Effects of intracellular pH, blood, and tissue oxygen tension on T1ρ relaxation in rat brain

Effects of intracellular pH, blood, and tissue oxygen tension on T1ρ relaxation in rat brain
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DOI:
10.1002/mrm.10233
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发表时间:
2002-09-01
影响因子:
3.3
通讯作者:
Kauppinen, RA
Kauppinen, RA
中科院分区:
医学3区
文献类型:
--
作者:
Kettunen, MI;Gröhn, OHJ;Kauppinen, RA

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在大鼠脑中研究了细胞内pH(pH(i))、顺磁宏观和微观磁化率对旋转框架(T-1 p)中T-1的影响。通过高碳酸血症诱导细胞内酸中毒,并定量pH(i)、T-1 p、T-2、弥散和脑血容量(CBV)。考虑到CBV的贡献,实质T-1 p延长4.5%归因于pH值(i)下降一个单位引起的组织水松弛变化。发现血T-1 p随血氧饱和度(Y)线性延长。通过BOLD和氧化铁造影剂AMI-227评估了对实质T-1 p的宏观敏感性贡献。来自这些实验的T-1 p数据可以用血管内效应来描述,磁化率梯度对组织水的影响微不足道。组织氧分压(PtO 2)的操纵和监测与微电极,以评估其合理的贡献,显微镜敏感性和放松。实质T-1 p几乎不受PtO 2变化的影响,但T-1在高氧下缩短,T-2在缺氧下表现出负BOLD效应。它表明,pH值,直接调节组织T-1 p,可能通过其对质子交换的影响,但是,无论是BOLD或PtO 2直接影响组织T-1 p。的观察结果进行了讨论,在光的物理化学机制有助于缺血性T-1 p的变化。(C)2002 Wiley-Liss,Inc.
The effects of intracellular pH (pH(i)), paramagnetic macroscopic, and microscopic susceptibility on T-1 in the rotating frame (T-1p) were studied in rat brain. Intracellular acidosis was induced by hypercapnia and pH(i), T-1p, T-2, diffusion, and cerebral blood volume (CBV) were quantified. Taking into account the CBV contribution, a prolongation of parenchymal T-1p by 4.5% was ascribed to a change in tissue water relaxation caused by a one unit drop in pH(i). Blood T-1p was found to prolong linearly with blood oxygenation saturation (Y). The macroscopic susceptibility contribution to parenchymal T-1p was assessed both through BOLD and an iron oxide contrast agent, AMI-227. The T-1p data from these experiments could be described by intravascular effects with insignificant effects of susceptibility gradients on tissue water. Tissue oxygen tension (PtO2) was manipulated and monitored with microelectrodes to assess its plausible contribution to microscopic susceptibility and relaxation. Parenchymal T-1p was virtually unaffected by variations in the PtO2, but T-1 was shortened in hyperoxia and T-2 showed a negative BOLD effect in hypoxia. It is demonstrated that pH, directly modulates tissue T-1p, possibly through its effect on proton exchange; however, neither BOLD nor PtO2 directly influence tissue T-1p. The observations are discussed in the light of physicochemical mechanisms contributing to the ischemic T-1p changes. (C) 2002 Wiley-Liss, Inc.