Vallance B D, Hume R, Weyers E
Br Heart J. 1978 Jan;40(1):64-68. doi: 10.1136/hrt.40.1.64.
After an acute myocardial infarction, there is an apparent acute fall in leucocyte ascorbic acid associated with an acute rise in white blood cells and serum cortisol. The apparent fall in leucocyte ascorbic acid is the result of the granulocytosis which occurs after the infarction. Estimations of ascorbic acid disclose that the granulocyte contains approximately half the ascorbic acid of the lymphocyte. When the granulocytosis subsides, the new population of white blood cells is depleted of ascorbic acid for at least 56 days, reflecting tissue desaturation which can be corrected by ascorbic acid supplements. Tissue desaturation is also reflected in subnormal serum ascorbic acid levels which persist also unless ascorbic acid supplements are given. Observations on normal subjects given infusions of tetracosactrin (Synacthen) show that adrenal stimulation can produce a similar rise in white blood cells and an apparent fall in leucocyte ascorbic acid concentration with the exception that the serum ascorbic acid remains unaltered. Therefore, while adrenal stimulation can mimic 'stress' with regard to the changes in the white blood cells, tissue depletion of ascorbic acid as reflected in the white blood cells and serum after a myocardial infarction requires a focus of damaged tissue.
急性心肌梗死后，白细胞中的抗坏血酸明显急性下降，同时白细胞和血清皮质醇急性升高。白细胞抗坏血酸的明显下降是梗死发生后粒细胞增多的结果。抗坏血酸的测定表明，粒细胞所含抗坏血酸约为淋巴细胞的一半。当粒细胞增多症消退时，新的白细胞群体至少56天缺乏抗坏血酸，这反映了组织不饱和状态，可通过补充抗坏血酸来纠正。组织不饱和状态也反映在血清抗坏血酸水平低于正常，除非给予抗坏血酸补充剂，否则这种情况会持续存在。对输注二十四肽促皮质素（合成促皮质素）的正常受试者的观察表明，肾上腺刺激可使白细胞产生类似的升高，白细胞抗坏血酸浓度明显下降，但血清抗坏血酸保持不变。因此，虽然肾上腺刺激在白细胞变化方面可模拟“应激”，但心肌梗死后白细胞和血清中反映的抗坏血酸组织耗竭需要有受损组织部位。
