Fragile Endothelium and Brain Dysregulated Neurochemical Activity in COVID-19.
Abdulrahman AlharthyFahad FaqihiZiad A MemishDimitrios KarakitsosPublished in: ACS chemical neuroscience (2020)
Immune system and renin-angiotensin-aldosterone system dysregulation with associated cytokine release syndrome may be a key feature of early stage of SARS-CoV-2 organotropism and infection. Following viral mediated brain injury, dysregulated neurochemical activity may cause neurogenic stress cardiomyopathy, which is characterized by transient myocardial dysfunction and arrhythmias. Cardiomyopathy along with acute acute inflammatory thromboembolism and endotheliitis (fragile endothelium) might at least partially explain the underlying mechanisms of rapidly evolving life-threatening COVID-19. Further studies are clearly required to explore these complex pathologies.
Keyphrases
- sars cov
- brain injury
- cerebral ischemia
- liver failure
- early stage
- subarachnoid hemorrhage
- respiratory syndrome coronavirus
- coronavirus disease
- respiratory failure
- nitric oxide
- heart failure
- angiotensin converting enzyme
- angiotensin ii
- oxidative stress
- drug induced
- aortic dissection
- left ventricular
- squamous cell carcinoma
- blood brain barrier
- deep learning
- radiation therapy
- resting state
- hepatitis b virus
- heat stress
- acute respiratory distress syndrome
- functional connectivity
- atrial fibrillation
- congenital heart disease