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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
1980-11-20
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pubmed:abstractText |
Perinatal hypoxic-ischemic brain damage and intraventricular hemorrhage (IVH) are important causes of death and neurologic and intellectual dysfunction. Both lesions are related to perinatal asphyxia, and the aim of our review is to establish a comprehensive pathogenetic model. Our previous finding that cerebral blood flow is pressure-passive in perinatal distress is crucial, as periods of hypertension and hypotension alternate in the distressed infant. In hypertension, transmural pressure increases in the capillaries, leading to edema and, in premature infants, eventual rupture of vessels and IVH. Intraventricular hemorrhage induces vasospasm and ischemia. Ischemia is the direct result of hypotension. Cerebral blood flow studies performed a few hours after birth with subsequent examinations at one year of age point to a decisive effect of neonatal ischemia on subsequent development.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
|
pubmed:issn |
0003-9942
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
37
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
585-7
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:7417061-Asphyxia Neonatorum,
pubmed-meshheading:7417061-Blood Pressure,
pubmed-meshheading:7417061-Blood-Brain Barrier,
pubmed-meshheading:7417061-Brain Damage, Chronic,
pubmed-meshheading:7417061-Brain Ischemia,
pubmed-meshheading:7417061-Cerebral Hemorrhage,
pubmed-meshheading:7417061-Cerebral Ventricles,
pubmed-meshheading:7417061-Cerebrovascular Circulation,
pubmed-meshheading:7417061-Child Development,
pubmed-meshheading:7417061-Homeostasis,
pubmed-meshheading:7417061-Humans,
pubmed-meshheading:7417061-Hypoxia, Brain,
pubmed-meshheading:7417061-Infant, Newborn
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pubmed:year |
1980
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pubmed:articleTitle |
Perinatal hypoxic-ischemic brain damage and intraventricular hemorrhage. A pathogenetic model.
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pubmed:publicationType |
Journal Article
|