Abstract
Objective The vagal, stellate, and cardiac ganglia cells changes following subarachnoid hemorrhage (SAH) may occur. This study aimed to investigate if there is any relation between vagal network/stellate ganglion and intrinsic cardiac ganglia insult following SAH. Materials and methods Twenty-six rabbits were used in this study. Animals were randomly divided as control (GI, n = 5); SHAM 0.75 cc of saline-injected (n = 5) and study with autologous 1.5 cc blood injection into their cisterna magna(GIII, n = 15). All animals were followed for three weeks and then decapitated. Their motor vagal nucleus, nodose, stellate, and intracardiac ganglion cells were estimated by stereological methods and compared statistically. Results Numerical documents of heart-respiratory rates, vagal nerve- ICG, and stellate neuron densities as follows: 276 ± 32/min-22 ± 3/min-10.643 ± 1.129/mm3-4 ± 1/mm3-12 ± 3/mm3 and 2 ± 1/cm3 in the control group; 221 ± 22/min-16 ± 4/min-8.699 ± 976/mm3-24 ± 9/mm3-103 ± 32/mm3 and 11 ± 3/cm3 in the SHAM group; and 191 ± 23/min-17 ± 4/min-9.719 ± 932/mm3-124 ± 31/mm3-1.542 ± 162/mm3 and 32 ± 9/cm3 in the SAH (study) group. The animals with burned neuro-cardiac web had more neurons of stellate ganglia and a less normal neuron density of nodose ganglia (p < 0.005). Conclusion Sypathico-parasympathetic imbalance induced vagal nerve-ICG disruption following SAH could be named as Burned Neurocardiac Web syndrome in contrast to broken heart because ICG/parasympathetic network degeneration could not be detected in classic broken heart syndrome. It was noted that cardiac ganglion degeneration is more prominent in animals’ severe degenerated neuron density of nodose ganglia. We concluded that the cardiac ganglia network knitted with vagal-sympathetic-somatosensitive fibers has an important in heart function following SAH. The neurodegeneration of the cardiac may occur in SAH, and cause sudden death.
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