Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Observational Study
The Compensatory Reserve Index for Predicting Hemorrhagic Shock in Prehospital Trauma.
Background: The compensatory reserve index (CRI) is a noninvasive, continuous measure designed to detect intravascular volume loss. CRI is derived from the pulse oximetry waveform and reflects the proportion of physiologic reserve remaining before clinical hemodynamic decompensation. Methods: In this prospective, observational, prehospital cohort study, we measured CRI in injured patients transported by emergency medical services (EMS) to a single Level I trauma center. ⋯ Conclusions: Low prehospital CRI-T predicts blood product transfusion by EMS or within 4 hours of hospital arrival but is less prognostic than EMS blood pressure or shock index. The evaluated version of CRI may be useful in an austere setting at identifying injured patients that require the most significant medical resources. CRI may be improved with noise filtering to attenuate the effects of vibration and patient movement.
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Observational Study
Cardiac output in critically ill patients can be estimated easily and accurately using the minute distance obtained by pulsed wave doppler.
Background: Cardiac output (CO) assessment is essential for management of patients with circulatory failure. Among the different techniques used for their assessment, pulsed-wave Doppler cardiac output (PWD-CO) has proven to be an accurate and useful tool. Despite this, assessment of PWD-CO could have some technical difficulties, especially in the measurement of left ventricular outflow tract diameter (LVOTd). ⋯ The percentage error was 17% in both cases. Conclusion: Measurement of MD in critically ill patients provides a simple and accurate estimate of CO, especially in patients with reduced or preserved LVEF. This would allow earlier cardiovascular assessment in patients with circulatory failure, which is of particular interest in difficult clinical or technical conditions.
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Introduction : Acute kidney injury (AKI) is a prevalent medical disorder characterized by a sudden decline in kidney function, often because of ischemia/reperfusion (I/R) events. It is associated with significant chronic complications, and currently available therapies are limited to supportive measures. Extracellular cold-inducible RNA-binding protein (eCIRP) has been identified as a mediator that potentiates inflammation after I/R injury. ⋯ In the 10-day survival study, mice in the treatment group showed a significant reduction in mortality as compared with vehicle group. Conclusion : In a murine renal I/R model, the administration of PS-OME miR130, a direct eCIRP antagonistic miRNA mimic, resulted in the reduction of kidney inflammation and injury, and improved survival. PS-OME miR130 holds promise to be developed as novel therapeutic for AKI as an adjunct to the standard of care.
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Cardiac macrophages with different polarization phenotypes regulate ventricular remodeling and neovascularization after myocardial infarction (MI). Annexin A2 (ANXA2) promotes macrophage polarization to the repair phenotype and regulates neovascularization. However, whether ANXA2 plays any role in post-MI remodeling and its underlying mechanism remains obscure. ⋯ In addition, ANXA2 directly interacted with integrin β3 in CMECs and enhanced their growth, migration, and tubule formation. Our results indicate that increased expression of ANXA2 could confer protection against MI-induced injury by promoting neovascularization in the infarcted area, partly through the inhibition of YAP in macrophages and activation of integrin β3 in endothelial cells. Our study provides new therapeutic strategies for the treatment of MI injury.
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Normal shear stress is essential for the normal structure and functions of the microcirculation. Hemorrhagic shock leads to reduced shear stress due to reduced tissue perfusion. ⋯ We consider how this reduced shear stress causes (1) a failure to restore normal vasomotor function and normal tissue perfusion thus leading to persistent tissue hypoxia and (2) increased microvascular endothelial permeability resulting in edema formation and impaired organ function. We discuss the need for clinical research into resuscitation strategies and solutions that aim to quickly restore endothelial shear stress in the microcirculation to normal.