Hyperdynamic severe intravascular sepsis depends on fluid administration in cynomolgus monkey

Abstract

A new model of high cardiac output septic shock in primates is presented that includes hemodynamic and metabolic effects of separate and combined infusions of normal saline and live Escherichia coli. In monkeys receiving ketamine anesthesia, cardiac output (QT) increased with saline loading but not significantly with bacterial infusion, and bacterial infusion without saline never significantly increased QT. Depressed oxygen consumption (VO2) was reversed with saline loading. In spite of continuing E. coli infusion, radiolabeled microspheres showed no increase in systemic anatomic shunt when QT was elevated. It is perceived that the tissue dysfunction associated with sepsis, which is called septic shock, and elevation of cardiac output are related only indirectly. High cardiac output only reflects an adequate volume status in a stressed individual; some of the afferent stress signals can be related to the septic state, but no specific or direct relationship is involved. In general, shock as indicated by a depression of VO2 does not appear to occur when QT is increased.

Systemic pressure-flow reactivity to norepinephrine in rabbits: impact of endotoxin and fluid loading

“…Consequently, the pathophysiologic determinants of the high systemic blood flow observed in the early phase of shock remain unclear. It can reasonably be concluded that this hyperdynamic profile mainly results from the fluid resuscitation [1,22,26], as suggested by our results. Fluid loading induced similar effects on flow in endotoxin and non-endotoxin animals, although the fluid-induced vasodilatation was more pronouned in endotoxic animals than in controls.…”

“…Using the same model, we have shown that, in the absence of fluid resuscitation, nitric oxide donors can induce similar hemodynamic patterns to fluid loading [11,12]. Several studies have shown a low systemic blood flow [11,15,21,22], rather than a high systemic blood flow [1,4,5,16], in septic shock, that might be related to fluid resuscitation [1,22,27]. Considering the pathophysiology of endotoxic shock, it is admitted that endotoxin induces a peripheral vascular hypocontractility [7][8][9][10]18], considerable vasodilation [4,5,7], an altered cardiac function [2][3][4], relative hypovolemia resulting from capillary leak [28,29] and increased resistance to venous return [17].…”

“…The hemodynamic pattern of septic shock is widely presented as an association of systemic hypotension and high systemic blood flow, which implies a decrease in calculated systemic vascular resistances [1][2][3][4][5]. The decrease in arterial blood pressure during sepsis may result from a combination between a reset of high pressure baroreflex [6], an abnormal contractile response of the vessels [7][8][9][10], a release of various substances dilating the peripheral vasculature [11][12][13] or the use of sedation and general anesthesia as an additional factor impairing the cardiovascular adaptation [14].…”

The role of the microcirculation in multiple organ dysfunction syndrome (MODS): a review and perspective

“…In addition, there are divergent views on the choice of initiating factor. The latter includes LPS, applied intravenously or intraperitoneally [24,166], live bacteria, given by the intravenous, intraperitoneal or intramuscular route [33,38,58,64], caecal ligation with perforation [157] and intravenous administration of TNF-c~ [48]. One of the major problems with some of these models is the discrepancy between the model and the human situation, not just in the choice of animal but, more importantly, in the relevance of the initiating factor.…”

Physiopathologie de la défaillance circulatoire

“…L'expansion volémique constitue ainsi le traitement symptomatique initial du choc septique [2]. Après sa réalisation, un état hémodynamique hyperdynamique est généralement observé [3].…”