The Extracorporeal Bio-Xeno Perfusion (myelo-timo-spleen) in Multi-organ Supportive Therapy (MOST) as a Modulator of Energy, for Immuno Correction Compensatory Anti-Inflammatory Response Syndromes, and Persistent Inflammation, Immuno suppression, Catabolism and Multi-organ Dysfunction

Role Of Acute Vascular Distress Syndrome In The Development Of Multisystem Inflammatory Syndrome In Sars-Cov-2 And Modern Views On The Research And Treatment Of Critical Coronavirus

“…As a result, we arrived at the universal Immunocompromised mechanism (IC CHAOS) of endothelial dysfunction. Which is considered Acute Vascular Distress Syndrome, unable to liquidate Local Inflammatory Response Syndrome (LIRS), and manifested as a trigger for spreading and initiating SIRS, with immune paralyzed Compensatory Anti-Inflammatory Response Syndrome (CARS) [33][34][35][36][37][38][39].…”

“…3) Gas exchange in tissues SvO2 ↑, BE ↑, PvO2 ↑, avSO2 ↓, avPO2 ↓ lactate/pyruvate ↑. At the same time the pressure/volume loop of the trachea is also considered which are presented in 4 types (cucumber, pod, pear, tomato) which means that the more the loop surface is expanded the more the respiratory pattern as well as the definition of the dynamic (Cdyn) and statistical (Cst) compliance confirming damage to the respiratory organs aggravating Mitochondrial Collapse Microcirculatory Mitochondrial Distress Syndrome and Recruitment of Microcirculatory-Mitochondrial in such cases are supplimented with MOST therapy in the EXTRACORPOREAL Life Support Organization (ELSO) with active detoxification methods:1) Alveolar recruitment with respiratory support in special modes of ventilation mainly APRV with permissive hypercapnia at normal pH, 2) Recruitment of Microcirculatory-Mitochondrial (RMM), 3) MOST Extracorporeal Life Support Organization (ELSO) extracorporeal oxygenation ECMO and CO2 elimination by type ECCO2R [74], 4) Active detoxification methods intra and extracorporeal electrochemical ultraviolet (laser) photomodulation of auto blood ultra diafiltration continuous intermittent filtering, hemodialysis, bioimmunoactivation and biodetoxification through the use of extracorporeal bio xenoperfusion (myelo-timospleen), enterosorption, volnerosorption, plasma sorption, plasma exchange, lympho sorption, liquoro sorption, peritoneal dialysis, oxygenation of the liver through the bougienized umbilical vein, hypothermia and others [33,[35][36][37][38][93][94][95][96]107] 5) Modeling of the index of extravascular pulmonary fluid (EVLWI). If EVLWI is <10 mL/kg this indicates alveolar atelectasis, which requires volemic resuscitation, bronchoscopy, alveolar recruitment, and surfactant therapy.…”

Intralipid in the Target Treatment of Lipid Peroxidation Disorder Caused by Oxidative and Nitro- Galogenic Stress in Patients with SARS-Cov2 / COVID / 19

“…Scientists Eldor J., Javid M.J., Zebardast J. has been published [1][2][3][4][5][6][7][8] the successful use of intralipid in postoperative cognitive impairments, the antitoxic effect of local anesthetics during neuraxial anesthesia, and also as an antidote to the toxic manifestations of calcium blockers, and since 2020, the anticovid / 19 effect.Coronavirus enters intracellularly thanks to both the molecule the protein Cluster of Differentiation (CD147) [also called extracellular matrix metalloproteinase inducers (EMMPRIN), or basigin (BSG), and belong to the immunoglobulin superfamily] and the Angiotensin-Converting Enzyme 2 (ACE2) receptors due to immunocompromising (IC) mechanisms. The predominance of the hyperinflammatory response (SIRS), due to the immune-paralysis of the anti-inflammatory response (CARS), manifests itself as IC CHAOS dissonance [9][10]. Vascular-pulmonary tissue is rich in ACE2 receptors, which contributes to rapid damage membranes to endothelium cells and alveocytes and the development of SARS-Cov2 / COVID19 respiratory failure, due to the accumulation of cytokine storm mediators.…”

Intralipid blocks the entry of the SARS-Cov2/COVID/19 virus into cells by maintaining receptor a leucine-rich repeat containing 15 (LRRC15), an angiotensin-converting enzyme 2 receptor competitor.

“…Thus, pharmacodynamically demonstrated not only anti-oxidative and anti-Nitro-Galogenic stress in patients with SARS-Cov2 / COVID /19 but also the antiviral effect of intralipid against SARS-Cov2/COVID/19, which prevents its penetration into cells, maintenance of LRRC15 receptors. Stopping the development of MODS caused by cytokine storm, immune dissonance CHAOS, Systemic Inflammatory Response Syndrome (SIRS) or immune paralysis, Compensatory Anti-inflammatory Response Syndrome (CARS), and Persistent Inflammation, immunosuppression and Catabolism Syndrome (PICS) [7][8][9].…”