HYPERK

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 该项目致力于了解胰岛素诱导的急性低血糖对人脑的生理影响和能量需求。我们在正常人正常血糖(90-105 mg/dl)-低血糖(60 mg/dl)钳夹中使用高场MR灌注和BOLD成像，以建立静息和任务激活脑的脑血流动力学和氧耗动力学。这项研究展示了在正血糖和低血糖条件下的一些非常有趣的发现。特别是，在正常血糖中，我们发现静息脱氧血红蛋白水平(通过R2‘的组织松弛测量来评估)与任务激活引起的血流量呈负相关。这可以被解释为：那些大脑氧提取效率高的志愿者(如果氧气提取高，静态脱氧血红蛋白水平更高)需要较少的血流上升来处理与任务相关的更大的氧气需求这提供了对观察到的R2‘、血流和潜在的大胆信号(到目前为止，通常认为是由于测量误差)中的可变性的生理学解释。 这项研究还表明，即使在相对温和的低血糖水平60 mg/dl，脑血流量也显著增加，从基线的56.8升至64.5‘b18.1ml/100g·min，(p&lt；0.02配对t检验)。在血流量增加的同时，松弛速率R2‘没有有效变化，这意味着在这种情况下，大脑代谢和血流量仍然是耦合的。

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. This projecte focuses on understanding the physiological effects and fuel needs of the human brain in acute insulin induced hypoglycemia. We have used high field MR perfusion and BOLD imaging in a euglycemic (90-105mg/dl)-hypoglycemic (60mg/dl) clamp in normal human subjeccts to establish the dynamics of cerebral blood flow, oxygen consumption in the resting and task-activated brain. This study has demostrated some very interesting findings under both the euglycemic and hypoglycemic conditions. In particular, in euglycemia we have found that the resting deoxyhemoglobin levels (as evaluated by tissue relaxation measure of R2') is inversely related to the task-activated provoked blood flow. This can be interpreted as: those volunteers who have high efficiency of cerebral oxygen extraction (static deoxyhemoglobin levels are greater if the extraction of oxygen is high) need less of a rise in blood flow to handle the greater demand of oxygen associated with a task This provides a physiological interpretation to the observed variability in R2', flow and potentially BOLD signals (which thus far has been generally assumed to be due to measurement error). This study has also demonstrated that even at a relatively mild hypoglycemic level of 60mg/dl, there is significant rise in cerebral blood flow, from a baseline of 56.8 to 64.5'b18.1ml/100g-min, (p<0.02 paired t-test). While the blood flow increase is seen, there is no effective change in the relaxation rate R2', implying that cerebral metabolism and blood flow remain coupled under these conditions.