Abstract
A pericyte-centered hypothesis suggests that embolisms occurring within microvasculature of a neurovascular unit can result in either parenchymal hemorrhage or intravascular congestion. Dysfunctional microvascular pericytes are featured depending on their location in the neurovascular unit. I extend the hypothesis by proposing a concept of pulmonary neurovascular unit (pNVU). In simulating pathophysiology in pulmonary embolisms, acute high-altitude illness and COVID-19, an existing local regulation of microvascular blood flow is believable. This control balances blood flow with oxygen supply to maintain physiological blood oxygen saturation level. We have reported a working module for the neurovascular unit in the sexually dimorphic nucleus of the preoptic area. Pericytes, labeled with alpha-smooth muscle actin immunoreactivity, are significantly denser within the microvasculature of the neurovascular unit in males, signifying their biological functions or potential pathophysiological role in diseases. Noticeably, an illustration provides an explanation of how malfunction of microvascular pericytes causes pulmonary focal hemorrhage, edema or microvascular congestion and thrombi [Fig. 1]. A bypass existing in the pNVU would autonomically deviate blood flow from COVID-19-affected pNVU to other healthy pNVU. Consequentially, systematically applied medicines including chloroquine and/or hydroxychloroquine became valueless due to low concentration of the medicine in the COVID-19-affected regions. Alternatively, a preventive, early antiviral therapy may be efficacious because dysfunctional blood-air exchange precedents and malfunction of pulmonary microcirculation follows. While testing the hypothesis with experimental evidence is urgently needed, supporting therapy aimed at improvement of microcirculation or rebuilding of microvascular pericytes’ physiological function may be recommended during the COVID pandemic.
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