Abstract
Sepsis causes long-term disability, such as immune dysfunction, neuropsychological disorders, persistent inflammation, catabolism, and immunosuppression, leading to a high risk of death in survivors, although the contributing factors of mortality are unknown. The purpose of this experimental study in rats was to examine renal (rSNA) and splanchnic (sSNA) sympathetic nerve activity, as well as baroreflex sensitivity, in acute and chronic post-sepsis periods. The rats were divided into two groups: control group with naïve Wistar rats and sepsis group with 2-mL intravenous inoculation of Escherichia coli at 108 CFU/mL. Basal mean arterial pressure, heart rate, rSNA, sSNA, and baroreflex sensitivity were evaluated in all groups at the acute (6 h) and chronic periods (1 and 3 months). Basal rSNA and sSNA were significantly reduced in the surviving rats, as was their baroreflex sensitivity, for both pressor and hypotensive responses, and this effect lasted for up to 3 months. A single episode of sepsis in rats was enough to induce long-term alterations in renal and splanchnic sympathetic vasomotor nerve activity, representing a possible systemic event that needs to be elucidated. These findings showed that post-sepsis impairment of sympathetic vasomotor response may be one of the critical components in the inability of sepsis survivors to respond effectively to new etiological illness factors, thereby increasing their risk of post-sepsis morbidity.
Highlights
Multiple systems, including neurological, hormonal, and metabolic pathways, are activated and/or depressed as a result of sepsis [1]
Basal sympathetic nerve activity (SNA) and macrocirculation During the acute phase of sepsis (6 h), spike variations were seen in both territories but in the opposite direction, with an rSNA reduction indicating a response to renal vasodilation and an increased sSNA indicating a vasoconstriction in the intestinal region, but neither was statistically significant when compared to their control value
This study reports changes in renal and splanchnic SNA in rats that survived an episode of sepsis, showing that, in addition to a change in the first hour after sepsis induction, this phenomenon persisted in surviving animals, at least until the third month after the episode
Summary
Multiple systems, including neurological, hormonal, and metabolic pathways, are activated and/or depressed as a result of sepsis [1]. The level of sympathetic nerve activity (SNA) is one of the determinants of renal blood filtration (RBF) and glomerular filtration rate (GFR). Through a differential innervation pattern of the afferent and efferent arterioles [5], whereas reflex stimulation of renal sympathetic nerve activation with hypoxia can selectively increase or decrease glomerular capillary pressure and GFR by differentially activating separate populations of renal nerves [8]. To better understand the causes of septic AKI, it is necessary to improve our knowledge of the hemodynamic changes in the renal micro-vasculature, the role of increased SNA and hormonal systems, and to investigate the importance of intra-renal shunting
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