Cerebral vasospasm: contractile activity of hemoglobin in isolated canine basilar arteries

1980 ◽  
Vol 53 (6) ◽  
pp. 787-793 ◽  
Author(s):  
Takeo Tanishima
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Contractile Activity ◽  
Cerebral Arteries ◽  
Adenosine Monophosphate ◽  
Active Species ◽  
Exchange Chromatography ◽  
Basilar Arteries ◽  
Chronic Cerebral Vasospasm

✓ Recent studies suggest the possible role of the red blood cell (RBC) in causing chronic cerebral vasospasm. However, the basic action of hemoglobin (Hb), the major component of the RBC, on cerebral arteries remains unknown. The present study was undertaken to analyze the contractile effects of human Hb (purified by ion-exchange chromatography) on canine arteries in vitro. The contractile activity of lysed RBC was shown to be derived from Hb. Hemoglobin in oxygenated form (oxyHb) caused a maximum contraction equal to about 70% of that induced by serotonin in the basilar artery. Ferrous Hb's (oxyHb and carboxyHb) produced much greater contraction than ferric Hb's (methemoglobin and cyanmethemoglobin), suggesting that superoxide radicals, an active species of oxygen, may be related to the contractile activity of Hb. Neither methysergide, phentolamine, mepyramine, nor aspirin inhibited the vasoconstrictive activity of oxyHb. This finding indicates that the activation of serotonergic, alpha-adrenergic, or histaminergic H1 receptors, or prostaglandin synthesis may not be involved in the mechanism of action of oxyHb. The constituents of Hb caused little or no contraction as compared with Hb as a whole. The basilar artery was more highly sensitive to Hb than arteries from other anatomical locations. Cyclic adenosine monophosphate caused a very slight decrease in the Hb-induced contraction. It is concluded that oxyHb can contract cerebral arteries in vitro. These results, coupled with recent reports on the participation of the RBC in producing chronic vasospasm, strongly suggest that oxyHb released from RBC's plays an important role in the pathogenesis of chronic cerebral vasospasm.

scholarly journals Endotoxin Decreases the Contractile Responses of the Porcine Basilar Artery to Vasoactive Substances

1993 ◽  
Vol 13 (4) ◽  
pp. 712-719 ◽  
Author(s):  
Masami Ueno ◽  
Tony J.-F. Lee
Keyword(s):  
Endothelial Cells ◽  
Basilar Artery ◽  
Muscle Tone ◽  
Cerebral Arteries ◽  
Contractile Responses ◽  
Vasoactive Substances ◽  
Basilar Arteries ◽  
Arterial Reactivity ◽  
Lps Treatment

The effects of endotoxin (lipopolysaccharide; LPS) on the reactivity of isolated porcine basilar artery were examined using in vitro tissue bath techniques. The active muscle tone of the basilar arterial rings with or without endothelial cells induced by U46619 (1 μ M) reached a plateau in 15 min, which was stable for the first hour and gradually decreased during the next 5 h. This time-dependent decrease in tone was significantly potentiated in the presence of LPS (20 μg/ml). The potentiation by LPS was blocked by Nw-nitro-l-arginine (l-NNA; 60 μ M), methylene blue (10 μ M), and dexamethasone (1 μ M) but not by hemoglobin (1 μ M). The effect of l-NNA was readily reversed by l-arginine but not by d-arginine. Furthermore, the contractile responses of porcine basilar arterial rings with or without intact endothelium to U46619 and KCl were decreased following incubation with LPS (20 μg/ml) for 4 h. Similar hyporeactivity was observed in cold storage–denervated cerebral arteries incubated with LPS for 4 h. This decrease in contractile responses in LPS-treated rings was reversed by 60 μ M l-NNA and 1 μ M dexamethasone. These results indicate that LPS treatment renders the porcine basilar arteries hyporesponsive to vasoconstrictors. Since effects of LPS were not modified by the presence of endothelial cells and perivascular neurons, the alteration in cerebral arterial reactivity may be due in part to an enhanced formation of nitric oxide from l-arginine in the vascular smooth muscle cells.

scholarly journals Upregulation of Relaxin after Experimental Subarachnoid Hemorrhage in Rabbits

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Yuichiro Kikkawa ◽  
Satoshi Matsuo ◽  
Ryota Kurogi ◽  
Akira Nakamizo ◽  
Masahiro Mizoguchi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Messenger Rna ◽  
Cerebral Arteries ◽  
Enzyme Linked Immunosorbent Assay ◽  
Endothelin 1 ◽  
Basilar Arteries ◽  
Experimental Subarachnoid Hemorrhage

Background. Although relaxin causes vasodilatation in systemic arteries, little is known about its role in cerebral arteries. We investigated the expression and role of relaxin in basilar arteries after subarachnoid hemorrhage (SAH) in rabbits.Methods. Microarray analysis with rabbit basilar artery RNA was performed. Messenger RNA expression of relaxin-1 and relaxin/insulin-like family peptide receptor 1 (RXFP1) was investigated with quantitative RT-PCR. RXFP1 expression in the basilar artery was investigated with immunohistochemistry. Relaxin concentrations in cerebrospinal fluid (CSF) and serum were investigated with an enzyme-linked immunosorbent assay. Using human brain vascular smooth muscle cells (HBVSMC) preincubated with relaxin, myosin light chain phosphorylation (MLC) was investigated with immunoblotting after endothelin-1 stimulation.Results. After SAH, RXFP1 mRNA and protein were significantly downregulated on day 3, whereas relaxin-1 mRNA was significantly upregulated on day 7. The relaxin concentration in CSF was significantly elevated on days 5 and 7. Pretreatment with relaxin reduced sustained MLC phosphorylation induced by endothelin-1 in HBVSMC.Conclusion. Upregulation of relaxin and downregulation of RXFP1 after SAH may participate in development of cerebral vasospasm. Downregulation of RXFP1 may induce a functional decrease in relaxin activity during vasospasm. Understanding the role of relaxin may provide further insight into the mechanisms of cerebral vasospasm.

scholarly journals Preclinical evaluation of Millipede 088 intracranial aspiration catheter in cadaver and in vitro thrombectomy models

2020 ◽  
pp. neurintsurg-2020-016218 ◽  
Author(s):  
Seán Fitzgerald ◽  
David Ryan ◽  
John Thornton ◽  
Raul G Nogueira
Keyword(s):  
Basilar Artery ◽  
Blood Clot ◽  
Cerebral Arteries ◽  
In Vitro Study ◽  
Cadaveric Study ◽  
Vitro Study ◽  
First Pass ◽  
Fresh Frozen ◽  
Basilar Arteries

BackgroundLarger bore aspiration catheters are expected to significantly improve the speed and completeness of acute stroke revascularization.ObjectiveTo evaluate the navigability and clot retrieval performance of a novel 8Fr aspiration catheter, Millipede 088 (Perfuze Ltd), using fresh-frozen cadavers and an in vitro thrombectomy model, respectively.MethodsCadaveric study: Transfemoral catheterization of the intracranial arteries was performed in six cadavers, allowing evaluation of navigation to 12 middle cerebral arteries (MCAs) and six basilar arteries. Commercially available 6Fr aspiration catheters (SOFIA Plus, Microvention) were used as controls. In vitro study: Three human blood clot phenotypes were created; red blood cell-rich, mixed, and fibrin/platelets-rich. Two clot sizes, resulting in occlusion of the internal carotid artery (ICA) and MCA-M1 were investigated. Endpoints were first-pass effect (FPE), first-pass complete ingestion, and second-pass recanalization.ResultsCadaveric study: Both the Millipede 088 and SOFIA Plus devices reached the distal MCA-M1 and the basilar artery in 10/12 and 2/2 of the navigation attempts, respectively. In the two instances of unsuccessful navigation, neither device was able to cross the ophthalmic artery. In vitro study: In 10 mm long M1 occlusions, Millipede 088 achieved 100% FPE versus 40% for 6Fr devices (p>0.001). In 20 mm long ICA occlusions, Millipede 088 achieved 100% removal success within two passes in each clot phenotype compared with an average of 27% for 6Fr devices (p>0.001).ConclusionsNavigation of the Millipede 088 catheter to the MCA-M1 and basilar artery is feasible in a cadaver model. Millipede 088 demonstrates superiority over 6Fr aspiration catheters for three representative clot phenotypes at the most common sites of occlusion in an in vitro vasculature model.

scholarly journals Identification, Characterization, and Functional Role of Phosphodiesterase Type IV in Cerebral Vessels: Effects of Selective Phosphodiesterase Inhibitors

1997 ◽  
Vol 17 (2) ◽  
pp. 210-219 ◽  
Author(s):  
Robert N. Willette ◽  
Aaron O. Shiloh ◽  
Charles F. Sauermelch ◽  
Anthony Sulpizio ◽  
Marcus P. Michell ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Cerebral Vessels ◽  
Type Iv ◽  
Canine Basilar Artery ◽  
Camp Hydrolysis ◽  
Phosphodiesterase Type ◽  
Chronic Cerebral Vasospasm

The role of the phosphodiesterase type IV isozyme (PDE IV) in the regulation of cerebrovascular tone was investigated in the canine basilar artery in vitro and in vivo. The PDE isozymes extracted from the canine basilar artery were isolated by diethylaminoethanol (DEAE)-Sepharose affinity chromatography and identified based on sensitivity to tsozyme-selective PDE inhibitors. [3H]cAMP hydrolysis was observed in one major and one minor peak of activity. The predominant peak was inhibited by the addition of cGMP (25%), siguazodan (26%), rolipram (39%), and the combination of siguazodan and rolipram (95%). Selective PDE IV inhibitors BRL 61063, rolipram, and denbufylline were equieffective inhibitors of [3H]-ccAMP hydrolysis mediated by PDE IV isolated from the canine basilar artery [concentrations producing 50% inhibition (IC50s) = 0.21 ± 0.05 μM, 0.67 ± 0.23 μM, and 0.73 ±0.16 μM, respectively]. In precontracted isolated ring segments of the canine basilar artery, selective PDE IV inhibitors produced potent and complete relaxation (IC50s <150 nM). In contrast, zaprinast (a selective PDE V inhibitor) and siguazodan (a selective PDE III inhibitor) produced only weak relaxation of the basilar artery (IC50s = 4.5 μM and >10 μM, respectively). Vasorelaxation produced by PDE IV inhibitors was not altered by removing the endothelium, l-NAME, or adenosine receptor antagonism. In a canine model of acute cerebral vasospasm, all three selective PDE IV inhibitors reversed basilar artery spasm produced by autologous blood without altering mean arterial blood pressure. In contrast, prolonged treatment with BRL 61063 failed to alter the development of basilar spasm in the two hemorrhage canine models of chronic cerebral vasospasm. Denbufylline-induced relaxation in vitro was also significantly impaired in basilar arteries obtained from the model of chronic vasospasm. In conclusion, PDE IV appears to be the predominant isozyme regulating vascular tone mediated by cAMP hydrolysis in cerebral vessels. In addition, vasorelaxation modulated by PDE IV is compromised in chronic cerebral vasospasm associated with subarachnoid hemorrhage.

scholarly journals Application of the 1-µsec pulsed-dye laser to the treatment of experimental cerebral vasospasm

1991 ◽  
Vol 75 (2) ◽  
pp. 271-276 ◽  
Author(s):  
Atsushi Teramura ◽  
Robert Macfarlane ◽  
Christopher J. Owen ◽  
Ralph de la Torre ◽  
Kenton W. Gregory ◽  
...  
Keyword(s):  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Laser Energy ◽  
Autologous Blood ◽  
Preliminary Investigation ◽  
Dye Laser ◽  
Pulsed Dye Laser ◽  
Content Type

✓ Laser energy of 480 nm was applied in 1-µsec pulses varying between 2.2 and 10 mJ to in vitro and in vivo models of cerebral vasospasm. First, the pulsed-dye laser was applied intravascularly via a 320-µm fiber to basilar artery segments from six dogs. The segments were mounted in a vessel-perfusion apparatus and constricted to, on average, 70% of resting diameter by superfusion with dog hemolysate. Immediate increase in basilar artery diameter occurred to a mean of 83% of control. In a second model, the basilar artery was exposed transclivally in the rabbit. In three normal animals, superfusion of the artery with rabbit hemolysate resulted in a reduction of mean vessel diameter to 81% of control. Following extravascular application of the laser, vessels returned to an average of 106% of the resting state. In six rabbits, the basilar artery was constricted by two intracisternal injections of autologous blood, 3 days apart. Two to 4 days after the second injection, the basilar artery was exposed. Extravascular laser treatment from a quartz fiber placed perpendicular to the vessel adventitia resulted in an immediate 53% average increase in caliber to an estimated 107% of control. No reconstriction was observed over a period of up to 5 hours. Morphologically, damage to the arterial wall was slight. This preliminary investigation suggests that the 1-µsec pulsed-dye laser may be of benefit in the treatment of cerebral vasospasm.

scholarly journals in vitro Effects of Calcium Antagonists PN 200-110, Nifedipine, and Nimodipine on Human and Canine Cerebral Arteries

1983 ◽  
Vol 3 (3) ◽  
pp. 354-361 ◽  
Author(s):  
E. Müller-Schweinitzer ◽  
P. Neumann
Keyword(s):  
Rank Order ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Mesenteric Arteries ◽  
Organ Bath ◽  
Vasoconstrictor Response ◽  
Dihydropyridine Derivative ◽  
Basilar Arteries ◽  
In Vitro Effects

PN 200–110 [4-(2, 1, 3-benzoxadiazol - 4 -) - 1,4-dihydro - 2,6 - dimethyl - pyridine - 3,5 - dicarboxylic acid methyl 1-methylethyl ester], a new dihydropyridine derivative, was investigated by recording isometric tension on spiral strips from human and canine arteries in tissue baths at 37°C. Responses to increasing concentrations of CaCl2 were investigated in calcium-free depolarizing solution (60 mmol/L KCl in equimolar replacement for NaCl, 50 mmol/L TRIZMA buffer, pH 7.4). Comparison of those concentrations that reduced the vasoconstrictor response to 1.6 mmol/L CaCl2 by 50% revealed the following order of potencies on both human and canine arteries: PN 200–110 > nimodipine > nifedipine. Responses to 5-hydroxytryptamine (5-HT) and blood were investigated in Krebs–Henseleit solution (NaHCO3 buffer). On canine arteries, PN 200–110 antagonized responses to 5-HT when used at 10–30 pmol/L; it was ∼70 times more potent on basilar than on mesenteric arteries, whereas both nifedipine and nimodipine were, respectively, ∼10 and 6 times more potent on basilar than on mesenteric arteries. When canine basilar arteries were constricted by the addition of blood to the organ bath, each of the investigated dihydropyridine derivatives elicited concentration-dependent relaxation, producing the following order of potencies: PN 200–110 > nifedipine = nimodipine. On human anterior cerebral arteries, the blood-induced contractions were counteracted in the following rank order: PN 200–110 = nimodipine > nifedipine. The results suggest that due to its potent calcium-blocking activity on cerebral arteries, PN 200–110 might be of value for the prevention and treatment of cerebrovascular spasms following subarachnoid hemorrhage.

Effects of ischemia and myogenic activity on active and passive mechanical properties of rat cerebral arteries

2002 ◽  
Vol 283 (6) ◽  
pp. H2268-H2275 ◽  
Author(s):  
Rebecca J. Coulson ◽  
Naomi C. Chesler ◽  
Lisa Vitullo ◽  
Marilyn J. Cipolla
Keyword(s):  
Contractile Activity ◽  
Cerebral Arteries ◽  
Biomechanical Properties ◽  
Short Term ◽  
Mechanical Stiffness ◽  
Middle Cerebral Arteries ◽  
Male Wistar Rats ◽  
Myogenic Activity ◽  
Activity Dependent

Passive (papaverine induced) and active (spontaneous pressure induced) biomechanical properties of ischemic and nonischemic rat middle cerebral arteries (MCAs) were studied under pressurized conditions in vitro. Ischemic (1 h of occlusion), contralateral, and sham-operated control MCAs were isolated from male Wistar rats ( n = 22) and pressurized using an arteriograph system that allowed control of transmural pressure (TMP) and measurement of lumen diameter and wall thickness. Three mechanical stiffness parameters were computed: overall passive stiffness (β), pressure-dependent modulus changes ( E inc,p), and smooth muscle cell (SMC) activity-dependent changes ( E inc,a). The β-value for ischemic vessels was increased compared with sham vessels (13.9 ± 1.7 vs. 9.1 ± 1.4, P < 0.05), indicating possible short-term remodeling due to ischemia. E inc,p increased with pressure in the passive vessels ( P < 0.05) but remained relatively constant in the active vessels for all vessel types, indicating that pressure-induced SMC contractile activity (i.e., myogenic reactivity) in cerebral arteries leads to the maintenance of a constant elastic modulus within the autoregulatory pressure range. E inc,a increased with pressure for all conditions, signifying that changes in stiffness are influenced by SMC activity and vascular tone.

scholarly journals Cerebrovascular responses in mice deficient in the potassium channel, TREK-1

2010 ◽  
Vol 299 (2) ◽  
pp. R461-R469 ◽  
Author(s):  
Khodadad Namiranian ◽  
Eric E. Lloyd ◽  
Randy F. Crossland ◽  
Sean P. Marrelli ◽  
George E. Taffet ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Linolenic Acid ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
K Channel ◽  
Whole Cell ◽  
Middle Cerebral Arteries ◽  
Basilar Arteries ◽  
Cerebrovascular Smooth Muscle Cells ◽  
Pore Domain

We tested the hypothesis that TREK-1, a two-pore domain K channel, is involved with dilations in arteries. Because there are no selective activators or inhibitors of TREK-1, we generated a mouse line deficient in TREK-1. Endothelium-mediated dilations were not different in arteries from wild-type (WT) and TREK-1 knockout (KO) mice. This includes dilations of the middle cerebral artery to ATP, dilations of the basilar artery to ACh, and relaxations of the aorta to carbachol, a cholinergic agonist. The nitric oxide (NO) and endothelium-dependent hyperpolarizing factor components of ATP dilations were identical in the middle cerebral arteries of WT and TREK-1 KO mice. Furthermore, the NO and cyclooxygenase-dependent components were identical in the basilar arteries of the different genotypes. Dilations of the basilar artery to α-linolenic acid, an activator of TREK-1, were not affected by the absence of TREK-1. Whole cell currents recorded using patch-clamp techniques were similar in cerebrovascular smooth muscle cells (CVSMCs) from WT and TREK-1 KO mice. α-linolenic acid or arachidonic acid increased whole cell currents in CVSMCs from both WT and TREK-1 KO mice. The selective blockers of large-conductance Ca-activated K channels, penitrem A and iberiotoxin, blocked the increased currents elicited by either α-linolenic or arachidonic acid. In summary, dilations were similar in arteries from WT and TREK-1 KO mice. There was no sign of TREK-1-like currents in CVSMCs from WT mice, and there were no major differences in currents between the genotypes. We conclude that regulation of arterial diameter is not altered in mice lacking TREK-1.

Neurogenically evoked cerebral artery constriction is mediated by neuropeptide Y

1994 ◽  
Vol 72 (9) ◽  
pp. 1086-1088 ◽  
Author(s):  
Ismail Laher ◽  
Peter Germann ◽  
John A. Bevan
Keyword(s):  
Neuropeptide Y ◽  
Cerebral Artery ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
Immune Serum ◽  
Nerve Endings ◽  
Transmural Stimulation ◽  
Basilar Arteries ◽  
Neurogenic Vasoconstriction ◽  
Stimulation Of

We examined the proposal that neuropeptide Y (NPY) released from nerve endings constricts cerebral arteries. Neurogenic vasoconstriction of rabbit basilar arteries is of adrenergic origin but is resistant to blockade by classical α-adrenoceptor antagonists. Tetrodotoxin-sensitive contractions of the rabbit basilar artery were elicited by transmural stimulation of nerves. The contractions were inhibited by incubation of tissues with an antiserum to NPY (0.32 μL undiluted immune serum/mL); addition of prazosin (0.1 μM) did not further attenuate the nerve-mediated contraction. The antiserum to NPY also antagonized vasoconstriction due to exogenously administered NPY and was without effect on responses due to histamine or angiotensin. Our results indicate that neurogenic vasoconstriction of the rabbit basilar artery is largely due to the release of NPY and that it is unlikely that other vasoconstrictors contribute significantly to the increased tone.Key words: cerebral artery, nerves, neuropeptide Y, norepinephrine.

scholarly journals Comparison of the Inhibitory Effects of Antithrombin III, α2-Macroglobulin, and Thrombin in Human Basilar Arteries: Relevance to Cerebral Vasospasm

1987 ◽  
Vol 7 (1) ◽  
pp. 68-73 ◽  
Author(s):  
Richard P. White
Keyword(s):  
Cerebral Vasospasm ◽  
Antithrombin Iii ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Vasorelaxant Effect ◽  
Basal Tone ◽  
At Iii ◽  
Basilar Arteries

Isolated human basilar arteries were used in this study to evaluate the inhibitory effect of antithrombin III (AT III), thrombin, and α2-macroglobulin (α2-M) on contractions elicited by K+, serotonin (5-HT), prostaglandin (PG) D2, PGF2α, and plasmin. α2-M (0.5–1.0 mg/ml) failed to affect the contractions produced by contractile agonists significantly but did notably reduce the basal tone of the arteries. Thrombin (1 and 10 U/ml) reduced basal tone and significantly inhibited the contractions elicited by K+, PGF2α, and plasmin. The relaxant effect of thrombin was abolished by procedures that destroy endothelium and by exposing the artery to thrombin for prolonged periods (tachyphylaxis). AT III (1–6 U/ml) reduced basal tone and significantly inhibited, in a concentration-dependent manner, the contractile responses to K+, 5-HT, PGD2, PGF2α, and plasmin. In sharp contrast to thrombin, AT III did not induce tachyphylaxis nor was its vasorelaxant effect significantly reduced by destruction of the endothelium. The results show AT III to be a potent and nonspecific inhibitor of human cerebral arteries and support the hypothesis that AT III may contribute to the delay of cerebral vasospasm seen in patients who experience aneurysmal hemorrhage.

Sign in / Sign up

Export Citation Format

Share Document