Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2000-3-22
pubmed:abstractText
To analyse the risk/benefit of cerebral thrombolysis the role of hemorrhagic transformation, either as clinically silent hemorrhagic infarction or disastrous parenchymal hemorrhage, is crucial. Thrombolysis in acute ischemic stroke increases the risk of severe, life-threatening hemorrhagic complications by up to 10 times compared to controls. In this paper, previous proposed concepts for the development of intracerebral hemorrhage and hemorrhagic transformation are presented. The role of the cerebral microvasculature will be emphasized. In experimental focal cerebral ischemia a significant loss of basal lamina components of the cerebral microvessels has been demonstrated. This loss in vessel wall integrity is associated with the development of petechial hemorrhage. The mechanisms for this microvascular damage may include plasmin-generated laminin degradation, matrix metalloproteinases activation, transmigration of leukocytes through the vessel wall, and other processes. We propose that attenuation of the microvascular integrity loss with subsequent reduction in hemorrhage is theoretically possible 1) by an improvement in the definition of an individual time window of therapy (by means of imaging techniques), 2) by a biochemical quantification of the basal lamina damage to avoid dangerous interventions, and 3) by pharmacological strategies to protect the basal lamina during thrombolysis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0340-6245
pubmed:author
pubmed:issnType
Print
pubmed:volume
82 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
92-4
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Hemorrhagic transformation of cerebral infarction--possible mechanisms.
pubmed:affiliation
Department of Neurology, Ludwig-Maximilians University, Klinikum Grosshadern, Munich, Germany. hamann@brain.nefo.med.uni-muenchen.de
pubmed:publicationType
Journal Article, Review