Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/23776
Title: The role of the central arachidonic acid-thromboxane A(2) cascade in cardiovascular regulation during hemorrhagic shock in rats
Authors: Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı.
0000-0002-5600-8162
0000-0002-3090-0099
Yalçın, Murat
Aydın, Cenk
AAG-6956-2021
57192959734
7005426982
Keywords: Biochemistry & molecular biology
Cell biology
Endocrinology & metabolism
Melittin
Phospholipase A(2)
Arachidonic acid
Cyclooxygenase
Thromboxane A(2)
Mean arterial pressure
Heart rate
Hemorrhage
Hypotensive
Intracerebroventricular
Central cholinergic system
Normotensive conscious rats
Blood-flow autoregulation
Hypotensive rats
Peripheral mechanisms
Cerebral-circulation
Injected U-46619
Newborn pigs
A2 analog
Rattus
Issue Date: Aug-2011
Publisher: Elsevier
Citation: Yalçın, M. ve Aydın, C. (2011). "The role of the central arachidonic acid-thromboxane A(2) cascade in cardiovascular regulation during hemorrhagic shock in rats". Prostaglandins Leukotrienes and Essential Fatty Acids, 85(2), 61-66.
Abstract: The aim of the current study was to elucidate the underlying central mechanism(s) of the cardiovascular effects evoked by centrally injected melittin and arachidonic acid (AA) in hemorrhaged hypotensive condition, specifically, from central AA release from the cell membrane under the influence of phospholipase A(2) (PLA(2)) to central thromboxane A(2) (TXA(2)) signaling via the cyclooxygenase (COX) pathway. As the main control of the study, melittin (3 mu g) or AA (150 mu g) was injected intracerebroventricularly (i.c.v.) after the hemorrhage procedure, which was performed by withdrawing a total volume of 2.2 ml of blood/100 g body weight over a period of 10 min. Both treatments generated a pressor response and abolished the hypotension-induced hemorrhage. Pretreatment with the PLA(2) inhibitor mepacrine (500 mu g; i.c.v.) completely blocked the pressor response to melittin in the hemorrhagic hypotensive state. Pretreatments with the nonselective COX inhibitor indomethacin (200 mu g; i.c.v.) or the TXA(2) synthesis inhibitor furegrelate (250 or 500 mu g; i.c.v.) were made to test the role of central COX activity and, subsequently, the TXA(2) signaling pathway in the melittin- or AA-mediated reversal of hemorrhagic hypotension. Indomethacin completely prevented the pressor response to melittin and AA in the hemorrhaged, hypotensive state, but furegrelate did so only partially. In conclusion, these findings suggest that central COX activity and, subsequently, the central TXA(2) signaling pathway, are, at least in part, involved in the melittin- or AA-induced reversal effect during hemorrhagic shock.
URI: https://doi.org/10.1016/j.plefa.2011.05.003
https://pubmed.ncbi.nlm.nih.gov/21658925/
http://hdl.handle.net/11452/23776
ISSN: 0952-3278
Appears in Collections:Scopus
Web of Science

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