PDF(Pubmed)
Abstract：
Postural orthostatic tachycardia syndrome (POTS) is a common accompaniment of a variety of chronic, inflammatory diseases, including long COVID, as are small, insoluble, \'fibrinaloid\' microclots. We here develop the argument, with accompanying evidence, that fibrinaloid microclots, through their ability to block the flow of blood through microcapillaries and thus cause tissue hypoxia, are not simply correlated with but in fact, by preceding it, may be a chief intermediary cause of POTS, in which tachycardia is simply the body\'s exaggerated \'physiological\' response to hypoxia. Similar reasoning accounts for the symptoms bundled under the term \'fatigue\'. Amyloids are known to be membrane disruptors, and when their targets are nerve membranes, this can explain neurotoxicity and hence the autonomic nervous system dysfunction that contributes to POTS. Taken together as a system view, we indicate that fibrinaloid microclots can serve to link POTS and fatigue in long COVID in a manner that is at once both mechanistic and explanatory. This has clear implications for the treatment of such diseases.
摘要：
体位性心动过速综合征(POTS)是多种慢性、炎症性疾病，包括长COVID，因为很小，不溶性,“纤维蛋白样”微凝块。我们在这里提出论点，伴随着证据，纤维蛋白样微凝块，通过它们阻断血液通过微毛细血管的流动，从而导致组织缺氧的能力，不仅与相关，而且事实上，在它之前，可能是POTS的主要中介原因，其中心动过速只是身体对缺氧的夸大的“生理”反应。类似的推理解释了术语“疲劳”下的症状。已知淀粉样蛋白是膜破坏剂，当它们的目标是神经膜时，这可以解释神经毒性以及导致POTS的自主神经系统功能障碍。作为一个系统视图，我们表明，纤维蛋白样微凝块可以将POTS与长COVID的疲劳联系起来，其方式既是机制性的，也是解释性的。这对于此类疾病的治疗具有明显的意义。
