Abstract
BackgroundThe truly popular consequence of management with the blood-thinning-drug, causation of lower blood-viscosity (BV), is bleeding and very frequently asymptomatic-hemorrhage (AH) and the acute-heart-failure (AHF) happen without any preceding symptoms.ObjectivesOur aim was to develop an infallible closed-form analytical model for demonstrating the proof of the concept of the Sanal flow choking in cardiovascular system (CVS) causing AH and AHF by correlating the blood pressure ratio (BPR), biofluid/blood-heat-capacity-ratio(BHCR), blood viscosity(BV), stenosis (in terms of vessel cross-sectional area (VCA)) and ejection fraction(EF). For establishing the proof of the concept we were planned in vitro and in silico studies. MethodsThe closed-form-analytical-methodology is used herein to establish the proof of the concept of Sanal-flow-choking. In vitro method is invoked for the speciation analyses of blood samples of healthy subjects (human being/Guinea pig) for the BHCR estimation. In silico method is used for demonstrating the asymptomatic pressure-overshoot in an artery due to the Sanal flow choking and shock wave generation. ResultsThe closed-form analytical, in vitro and in silico results are presented herein to establish the proof of the concept of internal flow choking in CVS causing cardiovascular risk without prejudice to the percutaneous coronary intervention (PCI). The analytical models reveal that the relatively high and low BV are risk factors of AH and AHF. In vitro study shows that nitrogen(N2), oxygen(O2), carbon dioxide(CO2) and argon(Ar) gases are predominant in fresh-blood samples of the healthy human-being and Guinea-pig at a temperature range of 37-400 C (98.6-1040 F), which increases the risk of flow-choking leading to AH and AHF. The thermal-tolerance level in terms of BHCR of Guinea-pig is found higher than the human being. In silico results demonstrated the Sanal flow choking and shock wave generation in an artery with the divergent/bifurcation region. ConclusionsAn overdose of blood-thinning drug for reducing the blood-viscosity(BV) augments Reynolds number leading to high-turbulence and enhanced boundary-layer-blockage(BLB), which increases the chances of cavitation and the Sanal-flow-choking leading to the shock wave and pressure-overshoot causing memory effect (stroke history) in viscoelastic vessels. Designing the precise blood-thinning regimen is vital for attaining the desired therapeutic efficacy and negating undesirable flow-choking leading to AH and AHF. Herein we established that the disproportionate blood-thinning treatment increases the risk of the Sanal-flow-choking due to the enhanced BLB factor. The cardiovascular risk could be diminished by concurrently lessening the BV and flow turbulence by rising thermal-tolerance-level in terms of BHCR or by decreasing the BPR. Condensed AbstractHerein, we provide a proof of the concept to establish that such asymptomatic diseases are due to the boundary-layer-blockage (BLB) induced flow choking (Sanal-flow-choking) at a critical blood-pressure-ratio (BPR). When the pressure of the nanoscale-fluid increases, average-mean-free-path decreases and thus, the Knudsen number reduces leading to a no-slip boundary condition with compressible-viscous (CV) flow effect. Sanal-flow-choking is a CV flow effect creating a physical situation of the sonic-fluid-throat, at a critical BPR. We concluded that AH and AHF are transient-events due to flow-choking, and not an illness. The cardiovascular risk could be diminished by concurrently lessening the BV and flow turbulence by rising thermal-tolerance-level in terms of BHCR or by decreasing the BPR.
Prokaryotic Expression and In Vitro Functional Analysis of IL-1β and MCP-1 from Guinea Pig