Role of Cerebral Microcirculation in Secondary Brain Damage

1986 ◽  
pp. 295-302 ◽  
Author(s):  
George Mchedlishvili
Keyword(s):  
Brain Damage ◽  
Cerebral Microcirculation ◽  
Secondary Brain Damage

Role of Vasopressin V1a and V2 Receptors for the Development of Secondary Brain Damage after Traumatic Brain Injury in Mice

2008 ◽  
Vol 25 (12) ◽  
pp. 1459-1465 ◽  
Author(s):  
Raimund Trabold ◽  
Sandro Krieg ◽  
Karsten Schöller ◽  
Nikolaus Plesnila
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Secondary Brain Damage

scholarly journals The Role of Bradykinin B1 and B2 Receptors for Secondary Brain Damage after Traumatic Brain Injury in Mice

2009 ◽  
Vol 30 (1) ◽  
pp. 130-139 ◽  
Author(s):  
Raimund Trabold ◽  
Christian Erös ◽  
Klaus Zweckberger ◽  
Jane Relton ◽  
Heike Beck ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcome ◽  
Brain Edema ◽  
Brain Damage ◽  
Secondary Brain Damage ◽  
Edema Formation ◽  
Receptor Mrna ◽  
B2 Receptors

Inflammatory mechanisms are known to contribute to the pathophysiology of traumatic brain injury (TBI). Since bradykinin is one of the first mediators activated during inflammation, we investigated the role of bradykinin and its receptors in posttraumatic secondary brain damage. We subjected wild-type (WT), B1-, and B2-receptor-knockout mice to controlled cortical impact (CCI) and analyzed tissue bradykinin as well as kinin receptor mRNA and protein expression up to 48 h thereafter. Brain edema, contusion volume, and functional outcome were assessed 24 h and 7 days after CCI. Tissue bradykinin was maximally increased 2 h after trauma ( P<0.01 versus sham). Kinin B1 receptor mRNA was upregulated up to four-fold 24 h after CCI. Immunohistochemistry showed that B1 and B2 receptors were expressed in the brain and were significantly upregulated in the traumatic penumbra 1 to 24 h after CCI. B2R−/− mice had significantly less brain edema (−51% versus WT, 24 h; P<0.001), smaller contusion volumes (∼50% versus WT 24 h and 7 d after CCI; P<0.05), and better functional outcome 7 days after TBI as compared with WT mice ( P<0.05). The present results show that bradykinin and its B2 receptors play a causal role for brain edema formation and cell death after TBI.

scholarly journals Angiotensin Receptor Type 1 Inhibition in Lymphopenia and in Neutropenia After Traumatic Brain Injury In Mice: a Randomized Controlled Study (ATLANTIS)

2021 ◽  
Author(s):  
Ralph Timaru-Kast ◽  
Shila P. Coronel-Castello ◽  
Tobias Krämer ◽  
André V. Hugonnet ◽  
Michael K.E. Schäfer ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Receptor Type ◽  
Wild Type ◽  
Secondary Brain Damage ◽  
Neutrophil Depletion ◽  
Cerebral Inflammation

Abstract Background: Cerebral inflammation with invasion of neutrophils and lymphocytes is an important factor in the process of secondary brain damage expansion after traumatic brain injury (TBI). Depletion of neutrophils in mice has been shown to reduce neurologic impairment after TBI. The intrinsic cerebral renin-angiotensin system is an important mediator of cerebral inflammation, as inhibition of the angiotensin II receptor type 1 (AT1) with candesartan improves neurologic recovery, and reduces secondary brain damage and cerebral neutrophil invasion after TBI. The present study was therefore designed to determine the role of immune cells in AT1 inhibition-mediated neuroprotection after TBI. Methods: In study A we assessed the effect of neutrophil depletion in mice after TBI. In study B we investigated the impact of RAG1 deficiency (RAG1-/-; mice without mature B- and T-lymphocytes) after TBI. In study C we investigated the role of neutrophils in candesartan mediated protection after TBI in wild-type mice with and without neutrophil depletion. In study D we examined the role of lymphocytes in AT1 inhibition mediated neuroprotection after TBI in RAG1-/-.Results: Neutropenic and RAG1-/- mice showed reduced brain damage compared to control groups. In control antibody treated wild type mice AT1 inhibition reduced lesion volumes and inflammation compared to vehicle, while in neutropenic mice, candesartan had no effect. In RAG1-/- mice AT1 inhibition resulted in reduction of brain damage and neuroinflammation compared to vehicle group. Conclusion: The present results demonstrate, that reduction of neutrophils and of lymphocytes as well as AT1 inhibition in wild type and RAG1-/- mice reduce brain damage and inflammation after TBI. However, AT1 inhibition was neuroprotective in RAG1-/- mice, but not in neutropenic mice. Therefore, the results indicate that AT1 inhibition mediated neuroprotection may be exerted by anti-inflammatory effects on neutrophils, with a subsequent reduction of neutrophil invasion.

scholarly journals Role of Cortical Spreading Depressions for Secondary Brain Damage after Traumatic Brain Injury in Mice

2008 ◽  
Vol 28 (7) ◽  
pp. 1353-1360 ◽  
Author(s):  
Louisa von Baumgarten ◽  
Raimund Trabold ◽  
Serge Thal ◽  
Tobias Back ◽  
Nikolaus Plesnila
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Low Frequency ◽  
Lesion Size ◽  
Secondary Brain Damage ◽  
Ipsilateral Hemisphere ◽  
Temporary Decrease ◽  
Electroencephalogram Eeg

In recent years, several studies have unequivocally shown the occurrence of cortical spreading depressions (CSDs) after stroke and traumatic brain injury (TBI) in humans. The fundamental question, however, is whether CSDs cause or result from secondary brain damage. The aim of the current study was, therefore, to investigate the role of CSDs for secondary brain damage in an experimental model of TBI. C57/BL6 mice were traumatized by controlled cortical impact. Immediately after trauma, each animal showed one heterogeneous direct current (DC) potential shift accompanied by a profound depression of electroencephalogram (EEG) amplitude, and a temporary decrease of ipsi- and contralateral regional cerebral blood flow (rCBF) suggesting bilateral CSDs. Within the next 3 h after TBI, CSDs occurred at a low frequency (0.38 CSD/h per animal, n = 7) and were accompanied by rCBF changes confined to the ipsilateral hemisphere. No significant relationship between the number of SDs and lesion size or intracranial pressure (ICP) could be detected. Even increasing the number of posttraumatic CSDs by application of KCl by more than six times did not increase ICP or contusion volume. We therefore conclude that CSDs may not contribute to posttraumatic secondary brain damage in the normally perfused and oxygenated brain.

Role of Mediator Compounds in Secondary Brain Damage — Current Evidence

1986 ◽  
pp. 139-150 ◽  
Author(s):  
Andreas Unterberg ◽  
K. Maier-Hauff ◽  
C. Dautermann ◽  
U. Hack ◽  
L. Schürer ◽  
...  
Keyword(s):  
Brain Damage ◽  
Current Evidence ◽  
Secondary Brain Damage

scholarly journals PROGNOSTIC MEANING OF SERUM NSE AS THE FACTOR OF BAD OUTCOME IN SECONDARY BRAIN DAMAGE

2021 ◽  
Vol 13 (08) ◽  
pp. 04-16
Author(s):  
Ainur Tokshilykova Ainur Tokshilykova ◽  
Zhanslu Sarkulova Zhanslu Sarkulova ◽  
Gulnara Kiliptari Gulnara Kiliptari
Keyword(s):  
Brain Damage ◽  
Significant Risk ◽  
Predictive Ability ◽  
Significant Risk Factor ◽  
Unfavorable Outcome ◽  
Secondary Brain Damage ◽  
Stroke Outcomes ◽  
Cerebral Pathology ◽  
The Mathematical Model

This research is dedicated to the study of brain neuronspecific markers and indicators of brain damage outcome. Purpose of the study: To examine the prognostic role of serum NSE as the predictor of unfavorable outcome in traumatic and vascular brain damages. Methods: Prospective cohort study with 219 patients. Blood serum neuronspecific markers (NSE,S100B),acid-base state, blood gas were derived during the period of observation: upon enrolment, on the 3-rd, 5-th and 7-th days spent in the hospital in the intensive care unit. Results: The most significant risk factor of unfavorable outcome is the marker NSE with the cut point 12,5 ng|ml. The results of the analysis indicate the presence of a statistically significant direct relationship between NSE> 12.5 ng / ml and LDH, compared to other variables, 3.7 times more often; with an increase in blood lactate more than 4,1 mmol/l almost 3,8 times; with GCS 13 points below by 1,7 times; S100≥0,2 by 2,8 times; with an increase of PCO2 <38,5 it was documented more than 3 times often. The measure of certainty the resulting model by the pseudo R2 Nagelkerke criterion-250.6; logLikelihood - 154.04 which corresponds to the excellent predictive ability of the mathematical model. The best predictive value of the model is a cut-off point of 88.89%, AuROC-0.809; Se-51.59%; Sp-95.06%; NPV-55.80%; PPV-94.20%. This model can be used to predict the outcome in patients with acute cerebral pathology. Keywords: strokes, brain traumatic damages, neuronspecific markers, diagnostic and prognostic criterias, stroke outcomes.

scholarly journals Role of Secondary Brain Damage Factors in Activation of VascularPlatelet Hemostasis in Traumatic Brain Injury

2016 ◽  
Vol 12 (5) ◽  
pp. 42-51 ◽  
Author(s):  
G. A. Boyarinov ◽  
L. V. Boyarinova ◽  
A. V. Deryugina ◽  
O. D. Solov'eva ◽  
R. R. Zaytsev ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Secondary Brain Damage

scholarly journals Experimental Antileukocyte Interventions in Cerebral Ischemia

1996 ◽  
Vol 16 (6) ◽  
pp. 1108-1119 ◽  
Author(s):  
Roger Härtl ◽  
Ludwig Schürer ◽  
Geert W. Schmid-Schönbein ◽  
Gregory J. del Zoppo
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Tissue Injury ◽  
Focal Cerebral Ischemia ◽  
White Blood Cells ◽  
Global Cerebral Ischemia ◽  
Secondary Brain Damage ◽  
Transient Focal Cerebral Ischemia ◽  
Insight Into

White blood cells (WBCs) play vital roles in host defense. Recently, increasing interest has been directed toward the question of whether WBCs, particularly polymorphonuclear leukocytes, could also act as mediators of secondary brain damage in the setting of focal and global cerebral ischemia with and without reperfusion. Considerable insight into the importance of WBC-mediated tissue injury has been gained from studies employing antileukocyte interventions in experimental cerebral ischemia. The purpose of this article is to survey the different approaches taken to interfere with WBC inflammatory function. Emphasis is laid on a discussion of the efficacy of these interventions, their effects and side effects on cerebral and systemic parameters, and the power of evidence they provide for identification of WBCs as important factors in cerebral ischemia. The role of WBCs has been investigated in a great variety of global and focal cerebral ischemia models with and without reperfusion, leading to spmetimes contradictory results. In the light of currently available data, it seems likely that WBCs contribute to secondary brain damage in the scenario of experimental transient focal cerebral ischemia, if the insult is not too severe.

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