Role of pCO2 (AV gap) of Multi Organ Dysfunction Syndrome
dc.contributor.author | Tarabrin, O. | |
dc.contributor.author | Vasiliev, I. | |
dc.contributor.author | Groppa, S. | |
dc.contributor.author | Ghicavii, V. | |
dc.contributor.author | D' Ambra, Mirta | |
dc.contributor.author | Friptu, V. | |
dc.contributor.author | Gladun, S. | |
dc.contributor.author | Diug, V. | |
dc.contributor.author | Spinei, L. | |
dc.contributor.author | Vartanov, V. | |
dc.contributor.author | Stavrou, I. | |
dc.contributor.author | Litarczek, G. | |
dc.date.accessioned | 2023-04-25T11:56:36Z | |
dc.date.available | 2023-04-25T11:56:36Z | |
dc.date.issued | 2019 | |
dc.description | Vasiliev I. Role of pCO2 (AV gap) of Multi Organ Dysfunction Syndrome / I. Vasiliev, S. Groppa, V. Ghicavii, I. Stavrov, O. Tarabrin et al. // Journal of Biomedical and Pharmaceutical Sciences. - 2019. - Vol. 2, Issue 2. - P. 1–5. | en_US |
dc.description.abstract | Recruitment of Microcirculatory-Mitochondrial (RMM) reduces Microcirculatory-Mitochondrial Distress Syndrome (MMDs), and Syndrome of Multi-Organ Dysfunction (MODs), by accelerated speed of delivery and return of blood flow which directly leads to a decrease in tissue hypoxia marker pCO2 (AV gap) and respectively with ↓ many other Endogenous Toxic Substances (ETS). In cases of pulmonary damage with ↑ pCO2 & ↓ Oxygenation Index PaO2 /FiO2 ↓ 300 the development of Acute Respiratory Distress Syndrome (ARDs), MMDs are also aggravated at ↑ with pCO2 AV gap. RMM also needs additional support of Multiple Organ Therapies-Multi-Organ Supportive Therapy (MOST), Alveolar Recruitment, Extracorporeal Life Support Organization (ELSO), Modeling of the Index of Extravascular Lung Fluid, EVLWI, Th4 - Th5 Thoracic Epidural Block, Active detoxification methods. The absence of decreasing of the pCO2 tissue hypoxia marker at the pCO2 AV gap ↓ 5.0 mmHg, after RMM proves the mitochondrial eu-energetic metabolic remodeling with the elimination of the hypo(an)ergic mitochondria performed by lysosomal clearance (mitophagy) makes the predominance eu-ergic mitochondria with the normalization of mitochondrial Ca++-uniporter-channel and mitochondrial permeability pore transition which productively inactivate the toxic forms of oxygen and nitrogen. | en_US |
dc.identifier.citation | Vasiliev I. Role of pCO2 (AV gap) of Multi Organ Dysfunction Syndrome / I. Vasiliev, S. Groppa, V. Ghicavii, I. Stavrov, O. Tarabrin et al. // Journal of Biomedical and Pharmaceutical Sciences. - 2019. - Vol. 2, Issue 2. - P. 1–5. | en_US |
dc.identifier.uri | https://hdl.handle.net/11300/24499 | |
dc.language.iso | en | en_US |
dc.subject | Microcirculatory-Mitochondrial Distress Syndrome | en_US |
dc.subject | Microcirculatory-Mitochondrial Recruitmen | en_US |
dc.subject | Multiple Organ Dysfunction Syndrome | en_US |
dc.subject | Marker of Tissue Hypoxia pCO2 (AV gap) | en_US |
dc.subject | Acute Respiratory Distress Syndrome | en_US |
dc.subject | Multi Organ Supportive Therapy | en_US |
dc.subject | Mitochondral Remodeling | en_US |
dc.subject | Mitochondrial Ca++ Uniporter Channel | en_US |
dc.subject | Toxic forms of Oxygen and Nitrogen | en_US |
dc.subject | Nascular Compliance ΔVP | en_US |
dc.title | Role of pCO2 (AV gap) of Multi Organ Dysfunction Syndrome | en_US |
dc.type | Article | en_US |
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