The Induction of the Heat Shock Protein under the Hypoxic Condition

众所周知，热休克蛋白（HSP）是对各种应激的诱导反应，而不仅仅是热休克，这是该蛋白名称的由来。诱导应力之一是缺血状态。在本研究中，我们使用之前研究中使用的5%吸氧缺氧模型和暂停呼吸机2分钟缺氧模型来研究低氧条件下热休克诱导的局部性。此外，我们还采用免疫印迹技术定量地说服了热休克蛋白诱导的波动。在沙鼠缺血模型中，本实验和文献报道均能强烈诱导热休克蛋白。另一方面，在大鼠缺氧模型中，甚至在大鼠缺血模型中，HSP的诱导作用都是轻微的。这一结果有两个可能的原因。此前有报道称，在低氧条件下，老鼠是一种比较强壮的动物。因此，HSP在缺氧大鼠脑中的诱导作用很小。另一个原因是，与脑缺血模型不同，我们的实验模型在低氧条件下伴随着心率的下降。因此，对整个身体施加影响。像这样的不完全缺血对消化器官系统尤其是小肠来说是致命的打击。Acker等人报告说，在血流量减少的情况下，血流优先流向大脑和心脏。因此，这些器官在不完全缺血中受到保护。当缺氧负荷程度较强时，HSP的诱导增加。它在一两天内达到顶峰。在发生严重缺血之前先进行弱缺血，就会出现缺血耐受现象。我们尝试在轻度缺氧事件后的一天内进行第二次负荷。HSP肯定是诱导的，但损伤是累积性的，而不是获得耐受性。虽然在小肠和盲肠可见充血和出血，但即使在这种情况下，分布在肠的神经末梢的神经细胞也没有变化。热休克蛋白获得的缺血耐受性可能仅限于一个神经细胞。少

It is known that heat shock protein (HSP) is induced responding to various stresses not only a heat shock which is the origin of a name of this protein. One of inducible stresses is the ischemic condition. In this study we investigate the locality of HSP induction under the low oxygen condition using a hypoxic model of 5 % oxygen inhalation that we have used since before in this research and 2 min anoxia model suspending the ventilator. Additionally, we persuaded the fluctuation of HSP induction quantitatively by the method of immunoblotting technique. In the ischemic model of gerbil the HSP was induced strongly in our experiment as well as previously reported. On the other hand, the induction of HSP was slight in the rat hypoxic model and even in the rat ischemic model. Two reasons are conceivable to this result. There are some reports since before that rat is a comparatively strong animal species in the low oxygen condition. Therefore,HSP induction was small in hypoxic rat's brain. A … More nother reason is that our experiment model of low oxygen condition accompanies a decrease of the heart rate unlike a brain ischemic model. Therefore an influence is exerted on a whole body. The incomplete ischemic condition like this becomes a fatal blow for a digestive organ system particularly the small intestine. Acker et al reported that in the case of a decreased blood flow a blood flow circulates to a brain and a heart preferentially. Therefore,these organs were protected in the incomplete ischemia. When an extent of a hypoxic load is strong,the induction of HSP increased. It peaked in a day or two. The phenomenon of ischemic tolerance well known if it gets weak ischemia done before severe ischemia is suffered. We tried to apply the 2nd load in a day after a mild hypoxic event. Surely the HSP was induced, but the injury was accumulative rather than the acquisition of tolerance. Although congestion and bleeding were seen at the small intestine and the cecum,there was not a change especially in a nerve cell of the nerve terminals which distributes to intestines even in such a case. The acquisition of ischemic tolerance by the HSP may limit to a nerve cell only. Less