Cerebral hemodynamic and metabolic changes after experimental subarachnoid hemorrhage

Hashi, Kazuo; Meyer, John Stirling; Shinmaru, S.; Welch, K. M. A.; Teraura, Tetsuaki

doi:10.1016/0022-510x(72)90016-0

Cited by 51 publications

(18 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our results support the conclusion of Weir et al, 17 Hashi et al, 21 and others 8 -25 that vasospasm is but one factor in the genesis of encephalopathy after SAH. Additional factors besides vasospasm are probably necessary and perhaps at times are more important in determining whether brain ischemia will complicate an SAH.…”

Section: Martins Doyle Newby Kobrine Ramirezsupporting

confidence: 92%

See 1 more Smart Citation

The Effect of a Simulated Subarachnoid Hemorrhage on Cerebral Blood Flow in the Monkey

Martins

Doyle

Newby

et al. 1975

Stroke

View full text Add to dashboard Cite

The hydrogen clearance method was used to measure local and total cerebral blood flow (CBF) in the rhesus monkey before and for five hours after a simulated subarachnoid hemorrhage (SAH). CBF remained stable after SAH unless SAH was associated with a fall in cerebral perfusion pressure. In addition, cerebrovascular resistance did not increase after SAH. These results suggest that vasoactive agents in fresh whole blood, and the arterial spasm they produce when added to cerebrospinal fluid (CSF), play only a limited role in the pathogenesis of ischemic encephalopathy that follows an SAH.

show abstract

Section: Martins Doyle Newby Kobrine Ramirezsupporting

confidence: 92%

“…Hashi et al, 21 who measured CBF in baboons for 60 minutes after a subarachnoid injection of blood and found CBF to increase and CVR to decrease during this time. Petruk et al 42 also studied the effect of SAH on CBF in the monkey.…”

Section: Martins Doyle Newby Kobrine Ramirezmentioning

confidence: 99%

The Effect of a Simulated Subarachnoid Hemorrhage on Cerebral Blood Flow in the Monkey

Martins

Doyle

Newby

et al. 1975

Stroke

View full text Add to dashboard Cite

show abstract

“…Furthermore, a non-discriminative dilation of the cerebral vasculature led to development of the 'steal syndrome' 4,36,68 , increased intracranial pressure (ICP) 19 and lower perfusion pressure. Thus, this technique of NO delivery did not spark clinical interest because of the high risk of potential ischemic complications (especially in hemodynamically unstable patients with cerebral vasospasm) and the difficulty of predicting pharmacokinetics because nitrates require an enzymatic step to release NO 5,29,93 .…”

Section: No Delivery: Systemicmentioning

confidence: 99%

RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Pluta

2008

Acta Neurochirurgica Supplement

View full text Add to dashboard Cite

Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation and chemoregulation. Subarachnoid hemorrhage (SAH) interrupts this regulation of cerebral blood flow. Hemoglobin, gradually released from erythrocytes in the subarachnoid space, destroys nNOS-containing neurons in the conductive arteries. This deprives the arteries of NO, leading to initiation of delayed vasospasm. But such vessel narrowing increases shear stress, which stimulates eNOS. This mechanism normally would lead to increased production of NO and dilation of arteries. However, a transient eNOS dysfunction evoked by an increase in the endogenous competitive NOS inhibitor, asymmetric dimethylarginine (ADMA), prevents this vasodilation. eNOS dysfunction has been recently shown to be evoked by increased levels of ADMA in cerebrospinal fluid (CSF) in response to the presence of bilirubin-oxidized fragments (BOXes). A direct cause of the increased ADMA CSF level is most likely decreased ADMA elimination owing to disappearance of ADMA-hydrolyzing enzyme [dimethylarginine dimethylaminohydrolase II (DDAH II)] immunoreactivity in the arteries in spasm. This eNOS dysfunction sustains vasospasm. CSF ADMA levels are closely associated with the degree and time course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of pre-clinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.

show abstract

“…The acute rise of intracranial pressure (ICP) during subarachnoid haemorrhage (SAH) is known experimentally2, 3,5,8,13,15,18 as well as clinically 6 ' 14, 16 A temporary but severe impairment of the cerebral circulation may supervene. Recently it has been demonstrated by our group, that the initial increase of ICP during SAH results from acute changes of the cerebrospinal fluid dynamics rather than from haemodynamic factors 3.…”

Section: Introductionmentioning

confidence: 99%

Cerebral blood flow and intracranial pressure during experimental subarachnoid haemorrhage

1992

View full text Add to dashboard Cite

The relationships of intracranial pressure (ICP), systemic blood pressure (SBP) and cerebral blood flow (CBF) during experimental subarachnoid haemorrhage were investigated in cats. Continuous monitoring of regional cerebral blood flow (rCBF) was done by a thermal diffusion method using a Peltier stack. During haemorrhage ICP rose within 5.4 +/- 0.97 minutes from 10.5 +/- 4.9 to 176.1 +/- 27.8 mmHg. This strong increase of ICP resulted in a temporary arrest of cerebral circulation. The Cushing response during the haemorrhage could not improve the cerebral circulation, but in contrast caused a further increase of ICP. After the haemorrhage the cerebral blood flow normalised within minutes. It is concluded, that the Cushing response during a subarachnoid haemorrhage should be regarded as a deleterious rather than a beneficial mechanism.

show abstract

Cerebral hemodynamic and metabolic changes after experimental subarachnoid hemorrhage

Cited by 51 publications

References 31 publications

The Effect of a Simulated Subarachnoid Hemorrhage on Cerebral Blood Flow in the Monkey

The Effect of a Simulated Subarachnoid Hemorrhage on Cerebral Blood Flow in the Monkey

RETRACTED CHAPTER: Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Cerebral blood flow and intracranial pressure during experimental subarachnoid haemorrhage

Contact Info

Product

Resources

About