Microangiographic changes following cerebral contusion in rats

Daneyemez, Mehmet

doi:10.1016/s0306-4522(99)00035-4

Cited by 13 publications

(5 citation statements)

References 20 publications

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“…Our present finding of a marked reduction in the fractional area occupied by immunoreactive vascular profiles within the contusion core and in peri-contusional areas (Fig. 3) confirms the observation of Daneyemez (1999) and is also consistent with edema-induced microvascular compression.…”

Section: Discussionsupporting

confidence: 92%

“…Focal ischemia is a component of brain contusion: avascular areas are apparent within injured regions together with irregular filling or nonfilling of superficial arteries (Daneyemez, 1999). At the periphery of a contusion, regional cerebral blood flow (rCBF) decreases to ischemic levels within 3 h after brain trauma, and microthrombosis is evident within the contused area (Maeda et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

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Quantitative Analysis of Microvascular Alterations in Traumatic Brain Injury by Endothelial Barrier Antigen Immunohistochemistry

Lin

Ginsberg

Zhao

et al. 2001

Journal of Neurotrauma

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Endothelial barrier antigen (EBA) is a protein triplet located in the plasma membrane of microvascular endothelium and selectively expressed in the normal nervous system. In this study, microvascular alterations following traumatic brain injury were studied using EBA immunohistochemistry. Anesthetized, physiologically regulated, normothermic Sprague-Dawley rats received moderate (1.5-2.0 atm) parieto-occipital parasagittal fluid-percussion traumatic brain injury (TBI). Control rats were subjected to similar anesthesia and physiological monitoring. Seven days after operative procedures, brains were perfusion-fixed, and coronal sections were reacted for EBA immunohistochemistry using a monoclonal antibody to rat EBA. Selected sections were reacted for isolectin B4 histochemistry. Computerized image analysis was used to compute numbers of EBA-immunopositive vascular profiles and mean vascular profile areas. In control brains, virtually all brain microvessels were clearly and positively immunostained, and antibody binding was specific for blood vessels. In rats with TBI, EBA immunoreactivity was greatly reduced in the zone of cortical contusion. Within the core contusion, fractional areas occupied by vascular profiles were markedly reduced (on average, by 57%), vascular profile counts were diminished, and lectin histochemistry revealed a robust inflammatory response with abundant macrophages. Taken together, these findings were thought to indicate frank microvascular destruction. At adjacent peri-contusional sites, the intensity of EBA immunostaining was also diminished; and vascular profile counts were reduced at adjacent cortical sites and homologous contralateral sites. The latter findings were interpreted as sublethal microvascular alterations possibly related to cerebral edema. The present results confirm that EBA is a specific immunohistochemical marker of normal central nervous system microvessels; that it is suitable for use in formaldehyde-fixed material; and that it is useful in quantitatively assessing microvascular alterations observed at contusional, peri-contusional and more remote sites following traumatic brain injury.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Quantitative Analysis of Microvascular Alterations in Traumatic Brain Injury by Endothelial Barrier Antigen Immunohistochemistry

Lin

Ginsberg

Zhao

et al. 2001

Journal of Neurotrauma

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“…31,34,35,37 Experimental models of TBI frequently exhibit ischemic changes and microvascular occlusion. 9,23,27,42 Although it is difficult to demonstrate while the patient is alive, cerebral ischemia has also been reported in nonfatal TBI 5,22,29 and most recently in pericontusional tissue. 40 Attributed to vasospasm by some investigators, early posttraumatic ischemia was shown by Schroder and associates 30 to be due largely to microvascular compromise.…”

Section: Discussionmentioning

confidence: 96%

Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury

Stein

Chen²,

Sinson³

et al. 2002

Journal of Neurosurgery

157

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“…Postmortem anatomical studies in both animal models and human patients consistently show thinning, shearing, or folding in smaller vessels, as well as microthrombi and microhemorrhages, (14–17). In human TBI, neuronal necrosis correlates strongly with the density of microthrombi (17), suggesting that vascular disruptions impact long-term cellular health and survival.…”

Section: Introductionmentioning

confidence: 99%

Rapid disruption of the cortical microcirculation after mild traumatic brain injury

Witkowski¹,

Erdener²,

Kılıç³

et al. 2019

Preprint

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Keywords: traumatic brain injury, mouse, weight drop injury, cerebral blood flow, capillary, in 21 vivo, laser speckle contrast imaging, optical coherence tomography, two-photon imaging 22 23 24 Acknowledgments: We thank Tim Otchy, Jennifer Morgan, and members of the Davison and 25 Boas laboratories for comments and discussion. This work was supported by Boston University 26 startup funds.Abstract 30 Traumatic brain injury (TBI) is a major source of cognitive deficits affecting millions annually. The 31 bulk of human injuries are mild, causing little or no macroscopic damage to neural tissue, yet can 32 still lead to long-term neuropathology manifesting months or years later. Although the cellular 33 stressors that ultimately lead to chronic pathology are poorly defined, one notable candidate is 34 metabolic stress due to reduced cerebral blood flow (CBF), which is common to many forms of 35 TBI. Here we used high-resolution in vivo intracranial imaging in a rodent injury model to 36 characterize deficits in the cortical microcirculation during both acute and chronic phases after 37 mild TBI. We found that CBF dropped precipitously during immediate post-injury periods, 38 decreasing to less than half of baseline levels within minutes and remaining suppressed for 1.5-39 2 hours. Repeated time-lapse imaging of the cortical microvasculature revealed further striking 40 flow deficits in the capillary network, where 18% of vessels were completely occluded for 41 extended periods after injury, and an additional >50% showed substantial stoppages. Decreased 42 CBF was paralleled by extensive vasoconstriction that is likely to contribute to loss of flow. Our 43 data indicate a major role for vascular dysfunction in even mild forms of TBI, and suggest that 44 acute post-injury periods may be key therapeutic windows for interventions that restore flow 45 and mitigate metabolic stress. 46 47 88 dysfunction across the cortical microvasculature, where a large fraction of individual capillaries 89were occluded for periods of minutes or longer, leading to localized regions with complete loss 90 5 of perfusion. CBF largely returned to normal by 3 hours after injury and showed no measurable 91 deficits when tracked until 3 weeks. Reduced CBF was paralleled by pronounced 92 vasoconstriction, identifying a potential mechanism contributing to disrupted flow. This rapid 93 and extensive vascular dysfunction highlights the importance of immediate post-injury periods 94 for delivering interventions, and suggests that relieving vasoconstriction will be a promising 95 avenue for countering the effects of mild injury. 96 97 Methods 98 99 Animals and surgical procedures 100 All experiments were performed in 2-5 month-old male and female C57BL6/J mice in accordance 101 with guidelines of the Boston University Institutional Animal Care and Use Committee. Animals 102 were group housed on a 12-hour light/dark cycle with ad libitum access to food and water. 103 Chronic cranial windows were implanted using standard procedures (30, 31). Brie...

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Microangiographic changes following cerebral contusion in rats

Cited by 13 publications

References 20 publications

Quantitative Analysis of Microvascular Alterations in Traumatic Brain Injury by Endothelial Barrier Antigen Immunohistochemistry

Quantitative Analysis of Microvascular Alterations in Traumatic Brain Injury by Endothelial Barrier Antigen Immunohistochemistry

Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury

Rapid disruption of the cortical microcirculation after mild traumatic brain injury

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