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• W2072131278 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).Beyin sapı herniasyonu sonucu gelişen solunum arresti, respiratuvar merkezlerde olan nöronal injuriye bağlanmıştır. Kemoreseptör yolunu oluşturan glossofaringeal sinir ve karotid cisim (GPN-CB) sinir ağlarının solunum düzenlenmesindeki hayati önemi kesin bilinmesine rağmen beyin sapı patolojilerinde oluşan solunum arrestindeki rolleri henüz araştırılmamıştır. Bu çalışmanın amacı, subaraknoid kanamalarda oluşması muhtemel GPN-CB nöral devrelerdeki hasarın solunum arresti gelişimindeki etkisini araştırmaktır.Bu çalışmada 18 hibrit tavşan incelendi. 4 tavşan GPN ve CB’nin normal yapısını belirlemek için kullanıldı. Kalan tavşanların sisterna mangalarına otolog kan verilerek subaraknoid kanama oluşturuldu ve 20 gün sonra tavşanlar incelendi. GPN’in akson sayısı ve CB’nin nöron sayısı stereolojik metotlarla hesaplandı. Sonuçlar Mann-Whitney U testi ile analiz edildi.Ondört tavşanın 6’sı ilk hafta içinde öldü. Ölen hayvanların beyin sapı ve komşu yapılarında ödem ve ezilme gözlendi. Normal tavşanlarda CB’nin ortalama nöronal yoğunluğu 4250±1250/mm3, GPN’in aksonal yoğunluğu 18000±5100/mm2 olarak hesaplandı. Ölen tavşanlarda CB’nin dejenere nöron sayısı 2100±500/mm3, GPN’in dejenere akson sayısı 8500±2550/mm2 olarak hesaplandı. GPN-CB nöral ağında oluşan hasar ölen tavşanlarda daha şiddetliydi.GPN ve CB’nin nörodejenerasyonu ve mortalite oranı arasında önemli bir ilişki vardır. Solunum regülasyonunda önemli bir nöral devre olan GPN-CP arkı subaraknoid kanamalarda iskemik ve mekanik hasarlara uğrayarak solunum arrestine neden olabilir." @default.
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• W2072131278 date "2010-08-01" @default.
• W2072131278 modified "2023-10-18" @default.
• W2072131278 title "The Contribution of Chemoreceptor-Network Injury to the Development of Respiratory Arrest Following Subarachnoid Hemorrhage" @default.
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• W2072131278 doi "https://doi.org/10.5152/eajm.2010.16" @default.
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