Hemodynamic effects of dopamine, norepinephrine, and fluids in a dog model of sepsis

Impaired pressor sensitivity to noradrenaline in septic shock patients with and without impaired adrenal function reserve

“…Noradrenaline acts predominantly on α‐adrenoreceptors [ 35]. If in theory noradrenaline may stimulate cardiac β 1 ‐receptors, in practice and as previously reported [ 36], in our septic shock patients after fluid rescusitation, noradrenaline induced a strong decrease of heart rate, probably as a result of the baroreflex activation secondary to the increase in mean systemic arterial pressure. Since simultaneously noradrenaline did not significantly change cardiac output, it can be concluded that it increased stroke volume, an effect which probably results of the Frank Starling mechanism and perhaps of the stimulation of β 1 ‐receptors.…”

“…Secondly, the above mentioned studies examined catecholamine responses immediately after an acute bolus of microbial toxins, a situation which is probably quite different from that of progressive sepsis, as seen in our patients. Indeed, one study in unanaesthetized dogs with chronic peritonitis suggests that sepsis did not affect the sensitivity of animals to noradrenaline as an α‐adrenoceptor agonist [ 36].…”

Cardiac Output Response to Norepinephrine in Postoperative Cardiac Surgery Patients

“…Still other studies demonstrated a NE-induced reduction in HR in healthy humans (30)(31)(32), normal and hypertensive subjects (33), and in several animal studies (14,(34)(35)(36). The HR reduction in all these studies was attributed to a baroreceptor-mediated central sympathetic withdrawal triggered by the NE-induced increased blood pressure (34,36). However, such baroreceptor-induced change in HR is accompanied by vasodilation of veins and arterioles (37).…”

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

“…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].…”