Journal of Cerebral Blood Flow and Metabolism最新文献

Reduced neurovascular coupling is associated with increased cardiovascular risk without established cerebrovascular disease: A cross-sectional analysis in UK biobank. 神经-血管耦合功能降低与心血管风险增加有关，但未确诊脑血管疾病：英国生物库横断面分析。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-22 DOI: 10.1177/0271678X241302172

Sheng Yang, Alastair John Stewart Webb

{"title":"Reduced neurovascular coupling is associated with increased cardiovascular risk without established cerebrovascular disease: A cross-sectional analysis in UK biobank.","authors":"Sheng Yang, Alastair John Stewart Webb","doi":"10.1177/0271678X241302172","DOIUrl":"10.1177/0271678X241302172","url":null,"abstract":"Mid-life vascular risk factors predict late-life cerebrovascular diseases and poor global brain health. Although endothelial dysfunction is hypothesized to contribute to this process, evidence of impaired neurovascular function in early stages remains limited. In this cross-sectional study of 31,934 middle-aged individuals from UK Biobank without established cerebrovascular disease, the overall 10-year risk of cardiovascular events was associated with reduced neurovascular coupling (p < 2 × 10-16) during a visual task with functional MRI, including in participants with no clinically apparent brain injury on MRI. Diabetes, smoking, waist-hip ratio, and hypertension were each strongly associated with decreased neurovascular coupling with the strongest relationships for diabetes and smoking, whilst in older adults there was an inverted U-shaped relationship with DBP, peaking at 70-80 mmHg DBP. These findings indicate that mid-life vascular risk factors are associated with impaired cerebral endothelial-dependent neurovascular function in the absence of overt brain injury. Neurovascular dysfunction, measured by neurovascular coupling, may play a role in the development of late-life cerebrovascular disease, underscoring the need for further longitudinal studies to explore its potential as a mediator of long-term cerebrovascular risk.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241302172"},"PeriodicalIF":4.9,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11585009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rapid oxygen titration following cardiopulmonary resuscitation mitigates cerebral overperfusion and striatal mitochondrial dysfunction in asphyxiated newborn lambs. 心肺复苏后的快速氧气滴定可减轻窒息新生羔羊的脑过度灌注和纹状体线粒体功能障碍。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-22 DOI: 10.1177/0271678X241302738

Shiraz Badurdeen, Robert Galinsky, Calum T Roberts, Kelly J Crossley, Valerie A Zahra, Alison Thiel, Yen Pham, Peter G Davis, Stuart B Hooper, Graeme R Polglase, Emily J Camm

{"title":"Rapid oxygen titration following cardiopulmonary resuscitation mitigates cerebral overperfusion and striatal mitochondrial dysfunction in asphyxiated newborn lambs.","authors":"Shiraz Badurdeen, Robert Galinsky, Calum T Roberts, Kelly J Crossley, Valerie A Zahra, Alison Thiel, Yen Pham, Peter G Davis, Stuart B Hooper, Graeme R Polglase, Emily J Camm","doi":"10.1177/0271678X241302738","DOIUrl":"10.1177/0271678X241302738","url":null,"abstract":"Asphyxiated neonates must have oxygenation rapidly restored to limit ongoing hypoxic-ischemic injury. However, the effects of transient hyperoxia after return of spontaneous circulation (ROSC) are poorly understood. We randomly allocated acutely asphyxiated, near-term lambs to cardiopulmonary resuscitation in 100% oxygen (\"standard oxygen\", n = 8) or air (n = 7) until 5 minutes after ROSC, or to resuscitation in 100% oxygen immediately weaned to air upon ROSC (\"rapid-wean\", n = 7). From 5 minutes post-ROSC, oxygen was titrated to target preductal oxygen saturation between 90-95%. Cerebral tissue oxygenation was transiently but markedly elevated following ROSC in the standard oxygen group compared to the air and rapid-wean groups. The air group had a delayed rise in cerebral tissue oxygenation from 5 minutes after ROSC coincident with up-titration of oxygen. These alterations in oxygen kinetics corresponded with similar overshoots in cerebral perfusion (pressure and flow), indicating a physiological mechanism. Transient cerebral tissue hyperoxia in the standard oxygen and air groups resulted in significant alterations in mitochondrial respiration and dynamics, relative to the rapid-wean group. Overall, rapid-wean of oxygen following ROSC preserved striatal mitochondrial respiratory function and reduced the expression of genes involved in free radical generation and apoptosis, suggesting a potential therapeutic strategy to limit cerebral reperfusion injury.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241302738"},"PeriodicalIF":4.9,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11584996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cerebral microvascular physiology associated with white matter lesion burden differs by level of vascular risk in typically aging older adults. 与白质病变负担相关的脑微血管生理学因典型老龄化老年人的血管风险水平而异。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-20 DOI: 10.1177/0271678X241300394

Gabriele M Gassner, Nikou L Damestani, Natalie S Wheeler, Jan A Kufer, Shrikanth M Yadav, Sarah F Mellen, Katherine N Maina, David H Salat, Meher R Juttukonda

{"title":"Cerebral microvascular physiology associated with white matter lesion burden differs by level of vascular risk in typically aging older adults.","authors":"Gabriele M Gassner, Nikou L Damestani, Natalie S Wheeler, Jan A Kufer, Shrikanth M Yadav, Sarah F Mellen, Katherine N Maina, David H Salat, Meher R Juttukonda","doi":"10.1177/0271678X241300394","DOIUrl":"10.1177/0271678X241300394","url":null,"abstract":"White matter lesions (WMLs) are prevalent with aging, and higher WML burden has been observed in older adults with vascular diseases. While the physiology underlying the formation of WMLs is not known, various risk factors are associated with high WML burden. Here, we investigated the relationship between vascular risk factors and microvascular physiology (i.e., oxygen supply and oxygen extraction fraction [OEF]) and their association with WML burden. Forty-one typically aging adults (60-80 years) were classified into high or low vascular risk based on common modifiable vascular risk factors (hypertension, diabetes, hyperlipidemia, and overweight). These groups were subdivided into high or low WML burden. Differences in microvascular physiology (oxygen supply and OEF) were then compared between and within groups. Overall, OEF was significantly higher in the high vascular risk group compared to the low vascular risk group (p < 0.01). In the low vascular risk subgroup, OEF was uniquely lower in the individuals with high WML versus low WML burden (p = 0.02), despite no differences in oxygen supply between these subgroups (p = 0.87). The coupling of impaired OEF with the absence of compensatory physiology, such as elevated oxygen supply, may represent an important mechanism underlying WML burden in individuals with low vascular risk factors.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241300394"},"PeriodicalIF":4.9,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11580122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Associations of life-course cardiovascular risk factors with late-life cerebral haemodynamics. 终生心血管风险因素与晚年脑血流动力学的关联。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-17 DOI: 10.1177/0271678X241301261

Mathijs Bj Dijsselhof, Jorina Holtrop, Sarah-Naomi James, Carole H Sudre, Kirsty Lu, Luigi Lorenzini, Lyduine E Collij, Catherine J Scott, Emily N Manning, David L Thomas, Marcus Richards, Alun D Hughes, David M Cash, Frederik Barkhof, Jonathan M Schott, Jan Petr, Henk Jmm Mutsaerts

{"title":"Associations of life-course cardiovascular risk factors with late-life cerebral haemodynamics.","authors":"Mathijs Bj Dijsselhof, Jorina Holtrop, Sarah-Naomi James, Carole H Sudre, Kirsty Lu, Luigi Lorenzini, Lyduine E Collij, Catherine J Scott, Emily N Manning, David L Thomas, Marcus Richards, Alun D Hughes, David M Cash, Frederik Barkhof, Jonathan M Schott, Jan Petr, Henk Jmm Mutsaerts","doi":"10.1177/0271678X241301261","DOIUrl":"10.1177/0271678X241301261","url":null,"abstract":"While the associations of mid-life cardiovascular risk factors with late-life white matter lesions (WMH) and cognitive decline have been established, the role of cerebral haemodynamics is unclear. We investigated the relation of late-life (69-71 years) arterial spin labelling (ASL) MRI-derived cerebral blood flow (CBF) with life-course cardiovascular risk factors (36-71 years) and late-life white matter hyperintensity (WMH) load in 282 cognitively healthy participants (52.8% female). Late-life (69-71 years) high systolic (B = -0.15) and diastolic (B = -0.25) blood pressure, and mean arterial pressure (B = -0.25) were associated with low grey matter (GM) CBF (p < 0.03), and white matter CBF (B = -0.25; B = -0.15; B = -0.13, p < 0.03, respectively). The association between systolic blood pressure and GM CBF differed between sexes (male/female B = -0.15/0.02, p = 0.04). No associations were found with early- or mid-life cardiovascular risk factors. Furthermore, WMHs were associated with cerebral haemodynamics but not cardiovascular risk factors. These findings suggest that cerebral blood flow autoregulation is able to maintain stable global cerebral haemodynamics until later in life. Future studies are encouraged to investigate why cardiovascular risk factors have differential effects on haemodynamics and WMH, and their implications for cognitive decline.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241301261"},"PeriodicalIF":4.9,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11571377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular and cellular mechanisms of mitochondria transfer in models of central nervous system disease. 中枢神经系统疾病模型中线粒体转移的分子和细胞机制。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-14 DOI: 10.1177/0271678X241300223

Takafumi Nakano, Keiichi Irie, Koichi Matsuo, Kenichi Mishima, Yoshihiko Nakamura

{"title":"Molecular and cellular mechanisms of mitochondria transfer in models of central nervous system disease.","authors":"Takafumi Nakano, Keiichi Irie, Koichi Matsuo, Kenichi Mishima, Yoshihiko Nakamura","doi":"10.1177/0271678X241300223","DOIUrl":"10.1177/0271678X241300223","url":null,"abstract":"In the central nervous system (CNS), neuronal function and dysfunction are critically dependent on mitochondrial integrity and activity. In damaged or diseased brains, mitochondrial dysfunction reduces adenosine triphosphate (ATP) levels and impairs ATP-dependent neural firing and neurotransmitter dynamics. Restoring mitochondrial capacity to generate ATP may be fundamental in restoring neuronal function. Recent studies in animals and humans have demonstrated that endogenous mitochondria may be released into the extracellular environment and transported or exchanged between cells in the CNS. Under pathological conditions in the CNS, intercellular mitochondria transfer contributes to new classes of signaling and multifunctional cellular activities, thereby triggering deleterious effects or promoting beneficial responses. Therefore, to take full advantage of the beneficial effects of mitochondria, it may be useful to transplant healthy and viable mitochondria into damaged tissues. In this review, we describe recent findings on the mechanisms of mitochondria transfer and provide an overview of experimental methodologies, including tissue sourcing, mitochondrial isolation, storage, and modification, aimed at optimizing mitochondria transplantation therapy for CNS disorders. Additionally, we examine the clinical relevance and potential strategies for the therapeutic application of mitochondria transplantation.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241300223"},"PeriodicalIF":4.9,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11565516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A dangerous liaison: Spreading depolarization and tissue acidification in cerebral ischemia. 危险的联系脑缺血时蔓延性去极化和组织酸化。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-13 DOI: 10.1177/0271678X241289756

Eszter Farkas, Christine R Rose

{"title":"A dangerous liaison: Spreading depolarization and tissue acidification in cerebral ischemia.","authors":"Eszter Farkas, Christine R Rose","doi":"10.1177/0271678X241289756","DOIUrl":"https://doi.org/10.1177/0271678X241289756","url":null,"abstract":"Brain pH is precisely regulated, and pH transients associated with activity are rapidly restored under physiological conditions. During ischemia, the brain's ability to buffer pH changes is rapidly depleted. Tissue oxygen deprivation causes a shift from aerobic to anaerobic metabolism and the accumulation of lactic acid and protons. Although the degree of tissue acidosis resulting from ischemia depends on the severity of the ischemia, spreading depolarization (SD) events emerge as central elements to determining ischemic tissue acidosis. A marked decrease in tissue pH during cerebral ischemia may exacerbate neuronal injury, which has become known as acidotoxicity, in analogy to excitotoxicity. The cellular pathways underlying acidotoxicity have recently been described in increasing detail. The molecular structure of acid or base carriers and acidosis-activated ion channels, the precise (dys)homeostatic conditions under which they are activated, and their possible role in severe ischemia have been addressed. The expanded understanding of acidotoxic mechanisms now provides an opportunity to reevaluate the contexts that lead to acidotoxic injury. Here, we review the specific cellular pathways of acidotoxicity and demonstrate that SD plays a central role in activating the molecular machinery leading to acid-induced damage. We propose that SD is a key contributor to acidotoxic injury in cerebral ischemia.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241289756"},"PeriodicalIF":4.9,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Macrovascular blood flow and microvascular cerebrovascular reactivity are regionally coupled in adolescence. 大血管血流量和微血管脑血管反应性在青春期具有区域耦合性。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-13 DOI: 10.1177/0271678X241298588

Kristina M Zvolanek, Jackson E Moore, Kelly Jarvis, Sarah J Moum, Molly G Bright

{"title":"Macrovascular blood flow and microvascular cerebrovascular reactivity are regionally coupled in adolescence.","authors":"Kristina M Zvolanek, Jackson E Moore, Kelly Jarvis, Sarah J Moum, Molly G Bright","doi":"10.1177/0271678X241298588","DOIUrl":"10.1177/0271678X241298588","url":null,"abstract":"Cerebrovascular imaging assessments are particularly challenging in adolescent cohorts, where not all modalities are appropriate, and rapid brain maturation alters hemodynamics at both macro- and microvascular scales. In a preliminary sample of healthy adolescents (n = 12, 8-25 years), we investigated relationships between 4D flow MRI-derived blood velocity and blood flow in bilateral anterior, middle, and posterior cerebral arteries and BOLD cerebrovascular reactivity (CVR) in associated vascular territories. As hypothesized, higher velocities in large arteries are associated with an earlier response to a vasodilatory stimulus (cerebrovascular reactivity delay) in the downstream territory. Higher blood flow through these arteries is associated with a larger BOLD response to a vasodilatory stimulus (cerebrovascular reactivity amplitude) in the associated territory. These trends are consistent in a case study of adult moyamoya disease. In our small adolescent cohort, macrovascular-microvascular relationships for velocity/delay and flow/CVR change with age, though underlying mechanisms are unclear. Our work emphasizes the need to better characterize this key stage of human brain development, when cerebrovascular hemodynamics are changing, and standard imaging methods offer limited insight into these processes. We provide important normative data for future comparisons in pathology, where combining macro- and microvascular assessments may better help us prevent, stratify, and treat cerebrovascular disease.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241298588"},"PeriodicalIF":4.9,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142620953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential vulnerability among cell types in the neurovascular unit: Description and mechanisms. 神经血管单元中不同类型细胞之间的脆弱性差异：描述与机制

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-09 DOI: 10.1177/0271678X241299960

Allison Brookshier, Patrick Lyden

引用次数: 0

Sensitivity assessment of QSM+qBOLD (or QQ) in detecting elevated oxygen extraction fraction (OEF) in physiological change. 对 QSM+qBOLD（或 QQ）检测生理变化中氧萃取分数（OEF）升高的灵敏度进行评估。

IF 4.9 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-05 DOI: 10.1177/0271678X241298584

Praveena Elanghovan, Thanh Nguyen, Pascal Spincemaille, Ajay Gupta, Yi Wang, Junghun Cho

{"title":"Sensitivity assessment of QSM+qBOLD (or QQ) in detecting elevated oxygen extraction fraction (OEF) in physiological change.","authors":"Praveena Elanghovan, Thanh Nguyen, Pascal Spincemaille, Ajay Gupta, Yi Wang, Junghun Cho","doi":"10.1177/0271678X241298584","DOIUrl":"https://doi.org/10.1177/0271678X241298584","url":null,"abstract":"The study investigated the sensitivity of a novel MRI-based OEF mapping, quantitative susceptibility mapping plus quantitative blood oxygen level-dependent imaging (QSM+qBOLD or QQ), to physiological changes, particularly increased oxygen extraction fraction (OEF) by using hyperventilation as a vasoconstrictive stimulus. While QQ's sensitivity to decreased OEF during hypercapnia has been demonstrated, its sensitivity to increased OEF levels, crucial for cerebrovascular disorders like vascular dementia and Parkinson's disease, remains unexplored. In comparison with a previous QSM-based OEF, we evaluated QQ's sensitivity to high OEF values. MRI data were obtained from 11 healthy subjects during resting state (RS) and hyperventilation state (HV) using a 3 T MRI with a three-dimensional multi-echo gradient echo sequence (mGRE) and arterial spin labeling (ASL). Region of interest (ROI) analysis and paired t-tests were used to compare OEF, CMRO2 and CBF between QQ and QSM. Similar to QSM, QQ showed higher OEF during HV compared to RS: in cortical gray matter, QQ-OEF and QSM-OEF was 36.4<math><mo> </mo><mo>±</mo><mo> </mo></math>4.7% and 35.3<math><mo> </mo><mo>±</mo><mo> </mo></math>12.5% at RS and 45.0<math><mo> </mo><mo>±</mo><mo> </mo></math>11.6% and 45.0<math><mo> </mo><mo>±</mo><mo> </mo></math>14.8% in HV, respectively. These findings demonstrate QQ's ability to detect physiological changes and suggest its potential in studying brain metabolism in neurological disorders.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241298584"},"PeriodicalIF":4.9,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impact of intracranial hypertension and cerebral perfusion pressure on spreading depolarization. 颅内高压和脑灌注压对展期去极化的影响

IF 5.4 2区医学

Journal of Cerebral Blood Flow and Metabolism Pub Date : 2024-11-05 DOI: 10.1177/0271678X241296799

Takuma Nishimoto, Fumiaki Oka, Takao Inoue, Hiroshi Moriyama, Reo Kawano, Michiyasu Suzuki, David Y Chung, Cenk Ayata, Hideyuki Ishihara

{"title":"Impact of intracranial hypertension and cerebral perfusion pressure on spreading depolarization.","authors":"Takuma Nishimoto, Fumiaki Oka, Takao Inoue, Hiroshi Moriyama, Reo Kawano, Michiyasu Suzuki, David Y Chung, Cenk Ayata, Hideyuki Ishihara","doi":"10.1177/0271678X241296799","DOIUrl":"10.1177/0271678X241296799","url":null,"abstract":"Spreading depolarization (SD) develops after stroke and traumatic brain injury and may contribute to secondary brain damage. These diseases are often accompanied by intracranial hypertension, but little is known about the effects of intracranial pressure (ICP) on SD. Here, we study the effect of increased ICP on hemodynamic and metabolic response to SD in rats. SDs were triggered at different ICPs and cerebral perfusion pressures (CPP). The regional cerebral blood flow (rCBF), partial pressure of brain tissue oxygen (PbtO2), cerebral extracellular glucose and lactate concentrations were recorded. Fluoro-Jade staining was used to quantify neuronal injury in cortex. At high ICP (50 mmHg) with low CPP (30 mmHg), rCBF and PbtO2 were monophasically decreased in contrast to a monophasically increased pattern under normal conditions. Neuronal death increased in both hemispheres but much more on the side where SDs were triggered. At high ICP (50 mmHg) with normal CPP (70 mmHg), CBF and metabolism during SD did not differ from baseline, and neuronal death did not increase even on the side of SD induction. These data suggest that maintaining CPP at 70 mmHg, even when the ICP is as high as 50 mmHg, preserves normal blood flow and metabolism during SD events and prevents neuronal degeneration.","PeriodicalId":15325,"journal":{"name":"Journal of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X241296799"},"PeriodicalIF":5.4,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142583093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0