]},"reference":[{"issue":"5","key":"e_1_3_3_2_2","first-page":"1039","article-title":"Ventilation-perfusion distributions in adult respiratory distress syndrome","volume":"120","author":"Dantzker DR","year":"1979","unstructured":"Dantzker DR, , Brook CJ, , Dehart P, , Lynch JP, , Weg JG. 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