Duration of ischemia influences the development and resolution of ischemic brain edema.

Todd, N. V.; Picozzi, Piero; Ha, Crockard; Russell, Ralph W. Ros S

doi:10.1161/01.str.17.3.466

Cited by 81 publications

(37 citation statements)

References 42 publications

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“…9 A relation between the duration of ischemia and the extent of damage to the BBB has also been shown previously. 31,32 The time between symptom onset and the scan series was shorter in our data (100 minutes versus 310 minutes). This difference suggests that the BBB damage already occurred early in patients who developed prominent space-occupying edema.…”

Section: Discussionmentioning

confidence: 55%

Imaging Findings Associated with Space-Occupying Edema in Patients with Large Middle Cerebral Artery Infarcts

Horsch¹,

Dankbaar²,

Stemerdink³

et al. 2016

American Journal of Neuroradiology

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on behalf of the DUST investigators ABSTRACT BACKGROUND AND PURPOSE: Prominent space-occupying cerebral edema is a devastating complication occurring in some but not all patients with large MCA infarcts. It is unclear why differences in the extent of edema exist. Better knowledge of factors related to prominent edema formation could aid treatment strategies. This study aimed to identify variables associated with the development of prominent edema in patients with large MCA infarcts.

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Section: Discussionmentioning

confidence: 55%

Imaging Findings Associated with Space-Occupying Edema in Patients with Large Middle Cerebral Artery Infarcts

Horsch¹,

Dankbaar²,

Stemerdink³

et al. 2016

American Journal of Neuroradiology

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“…Similar biphasic openings of the BBB have been shown in association with ischemia/reperfusion (Huang et al, 1999;Kuroiwa et al, 1985;Mossakowski et al, 1994). The biphasic time table and degree of paracellular opening associated with reoxygenation/ reperfusion has been shown to be dependent on the degree, period, and model of ischemic stress, as well as brain region affected (Marsala et al, 2004;Picozzi et al, 1985;Todd et al, 1986). It has been proposed that the first phase of increased BBB paracellular permeability subsequent to reperfusion is attributable to the loss of autoregulation and thereby "hemodynamic" in nature (Dirnagl and Pulsinelli, 1990;Kuroiwa et al, 1988).…”

Section: Discussionmentioning

confidence: 65%

Reoxygenation stress on blood–brain barrier paracellular permeability and edema in the rat

Witt

Mark

Sandoval

et al. 2008

Microvascular Research

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The blood-brain barrier (BBB) serves as a critical regulator of brain homeostasis. Following hypoxia (i.e. 6% oxygen/1hr) and reoxygenation (H/R), the BBB tight junctional complex is disrupted, resulting in increased BBB permeability and the development of vasogenic brain edema. In this study, we examined the effect of H/R on the in vivo rat BBB over a 36 hr time course in conjunction with paracellular permeability, grey matter edema, and systemic inflammatory activity. A biphasic increase was observed in the brain uptake of 14 C-sucrose, a paracellular permeability marker; with the first increase at the 10 min reoxygenation time point, and the second increase at the 6−18hr time points. Increased brain water weight gain (edema) also showed a biphasic response with the first increase at the 10 min-1 hr reoxygenation time points; and the second increase at only the 24 hr time point). Analysis of serum derived cytokines (IL-1β, TNFα, IL-6, IL-10, & IFNγ) demonstrated that only IL-1β and IL-6 were at detectable levels, but these levels were similar to controls. White bloodcell counts showed significant decreases in lymphocytes (10 min-3 hr), increases in monocytes (10 min-3 hr & 12 hr), and increases in polymorphonuclear cells (1hr & 3 hr). We have shown that H/R elicits a biphasic increase in paracellular permeability and edema, which parallel to post-stroke sequelae, despite the lack of occlusion or complete depletion of oxygen.

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“…9 Reperfusion with oxygenated blood after ischemia increases BBB damage, whereas permanent ischemia does not. 21 A unique feature of this phenomenon is demonstrated in our model by a biphasic opening of the blood-spinal cord barrier: the first opening was acute (30 minutes) after reperfusion and followed by a substantial recovery by 4 hours; the second opening, however, was a slow, progressive increase 8-24 hours after reperfusion. This finding was similar to observations made in cats in which the BBB was damaged 15 minutes after reperfusion of the ischemic brain.…”

Section: Discussionmentioning

confidence: 67%

Blood flow and vascular permeability during motor dysfunction in a rabbit model of spinal cord ischemia.

Jacobs

Kempski

McKinley

et al. 1992

Stroke

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Background and Purpose: Delayed deterioration of neurological function after central nervous system ischemia is a well-documented clinical problem. The purpose of our study was to elucidate the role of spinal cord blood flow and spinal cord-blood barrier integrity in the evolution of delayed neurological deterioration after transient spinal cord ischemia in rabbits.Methods: Anesthetized rabbits were subjected to lumbar spinal cord ischemia (25 minutes) and variable periods of reperfusion (30 minutes to 48 hours after ischemia). Regional spinal cord blood flow was monitored by carbon-14-labeled iodoantipyrine autoradiography; vascular permeability was assessed by quantitative microhistofluorescence of Evans blue-albumin in frozen sections of spinal cord. Hindlimb motor function was assessed by standard scoring system and tissue edema by wet/dry weight method.Results: Hindlimb motor function indicated complete paralysis during ischemia and partial gradual recovery upon reperfusion (up to 8 hours), followed by progressive deterioration to severe deficits over 48 hours. Severe vascular permeability disruption was noticed early (30 minutes) after reperfusion, but almost complete recovery reestablished at 8 hours was followed by a secondary progressive increase in vascular permeability. Blood flow was reduced by 20-30% (/?<0.01) 4 hours after ischemia in the gray matter, but hyperemia (200-300%, p<0.01) was observed 12-24 hours after ischemia. Spinal cord water content increased by 5.7% (p<0.05) 24 hours after ischemia.Conclusions: This study demonstrates that delayed neurological and motor deterioration after spinal cord ischemia is associated with severe progressive breakdown of spinal cord-blood barrier integrity that develops late (hours) after the injury. Our data suggest that no ischemic insult in early or late reperfusion is associated with delayed motor deterioration. (Stroke 1992;23:367-373) KEY WORDS • blood-brain barrier • spinal cord • rabbits

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Duration of ischemia influences the development and resolution of ischemic brain edema.

Cited by 81 publications

References 42 publications

Imaging Findings Associated with Space-Occupying Edema in Patients with Large Middle Cerebral Artery Infarcts

Imaging Findings Associated with Space-Occupying Edema in Patients with Large Middle Cerebral Artery Infarcts

Reoxygenation stress on blood–brain barrier paracellular permeability and edema in the rat

Blood flow and vascular permeability during motor dysfunction in a rabbit model of spinal cord ischemia.

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