糖尿病相关性低血糖PPT.ppt

我们几下来分别看看低血糖是如何影响各个系统的 我们看到近期低血糖发生，CNS脱敏就是阈值下降的另一种说法，直接的损伤就是知觉下降，此时自主神经过渡反应，选择性收缩血管，减少肾脏血流，促进糖尿病肾病的发展，连续的作用，使得自主神经衰竭，导致无意识性低血糖，最终导致心肌梗死风险增加；死亡率增加不过是个附属品。 低血糖对于神经系统的危害我们还仅仅局限在宏观水平，诸如认知功能障碍等等，在微观上的认识我们还远远不足。 下面将从脑组织内环境、神经元损伤等方面来讲述。 低血糖时通过氨基酸脱氨、代谢性酸消耗、乳酸形成等方面的作用使得脑组织内PH升高，形成碱性内环境，直接导致神经元细胞水肿，引起功能障碍，这种作用在短时间内通过酸碱平衡的缓冲对作用，碱环境是可逆的，如长期严重的的低血糖未及时纠正，会导致永久性神经系统损伤甚至死亡。 Auer RN曾在stroke上发表一篇名为Progress review: hypoglycemic brain damage.的综述。这篇综述指出，低血糖时神经元细胞死亡并不仅是由于细胞外环境，而是内生毒素的作用。文章引用电镜下小鼠海马组织在低血糖时改变的例子来说明他的观点。首先来看第一张图： 可以看到在低血糖时（脑电等电位时），10分钟后，海马突触周围的神经元树突线粒体肿胀，影响各突触间的递质释放。宏观上这就是产生认知障碍的原因。 Stroke. 1986 Jul-Aug;17(4):699-708.Links Progress review: hypoglycemic brain damage. Auer RN. The central question to be addressed in this review can be stated as How does hypoglycemia kill neurons? Initial research on hypoglycemic brain damage in the 1930s was aimed at demonstrating the existence of any brain damage whatsoever due to insulin. Recent results indicate that uncomplicated hypoglycemia is capable of killing neurons in the brain. However, the mechanism does not appear to be simply glucose starvation of the neuron resulting in neuronal breakdown. Rather than such an internal catabolic death current evidence suggests that in hypoglycemia, neurons are killed from without, i.e. from the extracellular space. Around the time the EEG becomes isoelectric, an endogenous neurotoxin is produced, and is released by the brain into tissue and cerebrospinal fluid. The distribution of necrotic neurons is unlike that in ischemia, being related to white matter and cerebrospinal fluid pathways. The toxin acts by first disrupting dendritic trees, sparing intermediate axons, indicating it to be an excitotoxin. Exact mechanisms of excitotoxic neuronal necrosis are not yet clear, but neuronal death involves hyperexcitation, and culminates in cell membrane rupture. Endogenous excitotoxins produced during hypoglycemia may explain the tendency toward seizure activity often seen clinically. The recent researc