BIOLOGICAL VARIATIONS OF REACTIVE HYPEREMIA IN CRITICALLY ILL PATIENTS

危重患者反应性高血症的生物学变异

基本信息

  • 批准号:
    7604916
  • 负责人:
  • 金额:
    $ 0.14万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2007
  • 资助国家:
    美国
  • 起止时间:
    2007-03-01 至 2007-09-16
  • 项目状态:
    已结题

项目摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Reactive hyperemia (RH) refers to arterial dilation in response to temporary stagnant ischemia, and is mediated in part through release of nitric oxide from endothelial cells. Near Infra-Red Spectroscopy (NIRS) can detect capillary hemoglobin concentration as well as capillary hemoglobin oxygen saturation. Tissue oxygen saturation falls during stagnant ischemia, and rises when flow returns; the rate of increase in tissue oxygen saturation represents reactive hyperemia. Our initial work has shown tht microvascular responses to reactive hyperemia are impaired in some critically ill patients. What is not known is the anatomic variation of these findings, and whether invasive catheters alter the blood flow response distal to the catheter. Furthermore, literature suggests that locally released soluble factors may be responsible for the microvascular responses in reactive hyperemia. We propose a pilot study to examine the anatomic and iatrogenic associated variation of microvascular reactive hyperemia in critically ill patients that have clinically indicated radial arterial catheters. Subjects will have NIRS measurements of reactive hyperemia in three locations, including one leg and both left and right forearms. Blood will be collected (ICU subjects only) before and during reactive hyperemia, simultaneously from arterial and venous catheters that demarcate the monitored tissue bed, and analyzed for candidate soluble factors purported to be associated with reactive hyperemia.
这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者(PI)可能从另一个NIH来源获得了主要资金, 因此可以在其他CRISP条目中表示。所列机构为 研究中心,而研究中心不一定是研究者所在的机构。 反应性充血(RH)是指对暂时性停滞性缺血作出反应的动脉扩张,并且部分通过内皮细胞释放一氧化氮介导。 近红外光谱(NIRS)可以检测毛细血管血红蛋白浓度以及毛细血管血红蛋白氧饱和度。 组织氧饱和度福尔斯在停滞性缺血期间下降,当血流恢复时上升;组织氧饱和度的增加率代表反应性充血。 我们的初步工作表明,在一些危重病人中,微血管对反应性充血的反应受损。 目前尚不清楚的是这些发现的解剖变异,以及侵入性导管是否会改变导管远端的血流反应。 此外,文献表明局部释放的可溶性因子可能是反应性充血中微血管反应的原因。 我们提出了一个试点研究,以检查解剖学和医源性相关的变化,微血管反应性充血的危重病人,有临床指征的桡动脉导管。 受试者将在三个位置(包括一条腿和左右前臂)进行反应性充血的NIRS测量。 在反应性充血之前和期间,同时从划分监测组织床的动脉和静脉导管采集血液(仅ICU受试者),并分析据称与反应性充血相关的候选可溶性因子。

项目成果

期刊论文数量(0)
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科研奖励数量(0)
会议论文数量(0)
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KEVIN C DOERSCHUG其他文献

A CASE OF COMPLICATIONS FROM COVID-19: DIFFUSE ALVEOLAR DAMAGE TO ANGIOINVASIVE ASPERGILLOSIS
  • DOI:
    10.1016/j.chest.2023.07.4000
  • 发表时间:
    2023-10-01
  • 期刊:
  • 影响因子:
  • 作者:
    SYDNEY M BOWMASTER;KEVIN C DOERSCHUG
  • 通讯作者:
    KEVIN C DOERSCHUG
COMPLICATIONS OF ENDOTRACHEAL INTUBATION: OSCILLATING ENDOBRONCHIAL OBSTRUCTION CAUSING DANGEROUS DYSSYNCHRONY
  • DOI:
    10.1016/j.chest.2023.07.1362
  • 发表时间:
    2023-10-01
  • 期刊:
  • 影响因子:
  • 作者:
    MILES D. HAGNER;DESMOND D. BARBER;KEVIN C DOERSCHUG
  • 通讯作者:
    KEVIN C DOERSCHUG
MIMICS OF SEPSIS: A RARE COMPLICATION OF CEFTRIAXONE PRESENTING WITH CHOLESTATIC LIVER INJURY AND DRUG-INDUCED HEMOLYTIC ANEMIA
  • DOI:
    10.1016/j.chest.2023.07.1375
  • 发表时间:
    2023-10-01
  • 期刊:
  • 影响因子:
  • 作者:
    YANA ZEMKOVA;KEVIN C DOERSCHUG;JOSALYN L CHO
  • 通讯作者:
    JOSALYN L CHO

KEVIN C DOERSCHUG的其他文献

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{{ truncateString('KEVIN C DOERSCHUG', 18)}}的其他基金

RAS dysregulation during HDIL2: a clinical model of sepsis-induced lung injury
HDIL2 期间 RAS 失调:脓毒症引起的肺损伤的临床模型
  • 批准号:
    9130382
  • 财政年份:
    2015
  • 资助金额:
    $ 0.14万
  • 项目类别:
Mechanisms and Meanings of Impaired Microvascular Responses in Human Sepsis
人类脓毒症微血管反应受损的机制和意义
  • 批准号:
    7894725
  • 财政年份:
    2009
  • 资助金额:
    $ 0.14万
  • 项目类别:
Mechanisms and Meanings of Impaired Microvascular Responses in Human Sepsis
人类脓毒症微血管反应受损的机制和意义
  • 批准号:
    8512769
  • 财政年份:
    2009
  • 资助金额:
    $ 0.14万
  • 项目类别:
Mechanisms and Meanings of Impaired Microvascular Responses in Human Sepsis
人类脓毒症微血管反应受损的机制和意义
  • 批准号:
    7581290
  • 财政年份:
    2009
  • 资助金额:
    $ 0.14万
  • 项目类别:
Mechanisms and Meanings of Impaired Microvascular Responses in Human Sepsis
人类脓毒症微血管反应受损的机制和意义
  • 批准号:
    8307936
  • 财政年份:
    2009
  • 资助金额:
    $ 0.14万
  • 项目类别:
Mechanisms and Meanings of Impaired Microvascular Responses in Human Sepsis
人类脓毒症微血管反应受损的机制和意义
  • 批准号:
    8150612
  • 财政年份:
    2009
  • 资助金额:
    $ 0.14万
  • 项目类别:
RENIN-ANGIOTENSIN SYSTEM AND VASCULAR REACTIVITY IN SEVERE SEPSIS
严重脓毒症中的肾素-血管紧张素系统和血管反应性
  • 批准号:
    7604871
  • 财政年份:
    2007
  • 资助金额:
    $ 0.14万
  • 项目类别:
OXIDATIVE STRESS AND PERFUSION IN SEPSIS
脓毒症中的氧化应激和灌注
  • 批准号:
    7604857
  • 财政年份:
    2007
  • 资助金额:
    $ 0.14万
  • 项目类别:
OXIDATIVE STRESS AND PERFUSION IN SEPSIS
脓毒症中的氧化应激和灌注
  • 批准号:
    7377076
  • 财政年份:
    2006
  • 资助金额:
    $ 0.14万
  • 项目类别:
PILOT STUDY OF ENTERIC PERFUSION DURING EXERCISE IN HYPOXIC CONDITIONS
缺氧条件下运动时肠灌注的试点研究
  • 批准号:
    7201354
  • 财政年份:
    2005
  • 资助金额:
    $ 0.14万
  • 项目类别:

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