Genesis of Antibiotic Resistance (AR) LXI:Turbulence Modelling: Mechanisms of E‐Complex [Ca2+/Mg2+Ecto‐ATPase (EC 3.6.1.15) /E‐NTPDase (NTPDase1) EC 3.6.1.6) regulated E‐kinase/PKA‐induced E‐NTPase∞CD36/E‐NTPDase∞CD39/CD73 Oligomeric Complex (E complex @ Ec)] activated leucocytes‐platelets‐erythrocytes (LPE) Augment “Hairpin Vortices of Tollmien–Schlichting waves(TSW)” for laminar to turbulent transition

Abstract

Here we present a plausible pathophysiological cascade initiating the transition of laminar to turbulent flow as a cause for, but not limiting other unknown clinical variable for an increased mortality rate in NCT01663701‐SSSP‐2. Based on the correlation between Perfused Boundary Region (PBR) and number of rolling leukocytes in post‐capillary venules in sepsis cohort, the PBR has been suggested as an index of glycocalyx shedding enhancing the leukocyte–endothelium interaction. NCT00793442 observed that average number of rolling leukocytes was 26 in the sepsis group and 9.8 in the non‐infected control group per field. The sepsis cohort, had an increased number of adhered leukocytes in non‐survivors compared to non‐sepsis cohort. Correlation of aforesaid hemodynamic parameters implicating the LPE impacting the damaged endothelial surface, tissue perfusion and organ dysfunction due to septic shock not withstanding “DIC”. After the LPE start forming in the arterial end of the capillary bed, rolling up and formation of vortex. Amplification of LPE involves the formation of a single vortex of greater strength through the pairing of vortices. As the vortices progress deregulating starling forces from the arterial region in the capillary bed towards the venous end, vortices to become heavily distorted and less distinct. Due to presence of damaged endothelial surface with adhered LPE, flow breaks down, generating a large number of small‐scale eddies, and the flow undergoes rapid transition to the fully turbulent regime. Mixing layers and wakes behind bluff bodies exhibit a sequence of events, leading to transition and turbulent flow. It has known that initial linear instability occurs around Rex, crit = 91 000 forming an unstable two‐dimensional disturbances are called TSW waves. Increased LPE adhesion, endothelial damage, possible scar tissue formation and/or necrotic lesions in the capillary bed are likely to be large enough a secondary, non‐linear, instability mechanism causes the TSW to become three‐dimensional and finally evolve into hairpin Λ‐vortices. In the most common mechanism of transition, would be K‐type transition, where the hairpin vortices are aligned. The hairpin vortices with a high shear region is induced which intensifies, elongates and rolls up. Regions of intense and highly localized changes occur at random times and locations near the damaged endothelial wall. These turbulent spots are carried along with the flow and grow by spreading across the capillary bed, which causes increasing amounts of laminar fluid to take part in the turbulent motion. Under progressive hypotensive state induced endothelial damage and abrupt collapse of interstitial space would result CCP ensuing hypoxia. Such scenario may have been the cause for mortality in NCT01663701‐SSSP‐2.Support or Funding InformationSupported by professional development funds and in part CME activities of Subburaj KannanMD PhD for www.aaets.org