Kurantsin-Mills J, Cassidy M M, Stafford R E, Weglicki W B
Department of Medicine, George Washington University Medical Center, Washington, DC 20037, USA.
Br J Nutr. 1997 Nov;78(5):845-55. doi: 10.1079/bjn19970200.
Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-alpha). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1-2) and chronic phases (week 3-4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.
以缺镁（Mg-D）饮食喂养的啮齿动物会出现心肌病性病变以及其他类型的心血管功能障碍。在大鼠中，心肌的炎性细胞浸润在第1周开始出现，并且在Mg-D饮食喂养的第3周和第4周病变广泛发展。尽管Mg-D心肌病的病因机制尚不清楚，但我们之前报道过，一旦血浆镁显著降低，病理生理过程最早的分子标志物之一就是血浆P物质、降钙素基因相关肽和前列腺素E2升高，随后是组胺和炎性细胞因子（白细胞介素-1、白细胞介素-6和肿瘤坏死因子-α）。为了评估特定循环炎性细胞亚群在Mg缺乏诱导的心肌病中观察到的病理生理变化机制中的潜在作用，我们通过流式细胞化学分析了这些细胞。Mg-D大鼠的白细胞亚群池逐渐增加。循环中嗜中性粒细胞和淋巴细胞水平升高似乎在炎症反应的急性期（第1 - 2周）和慢性期（第3 - 4周）都起作用；另一方面，单核细胞、嗜酸性粒细胞、嗜碱性粒细胞以及在染色涂片中呈淋巴细胞样的大未染色细胞在第3周和第4周显著增加，因此对慢性炎症期有影响。循环白细胞亚群的变化与心肌病性病变的时间进程平行，特别是在第3周和第4周。由于在心肌组织内白细胞浸润和沉积之前有明显的嗜中性粒细胞增多，微血管屏障的改变可能是这种神经源性炎症模型中心肌病的一个先决条件。
