Acute therapeutic modalities for experimental vasogenic edema

Harbaugh, R D; James, Hector E.; Marshall, Larry; Shapiro, Harvey M.; Laurin, Rita

doi:10.1097/00006123-197912000-00002

Cited by 4 publications

(5 citation statements)

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“…The smaller water‐content increase in the gray matter could also be a reason for the weaker correlation between D mono and T 1 in the mouse study. It appears that the small water content elevation in the penumbra is an inherent limitation of the cold injury model in mice since the peak of edema occurs 24 hours after the cold impact (28). The limitation of the cold injury model is one of the explanations for the relatively small number of animals used in this study.…”

Section: Discussionmentioning

confidence: 99%

In vivo brain edema classification: New insight offered by large b‐value diffusion‐weighted MR imaging

Schwarcz

Ursprung

Berente

et al. 2006

Magnetic Resonance Imaging

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Purpose:To assess the role of large b-value diffusion weighted imaging (DWI) in the characterization of the physicochemical properties of the water in brain edema under experimental and clinical conditions. Results: A strong linear correlation was found between T 1 and D mono in vasogenic brain edema, both in humans and in mice. After breakdown of D mono into fast and slow diffusing components, only D fast exhibited a strong correlation with T 1 ; D slow was unchanged in vasogenic brain edema. Conclusion:Large b-value DWI can furnish a detailed characterization of vasogenic brain edema, and may provide a quantitative approach for the differentiation of edema types on the basis of the physicochemical properties of the water molecules. Application of the DWI method may permit prediction and follow-up of the effects of antiedematous therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

In vivo brain edema classification: New insight offered by large b‐value diffusion‐weighted MR imaging

Schwarcz

Ursprung

Berente

et al. 2006

Magnetic Resonance Imaging

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show abstract

“…29 The effect of barbiturates on ICP is related to direct vasoconstriction or reduced cellular metabolism, [29][30][31][32][33][34][35] resulting in decreased intracranial volume. Stabilization of the lysosomal membrane may reduce cerebral swelling.…”

Section: Discussionmentioning

confidence: 99%

“…Stabilization of the lysosomal membrane may reduce cerebral swelling. 30,31,33,35 It has been reported that barbiturates may provide some benefit in the management of vasospasm-related deficits. 32 In the present study, although 2 of 6 patients who suffered early cerebral swelling failed to survive, the 4 survivors recovered to show GR or MD.…”

Section: Discussionmentioning

confidence: 99%

“…At Sumi Memorial Hospital, surgery for aneurysmal obliteration was performed in 60 patients between January 1, 1998 and April 30,2002. Of these 60 cases, 20 were unruptured aneurysm, 38 were ruptured aneurysm without ICH, and were ruptured MCA aneurysm accompanied by sylvian hematoma or ICH, 1 of which underwent decompressive craniotomy on aneurysmal obliteration.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Development of early cerebral swelling in surgically treated ruptured aneurysm of acute stage, its significance, and management

Niikawa¹,

Yasokawa

Ito

2005

Journal of Stroke and Cerebrovascular Diseases

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“…Mannitol and urea have also been shown consistently to decrease ICP and cerebral water content in the presence of a brain injury [63][64][65][66][67][68][69][70]. Mannitol appears to have a variable effect on CBF in brain injury, causing an increase when autoregulation is lost and no change when autoregulation is intact [66,71].…”

Section: Fluid Resuscitationmentioning

confidence: 93%

Analytic Reviews : Fluid Resuscitation in Head Injury

Shackford

1990

J Intensive Care Med

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Shackford SR Fluid resuscitation in head injury. J Intensive Care Med 1990:5:59-68.--------Head injury, either alone or in combination with hypovolemic shock, is the leading cause of traumatic death in this country. Factors contributing to mortality include the primary impact injury as well as subsequent ischemia and hypoperfusion. Intravenous fluid therapy is required in all of these patients. However, fluid therapy may increase brain swelling and cerebral edema formation which could lead to an increase in intracranial pressure and a reduction in cerebral perfusion pressure. The use of standard fluid therapy has been questioned, and novel therapies involving hyperosmolar and hypertonic solutions are now being investigated. This review covers recent advances in the understanding of the effects of fluid resuscitation on the brain. It also includes a brief summary of the determinants of transcapillary fluid exchange and a review of relevant cerebral circulatory physiology and the physiological aberrations produced by brain injury.From the Head injury and hemorrhage, either alone or in combination, are responsible for over 60% of civilian and military traumatic deaths [1,2]. Intravenous fluid therapy is necessary in all of these patients, especially those who require resuscitation from hypovolemic shock. Rapid fluid administration is lifesaving after hemorrhage but, when given in the large volumes necessary to restore perfusion, it may cause further harm to the injured brain by increasing edema formation. Although there is much information about the effects of asanguineous fluid therapy on the lung [3,4] and the kidney [5], relatively little information exists about the immediate and late effects of intravenous fluids on either the normal or the injured brain. There has recently been renewed interest in cerebral resuscitation after cardiac arrest [6] and brain injury [7]. The use of standard fluid therapy has been questioned, and novel therapies involving hyperosmolar and hypertonic solutions are now being investigated [8-12].This review covers recent advances in the understanding of the effects of fluid resuscitation on the brain. A brief summary of the determinants of transcapillary fluid exchange as well as a review of relevant cerebral circulatory physiology and the physiological aberrations produced by brain injury are necessary to interpret the relative importance of pertinent laboratory and clinical investigations of fluid therapy of brain injury with and without associated hypovolemia. Transcapillary Fluid ExchangeTranscapillary fluid exchange is governed by capillary permeability and the hydrostatic and oncotic pressure gradients that exist between the capillary and surrounding tissues. The relationship of these forces in determining net fluid movement across the capillary membrane is described by the Starling equation [13]: where Qj is net fluid flux across the membrane; Kf is the filtration coefficient of the membrane; S is the surface area of the membrane; Pc is the capillary hydrostatic pressure; P, is ...

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Acute therapeutic modalities for experimental vasogenic edema

Cited by 4 publications

References 0 publications

In vivo brain edema classification: New insight offered by large b‐value diffusion‐weighted MR imaging

In vivo brain edema classification: New insight offered by large b‐value diffusion‐weighted MR imaging

Development of early cerebral swelling in surgically treated ruptured aneurysm of acute stage, its significance, and management

Analytic Reviews : Fluid Resuscitation in Head Injury

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