{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T05:24:27Z","timestamp":1789536267293,"version":"build-2803163510"},"reference-count":79,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2015,5,15]],"date-time":"2015-05-15T00:00:00Z","timestamp":1431648000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"CIBERES ISCiii"},{"name":"MINECO (Spain)","award":["BFU2012-37459"],"award-info":[{"award-number":["BFU2012-37459"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2015,6]]},"abstract":"<jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Adult animals that have been perinatally exposed to oxygen\u2010rich atmospheres (hyperoxia), recalling those used for oxygen therapy in infants, exhibit a loss of hypoxic pulmonary vasoconstriction, whereas vasoconstriction elicited by depolarizing agents is maintained.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\n                            Loss of pulmonary hypoxic vasoconstriction is not linked to alterations in oxygen\u2010sensitive K\n                            <jats:sup>+<\/jats:sup>\n                            currents in pulmonary artery smooth muscle cells.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Loss of hypoxic vasoconstriction is associated with early postnatal oxidative damage and corrected by an antioxidant diet.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Perinatal hyperoxia damages carotid body chemoreceptor cell function and the antioxidant diet does not reverse it. The hypoxia\u2010elicited increase in erythropoietin plasma levels is not affected by perinatal hyperoxia.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>The potential clinical significance of the findings in clinical situations such as pneumonia, chronic obstructive pulmonary disease or general anaesthesia is considered.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Adult mammalians possess three cell systems that are activated by acute bodily hypoxia: pulmonary artery smooth muscle cells (PASMC), carotid body chemoreceptor cells (CBCC) and erythropoietin (EPO)\u2010producing cells. In rats, chronic perinatal hyperoxia causes permanent carotid body (CB) atrophy and functional alterations of surviving CBCC. There are no studies on PASMC or EPO\u2010producing cells. Our aim is to define possible long\u2010lasting functional changes in PASMC or EPO\u2010producing cells (measured as EPO plasma levels) and, further, to analyse CBCC functional alterations. We used 3\u2010 to 4\u2010month\u2010old rats born and reared in a normal atmosphere or exposed to perinatal hyperoxia (55\u201360% O\n                      <jats:sub>2<\/jats:sub>\n                      for the last 5\u20136\u00a0days of pregnancy and 4\u00a0weeks after birth). Perinatal hyperoxia causes an almost complete loss of hypoxic pulmonary vasoconstriction (HPV), which was correlated with lung oxidative status in early postnatal life and prevented by antioxidant supplementation in the diet. O\n                      <jats:sub>2<\/jats:sub>\n                      \u2010sensitivity of K\n                      <jats:sup>+<\/jats:sup>\n                      currents in the PASMC of hyperoxic animals is normal, indicating that their inhibition is not sufficient to trigger HPV. Perinatal hyperoxia also abrogated responses elicited by hypoxia on catecholamine and cAMP metabolism in the CB. An increase in EPO plasma levels elicited by hypoxia was identical in hyperoxic and control animals, implying a normal functioning of EPO\u2010producing cells. The loss of HPV observed in adult rats and caused by perinatal hyperoxia, comparable to oxygen therapy in premature infants, might represent a previously unrecognized complication of such a medical intervention capable of aggravating medical conditions such as regional pneumonias, atelectases or general anaesthesia in adult life.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp270274","type":"journal-article","created":{"date-parts":[[2015,4,2]],"date-time":"2015-04-02T17:59:54Z","timestamp":1427997594000},"page":"2459-2477","source":"Crossref","is-referenced-by-count":9,"title":["Hypoxic pulmonary vasoconstriction, carotid body function and erythropoietin production in adult rats perinatally exposed to hyperoxia"],"prefix":"10.1113","volume":"593","author":[{"given":"Jesus","family":"Prieto\u2010Lloret","sequence":"first","affiliation":[{"name":"Departamento de Bioqu\u00edmica y Biolog\u00eda Molecular y Fisiolog\u00eda\/Instituto de Biolog\u00eda y 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