scholarly journals Possible role of leukotrienes in hypoxic contraction of canine isolated basilar artery

1991 ◽  
Vol 103 (3) ◽  
pp. 1629-1632 ◽  
Author(s):  
Mai Gu ◽  
Douglas A. Elliott ◽  
Bill Y. Ong ◽  
Deepak Bose
Keyword(s):  
1997 ◽  
Vol 17 (10) ◽  
pp. 1089-1096 ◽  
Author(s):  
Kazunori Toyoda ◽  
Kenichiro Fujii ◽  
Setsuro Ibayashi ◽  
Tetsuhiko Nagao ◽  
Takanari Kitazono ◽  
...  

We tested the hypothesis that nitric oxide (NO) plays a role in CBF autoregulation in the brain stem during hypotension. In anesthetized rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and its branches were measured through an open cranial window during stepwise hemorrhagic hypotension. During topical application of 10−5 mol/L and 10−4 mol/L Nω-nitro-L-arginine (L-NNA), a nonselective inhibitor of nitric oxide synthase (NOS), CBF started to decrease at higher steps of mean arterial blood pressure in proportion to the concentration of L-NNA in stepwise hypotension (45 to 60 mm Hg in the 10−5 mol/L and 60 to 75 mm Hg in the 10−4 mol/L L-NNA group versus 30 to 45 mm Hg in the control group). Dilator response of the basilar artery to severe hypotension was significantly attenuated by topical application of L-NNA (maximum dilatation at 30 mm Hg: 16 ± 8% in the 10−5 mol/L and 12 ± 5% in the 10−4 mol/L L-NNA group versus 34 ± 4% in the control group), but that of the branches was similar between the control and L-NNA groups. Topical application of 10−5 mol/L 7-nitro indazole, a selective inhibitor of neuronal NOS, did not affect changes in CBF or vessel diameter through the entire pressure range. Thus, endothelial but not neuronal NO seems to take part in the regulation of CBF to the the brain stem during hypotension around the lower limits of CBF autoregulation. The role of NO in mediating dilatation in response to hypotension appears to be greater in large arteries than in small ones.


1998 ◽  
Vol 20 (1) ◽  
pp. 63-72 ◽  
Author(s):  
Ralf Hempelmann ◽  
Rainer Prade ◽  
Maximilian Mehdorn ◽  
Albrecht Ziegler

2006 ◽  
Vol 64 (3a) ◽  
pp. 572-574 ◽  
Author(s):  
Antônio Tadeu de Souza Faleiros ◽  
Francisco Humberto de Abreu Maffei ◽  
Luiz Antonio de Lima Resende

This study investigates the role of cervical sympathectomy in the prevention of acute vasospasm induced by meningeal haemorrhage in rabbits. Sixteen adult English Norfolk rabbits were divided into 2 experimental groups: bilateral cervical sympathectomy of the superior sympathetic ganglion (SSSG, n=8), and bilateral SSSG and sympathectomy of the inferior sympathetic ganglion (SISG, n=8). Other 24 animals were used as controls. Basilar artery diameter was evaluated by angiography. SSSG protected the animals against developing cerebral vasospasm; SSSG associated with SISG did not increase this effect.


2011 ◽  
Vol 165 (2) ◽  
pp. 163-167 ◽  
Author(s):  
Selim Kayaci ◽  
Ayhan Kanat ◽  
Mehmet Dumlu Aydin ◽  
Ahmet Murat Musluman ◽  
Mete Eseoglu ◽  
...  

1992 ◽  
Vol 445 (1) ◽  
pp. 169-179 ◽  
Author(s):  
M A Murray ◽  
F M Faraci ◽  
D D Heistad

2000 ◽  
Vol 279 (6) ◽  
pp. H2704-H2712 ◽  
Author(s):  
Sophocles Chrissobolis ◽  
James Ziogas ◽  
Yi Chu ◽  
Frank M. Faraci ◽  
Christopher G. Sobey

We tested whether activation of inwardly rectifying K+ (Kir) channels, Na+-K+-ATPase, or nitric oxide synthase (NOS) play a role in K+-induced dilatation of the rat basilar artery in vivo. When cerebrospinal fluid [K+] was elevated from 3 to 5, 10, 15, 20, and 30 mM, a reproducible concentration-dependent vasodilator response was elicited (change in diameter = 9 ± 1, 27 ± 4, 35 ± 4, 43 ± 12, and 47 ± 16%, respectively). Responses to K+ were inhibited by ∼50% by the Kir channel inhibitor BaCl2 (30 and 100 μM). In contrast, neither ouabain (1–100 μM, a Na+-K+-ATPase inhibitor) nor N G-nitro-l-arginine (30 μM, a NOS inhibitor) had any effect on K+-induced vasodilatation. These concentrations of K+ also hyperpolarized smooth muscle in isolated segments of basilar artery, and these hyperpolarizations were virtually abolished by 30 μM BaCl2. RT-PCR experiments confirmed the presence of mRNA for Kir2.1 in the basilar artery. Thus K+-induced dilatation of the basilar artery in vivo appears to partly involve hyperpolarization mediated by Kir channel activity and possibly another mechanism that does not involve hyperpolarization, activation of Na+-K+-ATPase, or NOS.


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