Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1984-2-14
pubmed:abstractText
In normothermic cats under light barbiturate anesthesia, cerebral blood flow was arrested for one hour by intrathoracal occlusion of the innominate, the left subclavian, and both mammary arteries. Recirculation of the brain after ischemia resulted in reactive hyperemia, followed by a decrease of blood flow to about 70% of control (post-ischemic hypoperfusion). During postischemic hypoperfusion, CO2-reactivity was completely abolished. Intravenous infusion of prostacyclin 2 hours after ischemia (1.8 micrograms/kg/min) decreased systemic arterial blood pressure and reduced platelet aggregability but did not improve cerebral blood flow, did not restore CO2-reactivity, and did not influence postischemic changes of blood coagulation. It is concluded that prostacyclin deficiency is not or not the only reason for the development of post-ischemic hypoperfusion and the associated disturbance of flow regulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0039-2499
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
724-30
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
No effect of prostacyclin on blood flow, regulation of blood flow and blood coagulation following global cerebral ischemia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't