De-installation of the multi-organic dysfunction syndrome by associating the mitochondrial microcirculatory recruitment with multiple organ support therapy in extracorporeal life support organization

Abstract

Introduction: The installation of macro-circulation centralization in MODS triggering in critical obstetric states caused by intravascular coagulation, HELLP, shock, SIRS, septicemia, CARS, embolism of the pulmonary artery, cerebral and other, – microcirculation will also be seriously damaged, as the reduction in blood flow perfusion affects the venous return to eliminate the waste of cellular metabolism, where a marker of tissue hypoxia is the increase in carbon dioxide. Objective: The mitochondrial microcirculatory recruitment with multiple organ support therapy in extracorporeal life support. Material and methods: This is a retrospective study over 35 years, in a lot of critical situations in obstetrics. Results: This disorder generates microcirculatory - mitochondrial distress syndrome, mitochondrial energy collapse, which can be recovered by microcirculation – mitochondrial recruitment to optimize systemic perfusion pressure (SPP), in turn, dependent on mean blood pressure and capillary resistance. Microcirculation - mitochondrial recruitment decentralizes macrocirculation benefits microcirculation in the capillary-cell metabolic area. In cases of manifestation respiratory-pulmonary CO2 ↑ (ARDS), confirmed ↓ PaO2/FiO2 ↓300 to Acute Respiratory Distress Syndrome (Berlin definition, 2012), thus also aggravates the microcirculatory-mitochondrial distress syndrome, mitochondrial collapse and the recruitment of the microcirculatory-mitochondrial is supplemented with multi-organ support therapy (MOST). 1. Alveolar recruitment through respiratory support in specific ventilation modes, predominantly APRV, with permissive hypercapnia at a normal pH. 2) MOST - extracorporeal with technical support. Extracorporeal Life Support Organization – ELSO. 3) Modeling of extra-vascular pulmonary fluid; 4) Th4 - Th5 thoracic epidural block. Conclusion: The absence of decreasing of the pCO2 tissue hypoxia marker at the A-V difference after microcirculatory - mitochondrial recruitment, rejects the necrosis /apoptosis, cellular hypo-(an)ergic and proves the mitochondrial eu-energetic metabolic remodeling with the elimination of the hypo (an) ergic mitochondria performed by clearance lysosomal (mitophagy), thus demonstrating eu-ergic mitochondria with the normalization of mitochondrial uniporter-Ca ++ and mitochondrial permeability pore transition, which productively inactivate the toxic forms of oxygen and nitrogen.

Rezumat. Instalarea centralizării macro-circulaţiei în declanşarea MODS în stări critice de obstetrică cauzate de coagularea intravasculară, HELLP, şoc, SIRS, septicemie, CARS, embolie a arterei pulmonare, cerebrală şi altele; - microcirculaţia va fi de asemenea grav afectată, iar perfuzia fluxului sanguin afectează revenirea venoasă pentru a elimina deşeurile de metabolism celular, unde un marker al hipoxiei tisulare este creşterea dioxidului de carbon, la diferenţa A-V. Această tulburare generează sindromul detresei microcirculator – mitocondriale (MMDs), colapsul energetic mitocondrial, care poate fi de-instalat (recuperat) prin recrutarea microcirculator - mitocondrială odată cu optimizarea presiunii de perfuzie sistemică, în dependenţă de tensiunea arterială medie şi rezistenţa capilară. Recrutarea microcirculator - mitocondrială descentralizează macrocirculaţia şi ameliorează microcrculaţia în spaţiul metabolic capilar-celulă. În cazurile de manifestare a ↑CO2-dependent respirator-pulmonar, confirmat ↓ PaO2 / FiO2 ↓ 300 pentru ARDS, sindromul de detresă respiratorie acută (definiţia de la Berlin, 2012), agravează de asemenea, şi sindromul detresei microcirculator-mitocondriale, colapsul mitocondrial iar recrutarea microcirculator - mitocondrială este suplimentată cu terapia de sprijin multi-organ (MOST). 1. Recrutarea alveolară prin suport respirator în moduri de ventilaţie specifice preponderent APRV, cu hipercapnie permisivă la un pH normal. 2) MOST - extracorporal cu suport tehnic în managmentul vital prin sprijin extracorporeal - ELSO. 3) modelarea fluidului pulmonar extra-vascular; 4) Blocul epidural T4-Th5 toracic. Reducerea markerului hipoxiei tisulare pCO2 la diferenţa A-V după recuperarea microcirculator - mitocondrială, respinge necroza / apoptoza, hipo-(an)ergicul celular şi dovedeşte remodelarea metabolică eu-energetică mitocondrială prin eliminarea hipo (an) mitocondriilor ergice efectuate prin clearance-ul lizozomal (mitofagie), demonstrând astfel mitocondriile eu-ergice cu normalizarea tranziţiei porilor permeabilităţii mitocondriale şi canalului uniporter-Ca ++ , care inactivează productiv formele toxice de oxigen şi azot.