Redox Changes Induced by General Anesthesia in Critically Ill Patients with Multiple Traumas

Abstract

The critically ill polytrauma patient is a constant challenge for the trauma team due to the complexity of the complications presented. Intense inflammatory response and infections, as well as multiple organ dysfunctions, significantly increase the rate of morbidity and mortality in these patients. Moreover, due to the physiological and biochemical imbalances present in this type of patients, the bioproduction of free radicals is significantly accelerated, thus installing the oxidative stress. In the therapeutic management of such patients, multiple surgical interventions are required and therefore they are being subjected to repeated general anesthesia. In this paper, we want to present the pathophysiological implications of oxidative stress in critically ill patients with multiple traumas and the implications of general anesthesia on the redox mechanisms of the cell. We also want to summarize the antioxidant treatments able to reduce the intensity of oxidative stress by modulating the biochemical activity of some cellular mechanisms.

Figure 1

Schematic representation of oxidative stress in the critically ill patient with multiple traumas. Primary trauma induces a series of secondary injuries due to the biological and biochemical imbalances. The first side effect installed is SIRS, followed by sepsis, and finally by MODS. The inflammations generated by the action of the polymorphonuclear cells, as well as by hypermetabolism, maintain and enhance the oxidative stress. Mitochondria are significantly affected thereby producing significant amounts of superoxide anion. Free radicals produced at the cellular level are neutralized by the number of antioxidant enzyme systems, such as SOD, CAT, Trx, Gpx, and Prx [11, 12].

Figure 2

The chemical structure of (a) desflurane, (b) halothane, (c) isoflurane, (d) sevoflurane, (e) ketamine, (f) midazolam, and (g) propofol.

Figure 3

The implications of general anesthetics in the cellular redox activity.

Figure 4

Biogenesis mechanism for miRNAs. The synthesis of miRNAs begins in the nucleus with the action of RNA polymerase II on a protein-coding. This forms a first species, called pri-miRNA. Through successive reactions of polyadenylation catalyzed by DGCR8 and Drosa, the precursor for the miRNAs species, called pre-miRNA, is obtained. pre-miRNA thus formed is transported into the cytoplasm through Exportin 5. In the cytoplasm, on the pre-miRNA acts the Dicer complex. Subsequently through the action of TRBP, AGO2 and Dicer is obtained the RNA induced silencing complex (RISC) and finnaly the mature miRNAs.