{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,3,13]],"date-time":"2025-03-13T04:09:43Z","timestamp":1741838983371,"version":"3.38.0"},"reference-count":45,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,1,4]],"date-time":"2025-01-04T00:00:00Z","timestamp":1735948800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>Robust preclinical models of asymmetric ventricular loading in late gestation reflecting conditions such as hypoplastic left heart syndrome are lacking. We characterized the morphometry and microvascular function of the hypoplastic left ventricle (LV) and remaining right ventricle (RV) in a sham\u2010controlled late gestation fetal lamb model of impaired left ventricular inflow (ILVI). Singleton fetuses were instrumented at \u223c120\u00a0days gestational age (dGA; term is \u223c147\u00a0days) with vascular catheters, an aortic flow probe and a deflated left atrial balloon. Balloons in ILVI fetuses were inflated over the 8\u00a0day study until aortic output was eliminated; Sham balloons remained deflated. At the study end\u2010point (\u223c134\u00a0dGA), cardiac function was assessed by echocardiography, microvascular perfusion of each free wall was measured by myocardial contrast echocardiography (MCE) and terminal morphometric data were collected. During the chronic study, flow through the ascending aorta of ILVI fetuses fell from 389 to \u221248\u00a0mL\u00a0min<jats:sup>\u22121<\/jats:sup> with minimal changes to other haemodynamics or blood chemistry. End\u2010point echocardiography and morphometry similarly showed significant and meaningful reductions in ILVI LV chamber volume and wall mass without statistically significant changes in RV size relative to Shams. MCE revealed modestly increased LV perfusion and profoundly increased RV perfusion in ILVI fetuses. Our model displays effective LV hypoplasia with preserved overall fetal health, and our finding of increased RV myocardial perfusion may indicate active vascular remodelling in response to the experimental lesion.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp16504-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Hypoplastic left heart syndrome can be caused by insufficient inflow of blood to the fetal left ventricle.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We found that eliminating fetal left ventricular input for 8\u00a0days reduced left ventricular size and volume, with minimal effects on the right ventricle or overall fetal health.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Blood and oxygen delivery increased significantly in the right ventricle and slightly in the hypoplastic left ventricle. Our results suggest functional and anatomical adaptation of the fetal coronary microvasculature to univentricular right heart conditions.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp286685","type":"journal-article","created":{"date-parts":[[2025,1,4]],"date-time":"2025-01-04T13:40:16Z","timestamp":1735998016000},"page":"971-987","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Enhanced myocardial perfusion in late gestation fetal lambs with impaired left ventricular inflow"],"prefix":"10.1113","volume":"603","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9812-2262","authenticated-orcid":false,"given":"Matthew W.","family":"Hagen","sequence":"first","affiliation":[{"name":"Center for Developmental Health Oregon Health &amp; Science University Portland OR USA"},{"name":"Knight Cardiovascular Institute Oregon Health &amp; Science University Portland OR USA"},{"name":"Division of Nephrology and Hypertension Oregon Health &amp; Science University Portland OR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2628-0085","authenticated-orcid":false,"given":"Samantha","family":"Louey","sequence":"additional","affiliation":[{"name":"Center for Developmental Health Oregon Health &amp; Science University Portland OR USA"},{"name":"Knight Cardiovascular Institute Oregon Health &amp; Science University Portland OR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sarah M.","family":"Alaniz","sequence":"additional","affiliation":[{"name":"Center for Developmental Health Oregon Health &amp; Science University Portland OR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6588-8798","authenticated-orcid":false,"given":"Eric B.","family":"McClellan","sequence":"additional","affiliation":[{"name":"Division of Pediatric Critical Care Oregon Health &amp; Science University Portland OR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jonathan R.","family":"Lindner","sequence":"additional","affiliation":[{"name":"Knight Cardiovascular Institute Oregon Health &amp; Science University Portland OR USA"},{"name":"Division of Cardiovascular Medicine University of Virginia Medical Center Charlottesville VA USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George D.","family":"Giraud","sequence":"additional","affiliation":[{"name":"Center for Developmental Health Oregon Health &amp; Science University Portland OR USA"},{"name":"Knight Cardiovascular Institute Oregon Health &amp; Science University Portland OR USA"},{"name":"Division of Cardiology VA Portland Health Care System Portland OR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1097-2562","authenticated-orcid":false,"given":"Sonnet S.","family":"Jonker","sequence":"additional","affiliation":[{"name":"Center for Developmental Health Oregon Health &amp; Science University Portland OR USA"},{"name":"Knight Cardiovascular Institute Oregon Health &amp; Science University Portland OR USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2025,1,4]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajog.2021.04.228"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cca.2006.02.018"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.2000.279.4.R1157"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.00656.2002"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.echo.2012.06.005"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1111\/j..2002.00053.x"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(96)70673-7"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpregu.1999.277.1.R306"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-5223(98)70448-9"},{"key":"e_1_2_6_11_1","article-title":"Regadenoson stress testing: A comprehensive review with a focused update","volume":"13","author":"Elkholy K. 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