Evaluating lung injury at increasing time intervals in a murine brain death model

Wauters, Shana; Somers, Jana; Vleeschauwer, Stéphanie De; Verbeken, Erik; Verleden, Geert M.; Loon, J. van; Raemdonck, Dirk Van

doi:10.1016/j.jss.2013.01.011

Cited by 17 publications

(21 citation statements)

References 19 publications

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“…As differences for inflammation are obvious between living and BD donors, we did not include living donor controls in our study and applied a syngeneic transplantation model in order to avoid notable inflammation caused by an allo-immune response in the recipient. Our observation that sham-operated mice suffer from a comparable inflammation to that in BD animals is supported by the documented induction of chemokines and leukocyte infiltration in sham-ventilated lungs [43,44]. This result supports recent studies suggesting that ventilation per se results in the inflammation of peripheral organs [45].…”

Section: Rv No Differences Between Bd and Sham Group Were Observed Fsupporting

confidence: 91%

Donor brain death leads to differential immune activation in solid organs but does not accelerate ischaemia-reperfusion injury

et al. 2016

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A comparative analysis of inflammation between solid organs following donor brain death (BD) is still lacking and the detailed influence of BD accelerating ischaemia-reperfusion injury (IRI) post-transplantation remains to be addressed. Applying a murine model of BD, we demonstrated that 4 h after BD organs were characterized by distinct inflammatory expression patterns. For instance, lipocalin 2 (LCN2), a marker of acute kidney injury, was selectively induced in BD livers but not in kidneys. BD further resulted in significantly reduced frequencies of CD3(+) CD4(+) , CD3(+) CD8(+) T cells and NKp46(+) NK cells in the liver, whereas BD kidneys and hearts were characterized by significantly lower frequencies of conventional dendritic cells (cDCs). Syngeneic models of kidney (KTx) and heart transplantation (HTx) illustrated stronger gene expression in engrafted BD hearts only, but 20 h post-transplantation both organs displayed comparable intragraft lymphocyte frequencies, except for NK cells and graft function. Moreover, the complement factor C3d deposit detected in small vessels and capillaries in cardiac syngrafts did not significantly differ between BD and sham-transplanted groups. Finally, no further influence of donor BD on graft survival was detected in an allogeneic heart transplantation setting (C57BL/6 grafts into BALB/c recipients). We show for the first time that BD organs are characterized by a varying inflammatory profile; however, BD does not accelerate IRI in syngeneic KTx and HTx.

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Section: Rv No Differences Between Bd and Sham Group Were Observed Fsupporting

confidence: 91%

Donor brain death leads to differential immune activation in solid organs but does not accelerate ischaemia-reperfusion injury

et al. 2016

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“…Herniation may develop if ICP increases greatly. BD models have been used in various animal studies previously (3,9,10,16). ICP was increased by a balloon catheter in this study and brain death was performed by creating herniation.…”

Section: Discussionmentioning

confidence: 99%

“…Techniques described by Pomper and Wauters were used in the experimental surgical procedure (9,10). Rats were placed in the prone position and a burr hole was drilled under the microscope in the right front parietal area of the scalp for a Fogarty catheter (3F, 0.20 ml) to be inserted through it (Fig.…”

Section: Preparation Periodmentioning

confidence: 99%

Role of ischemic modified albumin in the early diagnosis of increased intracranial pressure and brain death

Kara¹,

Pampal²,

Yıldırım³

et al. 2017

BLL

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AIM: Increased intracranial pressure following trauma and subsequent possible development of brain death are important factors for morbidity and mortality due to ischemic changes. We aimed to establish the role of ischemic modifi ed albumin (IMA) in the early diagnosis of the process, starting with increased intracranial pressure and ending with brain death. MATERIALS AND METHODS: Eighteen Wistar-Albino rats were divided into three groups; control (CG, n = 6), increased intracranial pressure (ICPG, n = 6), and brain death (BDG, n = 6). Intracranial pressure elevation and brain death were constituted with the infl ation of a balloon of a Fogarty catheter in the epidural space. In all three groups, blood samples were drawn before the procedure, and at minutes 150 and 240 for IMA and malondialdehyde (MDA) analysis. RESULTS: Serum IMA levels at 150 and 240 minutes were higher in ICPG than in CG (p < 0.05). IMA levels were similar in ICPG and BDG. Serum MDA levels at 150 and 240 minutes increased in ICPG and BDG groups compared to CG (p < 0.05). MDA levels were similar in ICP and BD groups. CONCLUSION: IMA should be considered as a biochemical parameter in the process starting from increased intracranial pressure elevation and ending at brain death (Tab. 3, Fig. 5, Ref. 31). Text in PDF www.elis.sk. KEY WORDS: ischemic modifi ed albumin, increased intracranial pressure, brain death.

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“…Late mortality is caused by injuries secondary to head trauma which impact distal organ function and increases susceptibility to infections. In particular, severe brain injury often produces a pronounced impact on lung function (16,124). The mechanisms by which TBI contributes to pulmonary dysfunction are poorly understood but are thought to involve a This article has been peer-reviewed and accepted for publication, but has yet to undergo copyediting and proof correction.…”

Section: Hmgb1 and Traumatic Brain Injurymentioning

confidence: 99%

The HMGB1-RAGE Inflammatory Pathway: Implications for Brain Injury-Induced Pulmonary Dysfunction

Weber

Allette

Wilkes

et al. 2015

Antioxidants & Redox Signaling

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Evaluating lung injury at increasing time intervals in a murine brain death model

Cited by 17 publications

References 19 publications

Donor brain death leads to differential immune activation in solid organs but does not accelerate ischaemia-reperfusion injury

Donor brain death leads to differential immune activation in solid organs but does not accelerate ischaemia-reperfusion injury

Role of ischemic modified albumin in the early diagnosis of increased intracranial pressure and brain death

The HMGB1-RAGE Inflammatory Pathway: Implications for Brain Injury-Induced Pulmonary Dysfunction

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