New experimental finding of dangerous autonomic ganglia changes in cardiac injury following subarachnoid hemorrhage; a reciprocal culprit-victim relationship between the brain and heart


AYDIN M. D. , KANAT A. , Sahin B., ŞAHİN M. H. , ERGENE Ş. , DEMİRTAŞ R.

INTERNATIONAL JOURNAL OF NEUROSCIENCE, 2022 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Publication Date: 2022
  • Doi Number: 10.1080/00207454.2022.2086128
  • Title of Journal : INTERNATIONAL JOURNAL OF NEUROSCIENCE
  • Keywords: Cardiac ganglia, nodose ganglia, vagal nerve, subarachnoid hemorrhage, ARTERY VASOSPASM, GLOSSOPHARYNGEAL NERVE, NODOSE GANGLION, CAROTID-BODY, DEGENERATION, HYDROCEPHALUS, MECHANISM, ANEURYSMS, DISRUPTION, SECONDARY

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/mm(3)-4 +/- 1/mm(3)-12 +/- 3/mm(3) and 2 +/- 1/cm(3) in the control group; 221 +/- 22/min-16 +/- 4/min-8.699 +/- 976/mm(3)-24 +/- 9/mm(3)-103 +/- 32/mm(3) and 11 +/- 3/cm(3) in the SHAM group; and 191 +/- 23/min-17 +/- 4/min-9.719 +/- 932/mm(3)-124 +/- 31/mm(3)-1.542 +/- 162/mm(3) and 32 +/- 9/cm(3) 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.