atterns of renal and splanchnic sympathetic vasomotor activity in an animal model of survival to experimental sepsi

Author(s)

Milanez, M. I. O. ^[1] ; Liberatore, A. M. A. ^[2] ; Nishi, E. E. ^[1] ; Bergamaschi, C. T. ^[1] ; Campos, R. R. ^[1] ; Koh, I. H. J. ^[2]

Affiliation

^[1] Univ Fed Sao Paulo, Dept Fisiol, Lab Fisiol Cardiovasc, Escola Paulista Med, Sao Paulo, SP - Brazil

^[2] Univ Fed Sao Paulo, Dept Cirurgia, Lab Pesquisa Expt, Escola Paulista Med, Sao Paulo, SP - Brazil

• Document type: Journal article
• Source: Brazilian Journal of Medical and Biological Research; v. 55, n. 1 2022.
• Web of Science Citations: 0

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 naive Wistar rats and sepsis group with 2-mL intravenous inoculation of Escherichia coli at 10(8) 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. (AU)

• FAPESP's process: 17/21052-0 - Sepsis: mechanisms, therapeutic targets and epidemiology
• Grantee: Reinaldo Salomão
• Support Opportunities: Research Projects - Thematic Grants
• FAPESP's process: 18/02671-3 - Functional and molecular actions of renal nerve in experimental chronic renal failure
• Grantee: Cassia Marta de Toledo Bergamaschi
• Support Opportunities: Regular Research Grants
• FAPESP's process: 18/01898-4 - Evaluation of brain-spinal projections in the temporal establishment of renal sympathetic hyperactivation in Renovascular Hypertension
• Grantee: Maycon Igor de Oliveira Milanez
• Support Opportunities: Scholarships in Brazil - Doctorate