Reduced Vagal Compound Action Potential Amplitude Is Associated with Glomerular Injury in an Experimental Rabbit Model of Severe Subarachnoid Hemorrhage

Background: Subarachnoid hemorrhage (SAH) induces a sympathetic surge and systemic inflammation that may impair renal perfusion and glomerular integrity. Although the vagus nerve is central to autonomic and anti-inflammatory regulation, its relationship to renal structural injury in severe SAH is unclear. This study evaluated whether electrophysiological vagal CAP amplitude correlates with glomerular integrity in an experimental SAH model. Methods: Nineteen rabbits were assigned to control (n = 5), sham (n = 5), and SAH groups (n = 9). SAH was induced by daily cisterna magna injections of autologous blood for three days, and animals were followed for 14 days; those that did not survive to the 14-day endpoint formed the SAH-Nonsurvivor subgroup (n = 4). Vagal compound action potential (CAP) amplitude (mV) was recorded electrophysiologically and used as the principal physiologic readout of vagal nerve integrity. Renal tissue and perirenal parasympathetic ganglia were analyzed histologically and stereologically to quantify degenerated neurons and atrophic glomeruli (per mm3). Vagal CAP amplitude decreased from 1.42 ± 0.36 mV in controls to 0.34 ± 0.11 mV in the SAH-Nonsurvivor subgroup (p < 0.001), while atrophic glomeruli increased from 4 ± 1 to 98 ± 11 per mm3. Degenerated neuronal density peaked in the SAH-Nonsurvivor subgroup (98 ± 19 per mm3). Vagal CAP amplitude was inversely correlated with glomerular injury (Spearman ρ = −0.89; 95% CI −0.96 to −0.73; p < 0.001). Conclusions: In this small exploratory study, reduced vagal CAP amplitude was associated with greater glomerular injury after severe SAH. These hypothesis-generating findings warrant confirmation in larger, adequately powered studies before any physiologic or translational interpretation can be made.