Abstract
Respiratory arrest following brainstem herniation has been attributed to injuries resulting from compression of the respiratory centers. While it is widely perceived that the chemoreceptor network, consisting of the glossopharyngeal nerve and carotid body (GPN-CB), is essential for the modulation of respiration, its contribution to the development of respiratory arrest has not been investigated. Therefore, the aim of this study was to investigate whether injury to the GPN-CB occurs in animals with respiratory arrest caused by experimentally-induced subarachnoid hemorrhage. Eighteen hybrid rabbits were used in this study. Four rabbits (n=4) were used to determine the normal structure of the GPN-CB. The remaining rabbits (n=14) received an autologous blood injection into the cisterna magna to produce a subarachnoid hemorrhage, after which they were observed for 20 days. The number of axons and the neuron density in the glossopharyngeal nerve and carotid body, respectively, were counted by stereological methods. The Mann-Whitney U test was used to analyze the results. Six of 14 rabbits died within the first week, likely due to brain swelling and crushing injuries that were observed in the brain stem and related structures. In control rabbits, the average neuronal density of the carotid body was 4250 ±1250/mm(3), while the axonal density in the glossopharyngeal nerve was 18000±5100 mm(2). Conversely, in the dead rabbits, the degenerated neuron density of the carotid body was 2100±500/mm(3), while the degenerated axon density in the glossopharyngeal nerve was 8500±2550 mm(2). In addition, histopathological lesions were more severe in the dead rabbits in terms of their glossopharyngeal nerve and carotid body. There is an important relationship between neurodegeneration in the GPN-CB and mortality rates following experimentally-induced hemorrhage. This relationship suggests that injury to the GPN-CB network disrupts the breathing reflex and results in respiratory arrest following a subarachnoid hemorrhage (SAH).
Highlights
The generation and continuation of respiration is dependent on a central driving force that consists of inspiratory and expiratory pump muscles
Histopathological lesions were more severe in the dead rabbits in terms of their glossopharyngeal nerve and carotid body
There is an important relationship between neurodegeneration in the glossopharyngeal nerve and carotid body (GPN-carotid body (CB)) and mortality rates following experimentally-induced hemorrhage
Summary
The generation and continuation of respiration is dependent on a central driving force that consists of inspiratory and expiratory pump muscles. Respiration is modulated by neural, chemical, behavioral, voluntary, and mechanical inputs. All respiratory inputs generated by baroreceptors, chemoreceptors, pulmonary receptors, mechanoreceptors, and respiratory centers are transmitted and integrated by the somatic, sympathetic, and parasympathetic nerves [1]. Defects of the glossopharyngeal and vagus nerves can result in significant impairments in speech, swallowing, and breathing [2]. One of the most important peripheral autonomic neural pathways for respiration consists of the carotid body (CB) and glossopharyngeal nerve (GPN) [3]. The CB contains chemoreceptors that can detect hypoxia, hypercarbia, and changes in blood pH. The primary afferent neurons of the GPN transmit information from the CB to the solitary nucleus. Some chemoreceptor afferents help mediate respiration in response to hypercarbia and hypoxia through their synaptic connections with
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