Institute of General Pharmacology and Toxicology, University Hospital Frankfurt am Main, Goethe-University, Theodor-Stern Kai 7, D-60590 Frankfurt am Main, Germany.
Medicina (Kaunas). 2024 Jan 23;60(2):194. doi: 10.3390/medicina60020194.
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a frequent, debilitating and still enigmatic disease. There is a broad overlap in the symptomatology of ME/CFS and the Post-COVID-19 Syndrome (PCS). A fraction of the PCS patients develop the full clinical picture of ME/CFS. New observations in microvessels and blood from patients suffering from PCS have appeared and include microclots and malformed pathological blood cells. Capillary blood flow is impaired not only by pathological blood components but also by prothrombotic changes in the vascular wall, endothelial dysfunction, and the expression of adhesion molecules in the capillaries. These disturbances can finally cause a low capillary flow and even capillary stasis. A low cardiac stroke volume due to hypovolemia and the inability of the capacitance vessels to adequately constrict to deliver the necessary cardiac preload generate an unfavorable low precapillary perfusion pressure. Furthermore, a predominance of vasoconstrictor over vasodilator influences exists, in which sympathetic hyperactivity and endothelial dysfunction play a strong role, causing the constriction of resistance vessels and of precapillary sphincters, which leads to a fall in capillary pressure behind the sphincters. The interaction of these two precapillary cardiovascular mechanisms causing a low capillary perfusion pressure is hemodynamically highly unfavorable in the presence of a primary capillary stasis, which is already caused by the pathological blood components and their interaction with the capillary wall, to severely impair organ perfusion. The detrimental coincidence of microcirculatory and precapillary cardiovascular disturbances may constitute the key disturbance of the Post-COVID-19 syndrome and finally lead to ME/CFS in predisposed patients because the interaction causes a particular kind of perfusion disturbance-capillary ischemia/reperfusion-which has a high potential of causing mitochondrial dysfunction by inducing sodium- and calcium-overload in skeletal muscles. The latter, in turn, worsens the vascular situation through the generation of reactive oxygen species to close a vicious cycle from which the patient can hardly escape.
肌痛性脑脊髓炎/慢性疲劳综合征（ME/CFS）是一种常见的、使人虚弱且仍然神秘的疾病。ME/CFS 和新冠后综合征（PCS）的症状有很大的重叠。PCS 患者中有一部分会发展为 ME/CFS 的完整临床症状。新的观察结果表明，PCS 患者的微血管和血液中出现了微血栓和畸形的病理血细胞。毛细血管血流受损不仅是由于病理性血液成分，还包括血管壁的促血栓形成变化、内皮功能障碍和毛细血管中黏附分子的表达。这些紊乱最终会导致毛细血管血流减少甚至停滞。由于低血容量和容量血管不能充分收缩以输送必要的心脏前负荷，导致心输出量降低，从而产生不利的低毛细血管前灌注压。此外，存在血管收缩素占优势于血管扩张素的影响，其中交感神经活性和内皮功能障碍起着重要作用，导致阻力血管和毛细血管前括约肌收缩，导致括约肌后面的毛细血管压力下降。这两种毛细血管前心血管机制的相互作用在原发性毛细血管停滞的情况下，对毛细血管灌注压产生了高度不利的影响，这种停滞已经是由病理性血液成分及其与毛细血管壁的相互作用引起的，严重损害了器官灌注。微循环和毛细血管前心血管紊乱的这种有害巧合可能构成新冠后综合征的关键紊乱，并最终导致易感患者发生 ME/CFS，因为这种相互作用导致了一种特殊的灌注紊乱——毛细血管缺血/再灌注，这通过在骨骼肌中引起钠和钙过载，具有很高的引发线粒体功能障碍的潜力。反过来，后者通过产生活性氧物质进一步恶化血管状况，从而形成一个恶性循环，使患者几乎无法逃脱。
