Does Renal Sympathetic Denervation Impact the Outcome in Sepsis-Induced Shock? An Experimental Porcine Model

Background/Objectives: Septic shock remains a life-threatening condition characterized by systemic inflammation and hemodynamic instability leading to multiorgan dysfunction with a high mortality rate. The sympathetic nervous system (SNS) plays a central role in septic shock pathophysiology, while the impact of renal sympathetic denervation (RSD) remains unclear. Methods: In this study, 14 Large White pigs were randomized to bilateral RSD (R group, n = 9) or control (C group, n = 5). Septic shock was induced by causing fecal peritonitis. Hemodynamic parameters (systolic and diastolic blood pressure, heart rate), urine output, laboratory biomarkers (inflammatory, coagulation, renal, hepatic, and electrolytes), and organ histopathology were evaluated preoperatively, postoperatively, and 6 h after shock induction. Results: RSD induced a significant reduction in systolic and diastolic blood pressure along with an increase in heart rate and a decrease in urine output. During septic shock, the R group demonstrated greater prolongation of prothrombin time and international normalized ratio. Renal dysfunction, inflammatory markers, hepatic injury, and electrolyte disturbances showed no significant differences, similar to the histopathological findings. Conclusions: RSD alters cardiovascular and coagulation parameters without confirmed alterations in progression of renal dysfunction or systemic inflammatory and hepatic responses, indicating a role of the SNS during septic shock.