According to this logic, the origins of irreversible, shock-related functional/structural defects should be located at the business end of the cardiovascular system, at the arteriolo-capillary and/or intracellular-mitochondrial junctions. Substrates and carrier capacity are necessary for the mitochondrion to produce energy. in this issue) non-invasive in vivo mitoPO 2 measurement is also possible. Protocols for high-resolution respirometry offer sensitive analyses of oxidative phosphorylation and diagnostics for the pathophysiology of a wide array of mitochondrial dysfunctions and with a novel technique (introduced by Baumbach et al. Several reliable techniques are now available to measure the respiratory properties of mitochondria in cells, tissue fractions or whole tissue samples. The human body employs a wide range of defense mechanisms which react to all types and levels of severity of external or internal insults that disrupt the physiological homeostasis, and, after various durations of compensation, the common denominator of shock states is the failure of energy production essential to maintaining a low-entropy intracellular state. Another related area to be explored in more detail is mitochondrial energetics. Therefore, according to our current understanding, the circulatory consequences of shock can be broadly categorized into those where the macrohaemodynamics are deranged and those where the microcirculation is malfunctioning. With these incremental technical advances, it is now recognized that shock-induced peripheral microcirculatory responses are not always connected to macrocirculatory changes, and, likewise, macrohaemodynamic variables cannot always be relied upon to monitor the outcome of shock conditions. Like the long evolutionary history of shock research itself, attempts to measure and characterize the performance of human microcirculation have spanned a number of decades, from the first reports on the use of capillary microscopy in 1916 (2) to the first handheld video microscope that provided real-time, dynamic observations at the bedside (3). Of these directions, the importance of microcirculatory investigations should be highlighted first. Nevertheless, shock classifications once thought appropriate and shock mechanisms based on clinical etiologies have been revised numerous times, and today it is perhaps timely to point in new directions again, which would conceivably improve our understanding of this still deadly syndrome. Today, their well-established tradition defines shock as circulatory failure, which results in inadequate cellular oxygen utilization and shock conditions, which are characterized by generalized hypoxia/dysoxia or by circulatory dysfunction leading to systemic hypoxia. The 280 years since then have seen numerous advances in the mechanism and treatment of this condition through meticulous experimental and clinical research, and our current knowledge on shock categories is deeply rooted in the classical work of George Crile, William Bayliss, Walter Cannon, and Alfred Blalock, to name just a few of the exceptional scientists in the field. When his treatise was published in London in 1743, this French term was translated as “shock and agitation,” the first noted description of a syndrome “ which suspends the laws of economy for a few moments” (1). Abstract: Editorial on the Research Topic Microcirculation Guided/Targeted Resuscitation In 1740, Henri-François Le Dran, a French surgeon, observed and described a peculiar state of “ saissisement,” which commonly follows gunshot wounds.
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