Relationship between presence of vasoconstrictor activity in cerebrospinal fluid and time after subarachnoid haemorrhage from rupture of cerebral arterial aneurysms.

Hunt, T M; Boulay, G. H. du; Blaso, William P.; Förster, David; Boullin, D J

doi:10.1136/jnnp.42.7.625

Cited by 18 publications

(1 citation statement)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4 Particular attention was paid to the time course of any resultant arterial narrowing, ~3 the in vitro reactivity of the major cerebral arteries (at postmortem examination), 7 their pathology, l'~~ and the pharmacological vasoconstrictor activity of the CSF. 2' 6' 11 We now report that intracisternal administration of oxyHb causes cerebral vasoconstriction in primates, but the duration of spasm is shorter than in the clinical situation, and the pathological changes associated with human vessels after prolonged spasm (post-SAH) are not observed.…”

mentioning

confidence: 86%

The role of hemoglobin in the etiology of cerebral vasospasm

Dj¹,

Tagari²,

G³

et al. 1983

Journal of Neurosurgery

View full text Add to dashboard Cite

Oxyhemoglobin was injected intracisternally into three baboons, and methemoglobin into one baboon, in an attempt to mimic the prolonged cerebral arterial spasm sometimes seen after subarachnoid hemorrhage due to aneurysm rupture. Cerebral angiography was performed for up to 7 days after injection of hemoglobin, and the degree of vasospasm was estimated from the angiograms. Oxyhemoglobin caused slight arterial narrowing, which lasted for 3 days. Methemoglobin had no significant effects. Motor neurological deficits and histopathological signs, characteristic of prolonged cerebral vasospasm, were not observed. It was concluded that hemoglobin alone is not capable of causing the cerebral vasospasm syndrome in these experimental animals.

show abstract

mentioning

confidence: 86%