Linked Life Data

3491340

Source:http://linkedlifedata.com/resource/pubmed/id/3491340

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1987-1-21
pubmed:abstractText
Nine millilitres of preclotted autologous blood was injected into the ventricles of 10 adult mongrel dogs (control dogs) to create subtotal ventricular casts with solid clots. The neurological status and systemic fibrinolytic profiles were closely monitored, and the changes in clot and ventricular volumes were measured by serial computed tomography (CT) for 3 months. The control animals showed severe neurological impairment for 7 to 9 days. No visible lysis of the intraventricular clots occurred for 5 to 7 days, after which slow clot lysis occurred at a constant rate. Complete lysis of the 10 clots took 38 to 65 days, indicating that canine cerebrospinal fluid normally possessed limited capacity for in situ fibrinolysis. Of the 10 control dogs, 8 developed progressive ventricular enlargement after a transient initial shrinkage parallel with initial clot lysis. Their final ventricular volume at 3 months was as much as 14 times the base line ventricular volume. Necropsy studies disclosed increased basal subarachnoid fibrosis and extensive ependymal and subependymal damage in the lateral ventricular walls of the hydrocephalic dogs. Ten other dogs (UK dogs) were given similar ventricular clot injections. Six hours later, each UK dog was begun on a regimen of 20,000 IU of intraventricular urokinase every 12 hours until solid clots were no longer seen in the ventricles on CT. In all 10 UK dogs, intraventricular urokinase induced complete lysis in 3 to 6 days without causing local or systemic hemorrhages. The neurological status of all 10 dogs also improved promptly. In 8 UK dogs, the ventricles that were initially distended by clots showed rapid shrinkage parallel with thrombolysis to a final volume at 3 months of less than four times the initial ventricular volume. Only 2 animals had persistently large or expanding ventricles. At necropsy, the ependymal and subarachnoid spaces of the UK dogs were remarkably free of damage and fibrosis. The possible mechanisms by which intraventricular urokinase may prevent posthemorrhagic hydrocephalus are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0148-396X
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
553-72
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Lysis of intraventricular blood clot with urokinase in a canine model: Part 3. Effects of intraventricular urokinase on clot lysis and posthemorrhagic hydrocephalus.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't