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作者通过4例心肺复苏病人及7只杂种犬动物实验发现均有不同程度血糖增高,认为是内源性儿茶酚胺释放增加和外源性儿茶酚胺的使用,使糖生成增加和组织利用降低,儿茶酚胺还抑制胰岛素的释放和增加对胰岛素的耐受性。它还抑制T_4和T_3的释放和/或转变,从而导致组织对糖的利用降低。在氧合和组织灌注正常的情况下,葡萄糖主要是有氧代谢,在能量代谢中起重要的作用。但在缺血、缺氧的情况下,葡萄糖以酵解途径分解,生成的能量仅是有氧代谢的1/19,并且生成大量乳酸,使细胞内pH降低,影响细胞功能,甚至导致细胞死亡,通过临床观察和实验,作者认为复苏期间高糖血症的存在已经明确,此时输入葡萄糖溶液无疑会加重高糖血症程度,加重缺血后脑损害,初级复苏阶段输入葡萄糖是不适当的,应避免,在高级复苏阶段,可根据血糖值输入适量葡萄糖作为供能物质。
The authors found in 4 cardiopulmonary resuscitation patients and 7 mongrel dogs animal experiments have increased blood glucose to varying degrees, that is, increased release of endogenous catecholamines and exogenous catecholamines use, increased sugar production and tissue utilization, catecholamines also inhibited Insulin release and increased insulin resistance. It also inhibits the release and / or turnover of T_4 and T_3, resulting in reduced tissue utilization of sugar. In the normal oxygenation and tissue perfusion, glucose is mainly aerobic metabolism, plays an important role in energy metabolism. However, in the condition of ischemia and hypoxia, glucose is decomposed by glycolysis and the energy produced is only 1/19 of that of aerobic metabolism, and a large amount of lactic acid is produced, lowering the intracellular pH, affecting cell functions and even cell death Through clinical observation and experiments, the authors believe that the existence of hyperglycemia during the recovery has been clear, then the input glucose solution will undoubtedly aggravate the degree of hyperglycemia, increase ischemic brain damage, glucose input during the initial recovery phase is inappropriate, Should be avoided in the advanced recovery phase, according to the amount of glucose into the amount of glucose as a feeding substance.