Endothelium-Dependent Contractions to NG-Monotnethyl-L-Arginine in Canine Basilar Artery

2015 ◽  
pp. 95-98 ◽  
Author(s):  
Zvonimir S. Katusic ◽  
Paul M. Vanhoutte
Keyword(s):  
Basilar Artery ◽  
Canine Basilar Artery

Evaluation of prostaglandin biosynthetic activity in canine basilar artery following subarachnoid injection of blood

1981 ◽  
Vol 55 (5) ◽  
pp. 771-778 ◽  
Author(s):  
Tomio Sasaki ◽  
Sei-itsu Murota ◽  
Susumu Wakai ◽  
Takao Asano ◽  
Keiji Sano
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Biosynthetic Activity ◽  
Content Type ◽  
Blood Injection ◽  
Canine Basilar Artery ◽  
Subarachnoid Blood ◽  
Fine Print

✓ Transformation of arachidonic acid into prostaglandins was investigated in the basilar artery by incubating sections of artery with carbon-14-labeled arachidonic acid. Thin-layer radiochromatography revealed that, in normal canine basilar arteries, 14C-arachidonic acid was transformed mainly to 6-ketoprostaglandin (PG)F1α, a spontaneous metabolite of prostacyclin (PGI2). Among other prostaglandins, only a small amount of PGF2α was detected, whereas PGD2, PGE2, and thromboxane B2 were not. Arteries removed on Days 3 and 8 after subarachnoid blood injection showed a prostaglandin synthesis profile similar to that in the normal cerebral artery. In borate-buffered saline (0.1M borate buffer, pH 9.0/0.15M NaCl = 1:9, vol/vol), canine basilar artery produced a PGI2-like substance that inhibited adenosine diphosphate (ADP)-induced platelet aggregation. Its anti-aggregatory activity was completely abolished by acidification. Aspirin likewise inhibited production of the anti-aggregatory substance. From these results, it was concluded that the anti-aggregatory activity was due solely to the production of PGI2 by the arterial specimen. Based on the above results, PGI2 biosynthetic activity in the cerebral artery exposed to subarachnoid blood injection was bioassayed by measuring the inhibitory activity of the incubation product upon ADP-induced platelet aggregation following incubation of the arteries in borate-buffered saline for 5 to 30 minutes at 20°C, using synthetic PGI2-Na as a standard. The synthetic activity of PGI2 in the artery exposed to subarachnoid blood injection had diminished remarkably by Days 3 and 8. This diminution of PGI2 synthesis in the cerebral artery may be involved in the pathogenesis of cerebral vasospasm.

Contraction of the Canine Basilar Artery following Linoleic, Arachidonic, 13-Hydroperoxylinoleic, or 15-Hydroperoxyarachidonic Acid

1981 ◽  
Vol 168 (3) ◽  
pp. 399-402 ◽  
Author(s):  
T. Koide ◽  
Y. Noda ◽  
S. Hata ◽  
K. Sugioka ◽  
S. Kobayashi ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Canine Basilar Artery

Expression and Function of Recombinant Endothelial Nitric Oxide Synthase Gene in Canine Basilar Artery

1997 ◽  
Vol 80 (3) ◽  
pp. 327-335 ◽  
Author(s):  
Alex F.Y. Chen ◽  
Timothy O’Brien ◽  
Masato Tsutsui ◽  
Hiroyuki Kinoshita ◽  
Vincent J. Pompili ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Basilar Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Canine Basilar Artery ◽  
And Function ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Calpain-calpastatin system of canine basilar artery in vasospasm

1993 ◽  
Vol 79 (4) ◽  
pp. 537-543 ◽  
Author(s):  
Ikuya Yamaura ◽  
Eiichi Tani ◽  
Takaomi C. Saido ◽  
Koichi Suzuki ◽  
Nobutaka Minami ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Early Stage ◽  
Local Application ◽  
Neutral Protease ◽  
Control Group ◽  
Calpain Activity ◽  
Fresh Blood ◽  
Content Type ◽  
Canine Basilar Artery ◽  
Fine Print

✓ Vasospasm was produced in the canine basilar artery by a two-hemorrhage method, while contraction was induced in the normal canine basilar artery by a local application of KCl or serotonin after transclival exposure. The control animals were injected with saline instead of fresh blood. The activation of μ-calpain, a Ca++-dependent neutral protease, in the basilar artery was studied by evaluating the conversion from its inactivated into its activated form on immunoblots. In addition, the activity of calpastatin, an intrinsic inhibitor of calpain, in the basilar artery was determined by assay. The majority of the μ-calpain was inactivated in the control group. In the spastic group, μ-calpain was generally activated markedly in the early stage of vasospasm and moderately thereafter. The contraction induced by KCl or serotonin application was classified into the early phasic and the later tonic stages; μ-calpain was usually activated in the phasic stage and inactivated in the tonic stage. Calpastatin activity was significantly decreased during vasospasm, whereas it was not significantly changed in KCl- or serotonin-induced contraction. The final activity of μ-calpain results from the balance of μ-calpain and calpastatin. This suggests that μ-calpain activity was enhanced continuously in the spastic group and transiently in the KCl or serotonin group, and that the continuous activation of μ-calpain during vasospasm probably induced more proteolytic changes compared to those in the KCl or serotonin group.

Effect of Endothelin on the Canine Basilar Artery

Neurosurgery ◽  
1990 ◽  
Vol 27 (3) ◽  
pp. 357-361 ◽  
Author(s):  
Hidenori Kobayashi ◽  
Minoru Hayashi ◽  
Shinjiro Kobayashi ◽  
Masanori Kabuto ◽  
Yuji Handa ◽  
...  
Keyword(s):  
Basilar Artery ◽  
Canine Basilar Artery

scholarly journals Activation of Protein Kinases in Canine Basilar Artery in Vasospasm

1999 ◽  
Vol 19 (1) ◽  
pp. 44-52 ◽  
Author(s):  
Hirokazu Fujikawa ◽  
Eiichi Tani ◽  
Ikuya Yamaura ◽  
Isao Ozaki ◽  
Katsuya Miyaji ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Basilar Artery ◽  
Molecular Mechanisms ◽  
Kinase Inhibitor ◽  
Polyacrylamide Gel Electrophoresis ◽  
Intracellular Ca ◽  
Canine Basilar Artery ◽  
Kinase Pathway

Subarachnoid hemorrhage (SAH) often leads to a long-term narrowing of cerebral artery called vasospasm. To understand the molecular mechanisms in vasospasm, signal transduction of tyrosine kinase pathway and phosphorylation of myosin light chain (MLC) and calponin (CaP) in the basilar artery were studied. Vasospasm was produced in the canine basilar artery by a two-hemorrhage method, and vasocontraction was induced by a local application of KCl or serotonin to the basilar artery after a transclival exposure. Intracellular substrates of tyrosine kinase pathway, including Shc, Raf1, and extracellular-regulated kinases in the basilar artery, were activated after SAH, and the activation of Shc suggests stimulation of signal transductions from tyrosine kinase receptors, G-coupled receptors, or both. The activation of tyrosine kinase pathway in vasospasm also was supported by dose-dependent dilation of the spastic basilar artery on days 0 and 7 by topical application of genistein, a tyrosine kinase inhibitor, and associated marked inhibition of tyrosine phosphorylation of intracellular substrates, including Shc. In addition, the generation of protein kinase M, catalytic fragment of protein kinase Cα (PKCα), in vasospasm on days 0 and 7 was inhibited in response to genistein, indicating an inactivation of μ-calpain. It is suggested, therefore, that the reversal of vasospasm by genistein is closely associated with the restoration of intracellular Ca2+ levels. However, the increased activities of Raf1 and extracellular-regulated kinases in vasospasm were declined on day 7 compared with those on day 0 or 2, suggesting that the activation of tyrosine kinase pathway is more closely associated with the early stage of vasospasm than with the late stage of vasospasm. The analysis by pyrophosphate polyacrylamide gel electrophoresis (PPi-PAGE) demonstrated three MLC bands in vasospasm on days 2 and 7, as well as in KCl- and serotonin-induced vasocontraction. Since PPi-PAGE resolves smooth muscle MLC into three bands in the MLC kinase (MLCK)-mediated phosphorylation and into a single band in the PKC-mediated phosphorylation based on the phosphorylation state, the current results suggest that MLC in vasospasm is phosphorylated by MLCK but not by PKC. In basilar artery, CaP was significantly down-regulated, and in addition, significantly phosphorylated on serine and threonine residues only in vasospasm on days 2 and 7. Although the significance of CaP phosphorylations in vivo still is controversial, CaP down-regulation and phosphorylation may attenuate the inhibition of Mg2+-ATPase activity by CaP and induce a potential enhancement of smooth muscle contractility in delayed vasospasm. Since CaP is phosphorylated vivo by PKC, activated PKC in vasospasm may phosphorylate CaP. Thus, SAH stimulates tyrosine kinase pathway to increase intracellular Ca2+ and activate PKC, and the former activates MLCK to phosphorylate MLC, whereas the latter phosphorylates CaP but not MLC.

scholarly journals Gene expression in a canine basilar artery vasospasm model: a genome-wide network-based analysis

2008 ◽  
Vol 31 (3) ◽  
Author(s):  
Atsushi Sasahara ◽  
Hidetoshi Kasuya ◽  
Boris Krischek ◽  
Atsushi Tajima ◽  
Hideaki Onda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Basilar Artery ◽  
Genome Wide ◽  
A Genome ◽  
Canine Basilar Artery

scholarly journals Levcromakalim decreases cytoplasmic Ca2+ and vascular tone in canine basilar artery of SAH model

1998 ◽  
Vol 76 ◽  
pp. 210
Author(s):  
Teruyuki Yanagisawa ◽  
Kazuyuki Sugai ◽  
Osamu Motohashi ◽  
Michiyasu Suzuki ◽  
Takashi Yoshimoto
Keyword(s):  
Basilar Artery ◽  
Vascular Tone ◽  
Canine Basilar Artery
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