Bu öğeden alıntı yapmak, öğeye bağlanmak için bu tanımlayıcıyı kullanınız: http://hdl.handle.net/11452/29819
Başlık: The effects of centrally injected arachidonic acid on respiratory system: Involvement of cyclooxygenase to thromboxane signaling pathway
Yazarlar: Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.
0000-0002-5600-8162
Erkan, Leman Gizem
Güvenç, Gökçen
Altınbaş, Burçin
Niaz, Nasır
Yalçın, Murat
AAR-6815-2021
AAG-6956-2021
56529371200
56529426800
55356919300
57060367600
57192959734
Anahtar kelimeler: Physiology
Respiratory system
Arachidonic acid
Cyclooxygenase
Thromboxane A2
Tidal volume
Respiratory rate
Respiratory minute ventilation
Partial oxygen pressure
Partial carbon dioxide pressure
Intracerebroventricular
Hemorrhaged hypotensive rats
Phospholipase A(2) activator
Central histaminergic system
Peripheral mechanism
Breathing movements
Fetal lambs
Melittin
Cascade
Pressor
Yayın Tarihi: 31-Ara-2015
Yayıncı: Elsevier
Atıf: Erkan, L. G. vd. (2016). "The effects of centrally injected arachidonic acid on respiratory system: Involvement of cyclooxygenase to thromboxane signaling pathway". Respiratory Physiology and Neurobiology, 225, 1-7.
Özet: Arachidonic acid (AA) is a polyunsaturated fatty acid that is present in the phospholipids of the cell membranes of the body and is abundant in the brain. Exogenously administered AA has been shown to affect brain metabolism and to exhibit cardiovascular and neuroendocrine actions. However, little is known regarding its respiratory actions and/or central mechanism of its respiratory effects. Therefore, the present study was designed to investigate the possible effects of centrally injected AA on respiratory system and the mediation of the central cyclooxygenase (COX) to thromboxane A2 (TXA2) signaling pathway on AA-induced respiratory effects in anaesthetized rats. Intracerebroventricular (i.c.v.) administration of AA induced dose- and time-dependent increase in tidal volume, respiratory rates and respiratory minute ventilation and also caused an increase in partial oxygen pressure (pO2) and decrease in partial carbon dioxide pressure (pCO2) in male anaesthetized Sprague Dawley rats. I.c.v. pretreatment with ibuprofen, a non-selective COX inhibitor, completely blocked the hyperventilation and blood gases changes induced by AA. In addition, central pretreatment with different doses of furegrelate, a TXA2 synthesis inhibitor, also partially prevented AA-evoked hyperventilation and blood gases effects. These data explicitly show that centrally administered AA induces hyperventilation with increasing pO2 and decreasing pCO2 levels which are mediated by the activation of central COX to TXA(2) signaling pathway.
URI: https://doi.org/10.1016/j.resp.2015.12.010
https://www.sciencedirect.com/science/article/pii/S1569904815301002
http://hdl.handle.net/11452/29819
ISSN: 1569-9048
1878-1519
Koleksiyonlarda Görünür:Scopus
Web of Science

Bu öğenin dosyaları:
Bu öğeyle ilişkili dosya bulunmamaktadır.


DSpace'deki bütün öğeler, aksi belirtilmedikçe, tüm hakları saklı tutulmak şartıyla telif hakkı ile korunmaktadır.