Changes in the subarachnoid space after experimental subarachnoid haemorrhage in the dog: Scanning electron microscopic observation

Suzuki, Shigeharu; Ishii, Masami; Ottomo, M; Iwabuchi, Takashi

doi:10.1007/bf01405236

Cited by 59 publications

(18 citation statements)

References 12 publications

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“…Also, thrombin is the most potent fibroblast mitogen and, therefore, might be responsible for the meningeal fibrosis and hydrocephalus that follows SAH. 27 OxyHb is believed to be of paramount importance in the generation of free radicals and prostaglandins in SAH. * 628 Hence, vasoconstriction may be only one effect of proteins that influences the course of SAH.…”

Section: Discussionmentioning

confidence: 99%

Vasodilator proteins: role in delayed cerebral vasospasm.

White¹

1986

Stroke

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Blood proteins could play a critical role in the pathogenesis of cerebral vasospasm in subarachnoid hemorrhage (SAH) as agonists and as antagonists of vasoconstriction. The present study was designed primarily to quantify the inhibition produced by antithrombin III of the phasic responses elicited by cumulative doses of KCl, serotonin (5-HT), uridine triphosphate (UTP), and thrombin in isolated canine basilar arteries, and to ascertain whether other proteins might act similarly. Antithrombin III (1 unit/ml and 3 units/ml) given 2 min beforehand inhibited all agonists. The inhibition was not dependent on a functional endothelium nor due to stimulation of the electrogenic sodium pump. Alpha2-macroglobulin (0.1 mg/ml and 0.4 mg/ml) inhibited the contractile responses to high K+, 5-HT and thrombin. Kallikrein (1 and 4 units/ml) did not inhibit UTP but inhibited high K+ and 5-HT through an effect on the endothelium. Kallikrein (1 unit/ml) irreversibly blocked the responses to thrombin. Globulins (3 mg/ml) and fibrinogen (0.3 mg/ml) were not inhibitory. The results demonstrate that anticoagulant proteins are very effective nonspecific inhibitors of the vasoconstriction, whereas the serine protease kallikrein selectively blocks thrombin. The remarkable potency of antithrombin III suggests that it may protect cerebral arteries from exhibiting vasospasm in SAH.

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Section: Discussionmentioning

confidence: 99%

Vasodilator proteins: role in delayed cerebral vasospasm.

White¹

1986

Stroke

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“…Therefore, it can be assumed that a sequence of events occurs, in which several different precipitating factors lead to the same final common pathway of injury progression. Although information about the process of cytotoxic damage in TBI is limited, considerable evidence exists that loss of calcium and potassium homeostasis, 5,12,15,16,19,32,34 release of excitotoxic amino acids 4,[15][16][17]18 and free radicals, 7,15,18,23,24 as well as acidosis, 36,37 give rise to parenchymal damage. Based on these findings Siesjö and colleagues 36 developed the notion that loss of cellular calcium homeostasis and enhanced production of free radicals are coupled events and that the detrimental effect of excessive tissue acidosis is, at least in part, secondary to the influence of hydrogen on calcium metabolism and free radical production.…”

Section: Potential For Development Of Neurotoxic Edemamentioning

confidence: 99%

Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging

Barzó

Marmarou²,

Fatouros³

et al. 1997

Journal of Neurosurgery

358

184

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The contribution of brain edema to brain swelling in cases of traumatic brain injury remains a critical problem. The authors believe that cellular edema, the result of complex neurotoxic events, is the major contributor to brain swelling and that vasogenic edema, secondary to blood-brain barrier compromise, may be overemphasized. The objective of this study, therefore, was to quantify temporal water content changes and document the type of edema that forms during the acute and late stages of edema development following closed head injury (CHI). The measurement of brain water content was based on magnetic resonance imaging-determined values of tissue longitudinal relaxation time (T1-weighted imaging) and their subsequent conversion to percentage of water, whereas the differentiation of edema formation (cellular vs. vasogenic) was based on the measurement of the apparent diffusion coefficient (ADC) by diffusion-weighted imaging. A new impact-acceleration model was used to induce CHI. Thirty-six adult Sprague-Dawley rats were separated into two groups: Group I, control (six animals); and Group II, trauma (30 animals). Fast ADC measurements (localized, single-voxel) were obtained sequentially (every minute) up to 1 hour postinjury. The T1-weighted images, used for water content determination, and the diffusion-weighted images (ADC measurement with conventional diffusion-weighted imaging) were obtained at the end of the 1st hour postinjury and on Days 1, 3, 7, 14, 28, and 42 in animals from the trauma and control groups. In the animals subjected to trauma, the authors found a significant increase in ADC (10 +/- 5%) and brain water content (1.3 +/- 0.9%) during the first 60 minutes postinjury. This is consistent with an increase in the volume of extracellular fluid and vasogenic edema formation as a result of blood-brain barrier compromise. This transient increase, however, was followed by a continuing decrease in ADC that began 40 to 60 minutes postinjury and reached a minimum value on Days 7 to 14 (10 +/- 3% reduction). Because the water content of the brain continued to increase during the first 24 hours postinjury (1.9 +/- 0.9%), it is suggested that the decreased ADC indicated cellular edema formation, which started to develop soon after injury and became dominant between 1 and 2 weeks postinjury. The study provides supportive evidence that cellular edema is the major contributor to posttraumatic swelling in diffuse CHI and defines the onset and duration of the increase in cellular volume.

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“…This can result in obliteration of the subarachnoid space or obstruction of arachnoid granulations hence increasing the resistance to CSF circulation and outflow hence elevating CSF pressure [24].…”

Section: Spinal Arachnoid Granulations -Increased Resistance To Outflowmentioning

confidence: 99%