Protection of cerebral microcirculation, mitochondrial function, and electrocortical activity by small-volume resuscitation with terlipressin in a rat model of haemorrhagic shock

Abstract

Resuscitation from haemorrhagic shock using terlipressin with small-volume LR was superior to high-volume LR, with regard to cerebral microcirculation, and mitochondrial and electrophysiological functions.

Therapeutic interventions to restore microcirculatory perfusion following experimental hemorrhagic shock and fluid resuscitation: A systematic review

“…Three of these effective treatment strategies targeted sex hormones with the use of testosterone receptor blocker flutamide 43,45 or by addition of 17B‐estradiol 42 . The remaining studies either reported no effect (44%) 13,19,46,47 or a decrease in blood flow (11%) following treatment with hormones 48 . One study did not report the used group size and could therefore not be shown in the forest plot 42 …”

“…7,10 Tissue edema increases diffusion distances between capillaries 11 leading to impaired tissue perfusion, reduced ATP production, and mitochondrial dysfunction. 12,13 Blood transfusion, hypothermia, and acidosis are other factors evoking the development of coagulopathy, complement activation, 14 and systemic inflammation. 7,15 The systemic inflammatory response is accompanied by the formation of ROS, which are normally neutralized by antioxidants.…”

“…To enable sufficient blood flow, restoration of the circulating volume is necessary; however, fluid resuscitation can also further aggravate fluid leakage and tissue edema 7,10 . Tissue edema increases diffusion distances between capillaries 11 leading to impaired tissue perfusion, reduced ATP production, and mitochondrial dysfunction 12,13 . Blood transfusion, hypothermia, and acidosis are other factors evoking the development of coagulopathy, complement activation, 14 and systemic inflammation 7,15 .…”

Exogenous vasopressin dose-dependently modulates gastric microcirculatory oxygenation in dogs via V1A receptor

“…An interaction of AVP with mitochondrial respiration was found, which may account for a reduced cellular oxygen demand. Supplemental AVP and terlipressin during resuscitation preserves renal [37] and cerebral mitochondrial function [38] in a rat model of hemorrhagic shock. Therefore, an AVP-induced, probably V1A receptor-mediated, modulation of cellular oxygen demand may account for the increased μHbO 2 observed in our study.…”

Brain Histology and Immunohistochemistry After Resuscitation From Hemorrhagic Shock in Swine With Pre-Existing Atherosclerosis and Sodium Thiosulfate (Na2S2O3) Treatment

“…Moreover, H 2 S and the oxytocin (OT)/ oxytocin receptor (OTR) systems interact in trauma in the heart and the brain (11)(12)(13)(14)(15) and are both reported to have anti-oxidative, and vasculo-protective effects (15). Hence, activation of either system could be beneficial in HS, since severe hypovolemia can induce at least transitory cerebral tissue hypoxia events (16- 19), redox imbalance (20), barrier dysfunction (18,21) and, upon resuscitation, ischemia/reperfusion (I/R) injury (22).…”