{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,23]],"date-time":"2025-05-23T23:28:30Z","timestamp":1748042910590},"reference-count":0,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[1993,7,1]]},"abstract":"<jats:p> Our objective was to determine whether chronic denervation associated with left lung autotransplantation (LLA) results in an alteration in sympathetic beta-adrenoreceptor regulation of the pulmonary circulation in conscious dogs. Continuous left pulmonary vascular pressure-flow (LPQ) plots were generated in conscious dogs 2\u20134 wk post-LLA and in sham-operated control conscious dogs. We tested the hypothesis that endogenous sympathetic beta-adrenoreceptor activation via circulating catecholamines acted to attenuate the chronic increase in pulmonary vascular resistance post-LLA. Administration of the sympathetic beta-adrenoreceptor antagonist propranolol had no significant effect on the LPQ relationship post-LLA. We also tested the hypothesis that pulmonary vascular reactivity to sympathetic beta-adrenoreceptor activation would be increased post-LLA. The thromboxane analogue U-46619 was used to acutely preconstrict (P &lt; 0.01) the pulmonary circulation in control dogs; this preconstriction shifted the LPQ relationship to the same position measured post-LLA. Under these conditions, cumulative doses of the beta-adrenoreceptor agonist isoproterenol caused pulmonary vasodilation (P &lt; 0.01) in the control group but had no effect post-LLA. However, after acute preconstriction with U-46619, the pulmonary vasodilator response (P &lt; 0.01) to isoproterenol post-LLA was not significantly different from that in the control group. These differential responses to isoproterenol with and without acute preconstriction indicate that a significant component of the chronic increase in pulmonary vascular resistance post-LLA is mediated by passive nonvasoactive mechanisms. Moreover, sympathetic beta-adrenoreceptor reactivity of the pulmonary circulation is not enhanced by chronic denervation resulting from the LLA procedure. <\/jats:p>","DOI":"10.1152\/jappl.1993.75.1.256","type":"journal-article","created":{"date-parts":[[2017,12,22]],"date-time":"2017-12-22T00:40:48Z","timestamp":1513903248000},"page":"256-263","source":"Crossref","is-referenced-by-count":3,"title":["Pulmonary vascular beta-adrenoreceptor activity in conscious dogs after left lung autotransplantation"],"prefix":"10.1152","volume":"75","author":[{"given":"K.","family":"Nishiwaki","sequence":"first","affiliation":[{"name":"Department of Anesthesiology\/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287\u20134961."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Rock","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology\/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287\u20134961."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. S.","family":"Stuart","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology\/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287\u20134961."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D. P.","family":"Nyhan","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology\/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287\u20134961."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W. P.","family":"Peterson","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology\/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287\u20134961."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. A.","family":"Murray","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology\/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287\u20134961."}],"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.1993.75.1.256","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T16:34:14Z","timestamp":1567960454000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/jappl.1993.75.1.256"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1993,7,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1993,7,1]]}},"alternative-id":["10.1152\/jappl.1993.75.1.256"],"URL":"https:\/\/doi.org\/10.1152\/jappl.1993.75.1.256","relation":{},"ISSN":["8750-7587","1522-1601"],"issn-type":[{"value":"8750-7587","type":"print"},{"value":"1522-1601","type":"electronic"}],"subject":[],"published":{"date-parts":[[1993,7,1]]}}}