{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T06:45:46Z","timestamp":1790145946398,"version":"4.0.1"},"reference-count":72,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,12,17]],"date-time":"2016-12-17T00:00:00Z","timestamp":1481932800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2017,1]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Prenatal alcohol exposure (PAE) can result in physical and neurocognitive deficits that are collectively termed \u201cfetal alcohol spectrum disorders\u201d (FASD). Although FASD is associated with lifelong intellectual disability, the mechanisms mediating the emergence of secondary mental health and physical disabilities are poorly understood. Based on our previous data showing that maternal ethanol (EtOH) exposure in mice resulted in an immediate reduction in cranially directed fetal blood flow, we hypothesized that such exposure would also result in persistent alterations in cranially directed blood flow in the prenatally alcohol\u2010exposed (PAE) adult. We also hypothesized that PAE adults exposed to an acute cerebrovascular insult would exhibit more brain damage and neurobehavioral impairment compared to non\u2010PAE adult controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Pregnant C57BL\/6 mice were exposed to EtOH, 3\u00a0g\/kg, or water by intragastric gavage. Blood flow in carotid, renal, and femoral arteries was assessed by ultrasound imaging in PAE and control adults at 3, 6, and 12\u00a0months of age. To mimic ischemic stroke in young adult populations, 3\u2010month\u2010old PAE and control animals were subject to transient middle cerebral artery occlusion (MCAo) and subsequently assessed for behavioral recovery, stroke infarct volume, and brain cytokine profiles.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>PAE resulted in a significant age\u2010related decrease in blood acceleration in adult mice, specifically in the carotid artery. A unilateral transient MCAo resulted in equivalent cortico\u2010striatal damage in both PAE and control adults. However, PAE adult mice exhibited significantly decreased poststroke behavioral recovery compared to controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our data collectively show that PAE adult mice exhibit a persistent, long\u2010term loss of cranially directed blood flow, and decreased capacity to compensate for brain trauma due to acute\u2010onset adult diseases like ischemic stroke.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.13277","type":"journal-article","created":{"date-parts":[[2016,12,17]],"date-time":"2016-12-17T17:34:28Z","timestamp":1481996068000},"page":"117-127","source":"Crossref","is-referenced-by-count":37,"title":["Fetal Alcohol Exposure Alters Blood Flow and Neurological Responses to Transient Cerebral Ischemia in Adult Mice"],"prefix":"10.1111","volume":"41","author":[{"given":"Shameena","family":"Bake","sequence":"first","affiliation":[{"name":"Women's Health in Neuroscience Program Department of Neuroscience and Experimental 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