The neuropathological mechanism of heart rhythm disorders, following spinal cord pathologies, to our knowledge, has not yet been adequately investigated. In this study, the effect of the ischemic neurodegeneration of the thoracic sympathetic nuclei (TSN) on the heart rate (HR) was examined following a spinal subarachnoid hemorrhage (SSAH).

This study was conducted on 22 rabbits. Five rabbits were used as a control group, five as SHAM, and twelve as a study group. The animals’ HRs were recorded via monitoring devices on the first day, and those results were accepted as baseline values. The HRs were remeasured after injecting 0.5 cc of isotonic saline for SHAM and 0.5 cc of autolog arterial blood into the thoracic spinal subarachnoid space at T4–T5 for the study group. After a three-week follow-up with continuous monitoring of their HRs, the rabbit's thoracic spinal cords and stellate ganglia were extracted. The specimens were evaluated by histopathological methods. The densities of degenerated neurons in the TSN and stellate ganglia were compared with the HRs.

The mean HRs and mean degenerated neuron density of the TSN and stellate ganglia in control group were 251±18/min, 5±2/mm³, and 3±1/mm³, respectively. The mean HRs and the mean degenerated neuron density of the TSN and stellate ganglia were detected as 242±13/min, 6±2/mm³, and 4±2/mm³ in SHAM (P>0.05 vs. control); 176±19/min, 94±12/mm³, and 28±6/mm³ in the study group (P<0.0001 vs. control and P<0.005 vs. SHAM), respectively.

SAH induced TSN neurodegeneration may have been responsible for low HRs following SSAH. To date this has not been mentioned in the literature.