Background: In the current proposal, we used the intralipid in standard therapy against COVID / 19 as an energy carrier for parenteral nutrition in critically ill patients. In patients receiving intralipid, there was an accelerated recovery of the lungs, a decrease in markers of endogenous intoxication (EI), tissue hypoxia and an improvement in general condition. In the absence of Intralipid in the intensive care unit, there was a slow recovery of the lungs and a more prolonged improvement in the general condition with the preservation of EI markers (cytolytic enzymes, C-reactive protein, platelets) and tissue hypoxia (pCO2 AV> 6 mm Hg). Collectively, Intralipid has been seen in the targeted LPO treatment plan for oxidative and nitro-galogenic stress in SARS-Cov2 / COVID / 19 patients.

The effectiveness of Intralipid against SARS-Cov2/COVID/19 with Multiple Organ Dysfunction Syndrome (MODS) prevention or regression is described in the original scientific paper [1]. Intralipid at Oxidative and Nitro-Galogenic stress in patients with SARS-Cov2 / COVID /19, favors the predominance of the membrane-cytoprotective action of Reactive Oxygen Species (ROS) / Reactive Nitrogen Species (ROS/RNS) over the membrane-to-destructive action, restoring the balance between [ROS /AS] / [RNS / ANOS]. Membrane-cytoprotective mechanism Intralipid is due to a decrease in ROS and RNS and an increase in the activity of the Antioxidant System (AS) and Anti Nitro Oxidant System (ANOS), stopping lipid peroxidation (LPO), reducing Electro-Ion Membrane Distress Syndrome (Maria&Irina Vasilieva syndrome) [2], accelerates the regeneration of endothelial and epithelial cells of the alveolar acinus, restoring gas-respiratory metabolism and the predominance of physiological cell apoptosis over necrosis. Intralipid at SARS-Cov 2 / COVID / 19 opposes Microcirculatory Mitochondrial Distress syndrome (MMDS) by Microcirculatory - Mitochondrial Recruitment; as a result of which pCO2 (AVgap) <6 mm Hg, since LPO decreases and at the level of mitochondrial membranes, improving the function of Mitochondrial permeability transition pore-dependent Ca uniporter, mPT pore, support energy metabolism, eliminating energy deficits, restoring Extreme / Abnormal myelopoiesis and impaired autophagy (mitophagy). Thus, Intralipid has been shown in the strategy of targeted treatment of LPO in Oxidative and Nitro-Galogenic stress in patients with SARS-Cov2 /COVID / 19.

Ca ++ mPT pore damage leads to ↑ Ca ++ in the mitochondria (M), where Ca ++ pumps ↓H + and ↑pH, through the disordered depolarization ↓electric potential of the internal M membrane, ATP synthesis is also afect, which is manifested by a mitochondrial energy deficit (MED). MED provoke→ cell hypo -anergy→oxidative stress, OS→ collapse M→M swells → osmotic demyelination→membrane rupture M→detritus mass output with large molecule in intermembrane space M→in cell cytosol→apoptosis-inducing factor→cytochrome C→which are the predictors of programmed cell death. Contributing to the increase in blood pressure to OS not only hyperadrenalinemia, but also the reduction of the effect of vasorelaxation by NO, which ↓ as it becomes becomes a trap for the excess oxygen free radicals, especially for oxygen superoxide. Triphosphoric acid (ATP), donated, as an energetic carrier, mitochondrial permeability transition pore-dependent Ca++uniporter, mPT pore, restores the disorder of electrical cardiac potentials: ↓Conductivity, ↑refractoriness of the atrioventricular node, ↓sinus nodule automatism, and primary hypertension, caused by MED and, further, manifested by the microcirculatory and mitochondrial distress syndrome. Simultaneously, ATP influences: Mitochondrial ATP-dependent potassium channel, mitoKATP; acetylcholinedependent potassium channel, KACh cholinergic-M receptor; receptors: Adenosine A1; and purine P2. M myocardial cells create mesh nets that limit the disordered energy flow in the reduced M space, avoiding damage to the entire heart muscle. As a result, M also plays the role of the electroconductivity switch, which protects the heart from the extent of the damage of a "short circuit" in area necrotizing myocardiocytes and M hypoanergic. Hence, the anti-arrhythmogenic effect of ATP-energetic

Hibernation proposed by Irving and Krog (1954) was developed by H. Laborit and P. Huguenard, which, today, is very current and important in modern medicine as neurovegetative correction (NVC): Curative anesthesia, neurovegetative blockade, artificial hibernation, capable of providing the minimal metabolic rate at the parabiosis level, and phylogenetic descending cerebral activity. It is important! NVC is not block-free and inhibits excessive impulses, prevents them from attenuating, and installs normal blood pressure, heart rate, body temperature (T°C), blood (pH), adrenal-cholinergic balance, maintaining hibernation homeostasis. From the multiple neurovegetative correction (NVC) schemes of cerebral insufficiency (CI) of various causes (traumas, onco, stroke, neuroinfections, metabolic, hypoxic, etc.), ongoing 35 years, retrospectively, arranged the pattern, with three essential syndromes manifestation of CI: Diencephal -hyperkinetic (catabolic adrenergic), extrapyramidal -eukinetic (balanced), and mezencephal -hypokinetic (anabolic cholinergic). NVC is multimodal and selective inhibition, correction, and analgesia. Thus, by performing the loco-regional correction of the three symptoms of CI and systemic by appropriate medications, NVC can be obtained. Here we describe, diencephal -hyperkinetic syndrome (catabolic adrenergic) → psychic, motor, and vegetative agitation (↑blood pressure [BP], heart rate [HR], T0C) return to normal by administering the usual doses of dexmedetomidine,D with the influence of G-protein and super selective α2-Adreno agonists, as a cerebrospinal locoregional neurotransmitter, D installs anxiolysis, anesthesia, ↓ T0C (central) produces sedation without inhibiting the respiratory center (important in patients with sleep apnea) and central and systemic cerebral effect, α2-Adreno agonist (previously used clonidine) ↓BP, HR, T0C (peripheral), to optimize systemic perfusion pressure, in turn dependent on mean BP and capillary resistance, also stimulates the elimination by endotheliocytes of the NO vasorelaxant → antioxidant, which catches the superoxide O 2 -, at the same time influencing and mitochondrial permeability transition pore dependent Ca++uniporter, mPT pore.

The effectiveness of Intralipid against SARS-Cov2/COVID/19 with Multiple Organ Dysfunction Syndrome (MODS) prevention or regression is described in the original scientific paper [1]. Intralipid at Oxidative and Nitro-Galogenic stress in patients with SARS-Cov2 / COVID /19, favors the predominance of the membrane-cytoprotective action of Reactive Oxygen Species (ROS) / Reactive Nitrogen Species (ROS/RNS) over the membrane-to-destructive action, restoring the balance between [ROS /AS] / [RNS / ANOS]. Membrane-cytoprotective mechanism Intralipid is due to a decrease in ROS and RNS and an increase in the activity of the Antioxidant System (AS) and Anti Nitro Oxidant System (ANOS), stopping lipid peroxidation (LPO), reducing Electro-Ion Membrane Distress Syndrome (Maria&Irina Vasilieva syndrome) [2], accelerates the regeneration of endothelial and epithelial cells of the alveolar acinus, restoring gas-respiratory metabolism and the predominance of physiological cell apoptosis over necrosis. Intralipid at SARS-Cov 2 / COVID / 19 opposes Microcirculatory Mitochondrial Distress syndrome (MMDS) by Microcirculatory - Mitochondrial Recruitment; as a result of which pCO2 (AVgap) <6 mm Hg, since LPO decreases and at the level of mitochondrial membranes, improving the function of Mitochondrial permeability transition pore-dependent Ca uniporter, mPT pore, support energy metabolism, eliminating energy deficits, restoring Extreme / Abnormal myelopoiesis and impaired autophagy (mitophagy). Thus, Intralipid has been shown in the strategy of targeted treatment of LPO in Oxidative and Nitro-Galogenic stress in patients with SARS-Cov2 /COVID / 19.