scholarly journals Effects of Pentobarbital on Contractile Responses of Feline Cerebral Arteries

1981 ◽  
Vol 1 (4) ◽  
pp. 437-440 ◽  
Author(s):  
L. Edvinsson ◽  
J. McCulloch
Keyword(s):  
Anaesthetic Agent ◽  
Cerebral Arteries ◽  
Cerebrovascular Reactivity ◽  
Contractile Responses ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

The effects of pentobarbital on the contractile responses of isolated feline middle cerebral arteries have been examined. In the presence of pentobarbital (3 × 10−4 M), the maximum contractions effected by potassium, noradrenaline, and prostaglandin F2α were reduced by 37 ± 3, 69 ± 3, and 10 ± 6%, respectively. The results caution against the use of pentobarbital as an anaesthetic agent in investigations of cerebrovascular reactivity.

scholarly journals Contractile and Endothelium-Dependent Dilatory Responses of Cerebral Arteries at Various Extracellular Magnesium Concentrations

1991 ◽  
Vol 11 (1) ◽  
pp. 161-164 ◽  
Author(s):  
Mária Faragó ◽  
Csaba Szabó ◽  
Eörs Dóra ◽  
Ildikó Horváth ◽  
Arisztid G. B. Kovách
Keyword(s):  
Smooth Muscle ◽  
Vascular Reactivity ◽  
Calcium Influx ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Contractile Responses ◽  
Middle Cerebral Arteries ◽  
The Right ◽  
Endothelial Receptor

To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10−8-10−5 M norepinephrine, were significantly potentiated at low Mg2+ (0.8 m M v. the normal, 1.2 m M). High (1.6 and 2.0 m M) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 108–10−5 M acetylcholine were inhibited by high (1.6 and 2.0 m M) Mg2+. Lowering of the Mg2+ concentration to 0.8 m M or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.

scholarly journals Effects of GV14 Acupuncture on Cerebral Blood Flow Velocity in the Basilar and Middle Cerebral Arteries and CO2 Reactivity during Hypercapnia in Normal Individuals

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Hyun Ku Lee ◽  
Sang-Kwan Moon ◽  
Chul Jin ◽  
Seung-Yeon Cho ◽  
Seong-Uk Park ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Arteries ◽  
Transcranial Doppler Sonography ◽  
Cerebrovascular Reactivity ◽  
Acupuncture Points ◽  
Co2 Reactivity ◽  
Middle Cerebral Arteries

The Governing Vessel 14 (GV14) (Dazhui) is one of the acupuncture points referred to as “seven acupoints for stroke.” Nevertheless, there is a scarcity of research on the effects of acupuncture treatment at GV14. This study investigated the effects of acupuncture at GV14 on cerebral blood flow (CBF), especially that in the basilar artery (BA) and the middle cerebral arteries (MCA). Sixteen healthy men aged 20 to 29 years were enrolled in this study. CBF velocity and cerebrovascular reactivity (CVR) were measured using transcranial Doppler sonography (TCD). The following were assessed: closed circuit rebreathing- (CCR-) induced carbon dioxide (CO2) reactivity, modified blood flow velocity at 40 mmHg (CV40) on BA and MCAs, blood pressure (BP), and heart rate (HR). Observed results were obtained after comparison with the baseline evaluation. Statistically significant elevations in CO2 reactivity were recorded in the BA (3.28 to 4.70, p < 0.001 ) and MCAs (right: 3.81 to 5.25, p = 0.001 ; left: 3.84 to 5.12, p = 0.005 ) after acupuncture at GV14. The CV40 increased statistically significantly only in the BA (45.49 to 50.41, p = 0.003 ). No change was observed in BP (106.83 to 107.08 (mmHg), p = 0.335 ) and HR (77 to 75 (bpm), p = 0.431 ). Acupuncture at GV14 improved CBF velocity. These results could be explained by the regulation of endothelium-dependent vessel dilation effected by acupuncture. This trial is registered with Korean Clinical Trial Registry (http://cris.nih.go.kr; registration number: KCT0004787).

scholarly journals Regulation of Ca2+sensitization by PKC and rho proteins in ovine cerebral arteries: effects of artery size and age

1998 ◽  
Vol 275 (3) ◽  
pp. H930-H939 ◽  
Author(s):  
Sergey E. Akopov ◽  
Lubo Zhang ◽  
William J. Pearce
Keyword(s):  
G Protein ◽  
Cerebral Arteries ◽  
Rho Kinase ◽  
Cerebrovascular Reactivity ◽  
Rho Proteins ◽  
Experimental Conditions ◽  
Fetal Sheep ◽  
Middle Cerebral Arteries ◽  
Near Term ◽  
Nonpregnant Adult

G protein-regulated Ca2+ sensitivity of vascular contractile proteins plays an important role in cerebrovascular reactivity. The present study examines the intracellular mechanisms that govern G protein-regulated Ca2+ sensitivity in cerebral arteries of different size and age. We studied β-escin-permeabilized segments of common carotid, basilar, and middle cerebral arteries from nonpregnant adult and near-term fetal sheep. Activation of protein kinase C (PKC) by (−)-indolactam V or a phorbol ester produced receptor-independent increases in Ca2+ sensitivity. Such increases were more marked in immature arteries and were inversely correlated with artery size in both mature and immature arteries. However, inhibitors of PKC did not significantly affect increases in Ca2+ sensitivity in responses to either serotonin (5-hydroxytryptamine, 5-HT) or guanosine 5′- O-(3-thiotriphosphate) (GTPγS). Alternatively, deactivation of rho p21, a small G protein associated with Rho kinase, by exotoxin C3 fully prevented increases in Ca2+ sensitivity in responses to 5-HT or GTPγS in both adult and fetal arteries of all types. Neither inhibitors of PKC nor exotoxin C3 altered baseline Ca2+ sensitivity. We conclude that patterns of receptor- and/or G protein-mediated modulation of Ca2+ sensitivity are dependent on an intracellular pathway that involves activation of small G proteins and Rho kinase. In contrast, PKC has little, if any, role in agonist-induced Ca2+ sensitization under the present experimental conditions.

Testosterone suppresses endothelium-dependent dilation of rat middle cerebral arteries

2004 ◽  
Vol 286 (2) ◽  
pp. H552-H560 ◽  
Author(s):  
Rayna J. Gonzales ◽  
Diana N. Krause ◽  
Sue P. Duckles
Keyword(s):  
Vascular Tone ◽  
Cerebral Arteries ◽  
Cerebrovascular Reactivity ◽  
Male Rats ◽  
Intraluminal Pressure ◽  
Vascular Effects ◽  
Additional Increase ◽  
Testosterone Treatment ◽  
Cox Inhibitor ◽  
Middle Cerebral Arteries

Little is known about vascular effects of testosterone. We previously reported chronic testosterone treatment increases vascular tone in middle cerebral arteries (MCA; 300 μm diameter) of male rats. In the present study, we investigated the hypothesis that physiological levels of circulating testosterone affect endothelial factors that modulate cerebrovascular reactivity. Small branches of MCA (150 μm diameter) were isolated from orchiectomized (ORX) and testosterone-treated (ORX+T) rats. Intraluminal diameters were recorded after step changes in intraluminal pressure (20–100 Torr) in the absence or presence of NG-nitro-l-arginine-methyl ester (l-NAME), a nitric oxide synthase (NOS) inhibitor; indomethacin, a cyclooxygenase (COX) inhibitor; and/or apamin and charybdotoxin (CTX); and KCa channel blockers used to inhibit endothelium-derived hyperpolarizing factors (EDHF). At intraluminal pressures ≥60 Torr, arteries from ORX+T developed greater tone compared with ORX arteries. This difference was abolished by removal of the endothelium but remained after treatment of intact arteries with indomethacin or l-NAME. In addition, testosterone treatment had no effect on cerebrovascular production of endothelin-1 or prostacyclin nor did it alter protein levels of endothelial NOS or COX-1. Endothelium removal after l-NAME/indomethacin exposure caused an additional increase in tone. Interestingly, the latter effect was smaller in arteries from ORX+T, suggesting testosterone affects endothelial vasodilators that are independent of NOS and COX. Apamin/CTX, in the presence of l-NAME/indomethacin, abolished the difference in tone between ORX and ORX+T and resulted in vessel diameters similar to those of endothelium-denuded preparations. In conclusion, testosterone may modulate vascular tone in cerebral arteries by suppressing EDHF.

Altered reactivity of human cerebral arteries after subarachnoid hemorrhage

1995 ◽  
Vol 83 (3) ◽  
pp. 510-515 ◽  
Author(s):  
Hisashi Onoue ◽  
Nobuyoshi Kaito ◽  
Masahiko Akiyama ◽  
Masato Tomii ◽  
Shogo Tokudome ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Vasoactive Agents ◽  
Content Type ◽  
Vasoactive Substances ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F ◽  
Human Cadavers ◽  
Endothelium Dependent Relaxation

✓ To investigate the effects of subarachnoid hemorrhage (SAH) on the responsiveness of human cerebral arteries to vasoactive substances, the authors measured the isometric tension generated in helical strips of basilar and middle cerebral arteries isolated from human cadavers Contractions caused by KCl, prostaglandin F2α, noradrenaline, and serotonin were reduced in arteries obtained from cadavers with aneurysmal SAH damage and compared to those obtained from cadavers with no indication of intracranial diseases. Endothelium-dependent relaxation elicited by substance P and bradykinin, and endothelium-independent relaxation induced by prostaglandin I2 and nitroglycerin were also markedly decreased in arteries affected by SAH. However, the reduction in relaxation response to prostaglandin I2 was significantly less than that to the other vasodilator agents. These results indicate that human cerebral artery functions are severely impaired after SAH and that poor responses to vasoactive agents may result primarily from dysfunction of smooth-muscle cells.

scholarly journals PACAP, a VIP-like Peptide: Immunohistochemical Localization and Effect upon Cat Pial Arteries and Cerebral Blood Flow

1993 ◽  
Vol 13 (2) ◽  
pp. 291-297 ◽  
Author(s):  
R. Uddman ◽  
P. J. Goadsby ◽  
I. Jansen ◽  
L. Edvinsson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Arteries ◽  
Immunohistochemical Localization ◽  
Nerve Fibers ◽  
Moderate Increase ◽  
Pial Arteries ◽  
Maximal Increase ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

Pituitary adenylate cyclase activating peptide (PACAP) is a vasoactive intestinal polypeptide (VIP)–like peptide recently isolated from ovine hypothalami. Nerve fibers containing PACAP immunoreactivity were present in the adventitia and the adventitia-media border of cat cerebral arteries. Double immunostaining revealed that PACAP-immunoreactive nerve fibers constituted a sub-population of the VIP-containing fibers. PACAP effected a concentration-dependent relaxation of feline middle cerebral arteries that had been precontracted with prostaglandin F2α. The maximum relaxation, 24 and 34% of precontraction, was achieved with PACAP-38 and PACAP-27, respectively, at a concentration of 10−6 M. In cats anesthetized with α-chloralose, intracerebral microinjection of PACAP effected a moderate increase in cerebral blood flow. The maximal increase (18.6 ± 6%) was observed following the injection of 5 μg PACAP.

scholarly journals Effects of Kininase II Inhibitors on the Vasomotor Response to Bradykinin of Feline Intracranial and Extracranial Arteries in vitro and in situ

1983 ◽  
Vol 3 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Michael Wahl ◽  
Alan R. Young ◽  
Lars Edvinsson ◽  
Franz Wagner
Keyword(s):  
Cerebral Arteries ◽  
Surrounding Tissue ◽  
Experimental Conditions ◽  
Pial Arteries ◽  
Simultaneous Application ◽  
Kininase Ii ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

Bradykinin is known to effect a vasodilatation of feline cerebral arteries in situ and of both human and feline pial arteries in vitro. In order to demonstrate whether kininase II (localized within the vessel wall or in the surrounding tissue or fluid) influences the response to bradykinin, two different inhibitors of this bradykinin degradation enzyme were tested. Perivascular microapplication of potentiator C (10−10–10−4 M) or captopril (10−10–10−3 M) did not, by itself, change the diameter of feline pial arteries (87–305 μm) in situ. In a similar investigation, the dilating action of bradykinin (10−8–10−5 M) was not modified by the simultaneous application of potentiator C or captopril (10−5 M). Furthermore, the relaxing effect of bradykinin (10−10–10−4 M) on isolated feline middle cerebral arteries (preconstricted with 5-hydroxytryptamine or prostaglandin F2α) was not influenced by the presence of captopril (10−7 M). In contrast, when studied on isolated extracranial vessel segments (feline sublingual artery), bradykinin caused a concentration-dependent constriction of the artery. This constriction was completely reversed to dilatation in the presence of captopril (10−7 M). Moreover, the characteristic effect of kininase II inhibition was demonstrated in the isolated guinea pig ileum preparation. In this instance, bradykinin induced a concentration-dependent contraction that was enhanced by potentiator C or captopril. We conclude, therefore, that bradykinin exerts variable responses on vascular smooth muscle, depending on the species used, the muscle location and experimental conditions. Finally, the in situ and in vitro findings for pial and middle cerebral arteries demonstrate that kininase II does not modify the dilating effect of bradykinin under our experimental conditions.

scholarly journals Cerebrovascular Vasodilation to Extraluminal Acidosis Occurs via Combined Activation of ATP-Sensitive and Ca2+-Activated Potassium Channels

2003 ◽  
Vol 23 (10) ◽  
pp. 1227-1238 ◽  
Author(s):  
Ute Lindauer ◽  
Johannes Vogt ◽  
Sigrid Schuh-Hofer ◽  
Jens P Dreier ◽  
Ulrich Dirnagl
Keyword(s):  
Potassium Channels ◽  
Cerebral Arteries ◽  
Vessel Diameter ◽  
Cerebrovascular Reactivity ◽  
Channel Function ◽  
Inward Rectifier Potassium Channels ◽  
Flow Response ◽  
Channel Opener ◽  
Middle Cerebral Arteries

Albeit controversely discussed, it has been suggested by several authors that nitric oxide (NO) serves as a permissive factor in the cerebral blood flow response to systemic hypercapnia. Potassium channels are important regulators of cerebrovascular tone and may be modulated by a basal perivascular NO level. To elucidate the functional targets of the proposed NO modulation during hypercapnia-induced vasodilation, the authors performed experiments in isolated, cannulated, and pressurized rat middle cerebral arteries (MCA). Extracellular pH was reduced from 7.4 to 7.0 in the extraluminal bath to induce NO dependent vasdilation. Acidosis increased vessel diameter by 35 ± 10%. In separate experiments, ATP-sensitive potassium channels (KATP) were blocked by extraluminal application of glibenclamide (Glib), Ca2+-activated potassium channels (KCa) by tetraethylammonium (TEA), voltage-gated potassium channels (Kv) by 4-aminopyridine, and inward rectifier potassium channels (KIR) by BaCl2. Na+-K+-ATP-ase was inhibited by ouabain. Application of TEA slightly constricted the arteries at pH 7.4 and slightly but significantly attenuated the vasodilation to acidosis. Inhibition of the other potassium channels or Na+-K+-ATP-ase had no effect. Combined blockade of KATP and KCa channels further reduced resting diameter, and abolished acidosis induced vasodilation. The authors conclude that mainly KCa channels are active under resting conditions. KATP and KCa channels are responsible for vasodilation to acidosis. Activity of one of these potassium channel families is sufficient for vasodilation to acidosis, and only combined inhibition completely abolishes vasodilation. During NO synthase inhibition, dilation to the KATP channel opener pinacidil or the KCa channel opener NS1619 was attenuated or abolished, respectively. The authors suggest that a basal perivascular NO level is necessary for physiologic KATP and KCa channel function in rat MCA. Future studies have to elucidate whether this NO dependent effect on KATP and KCa channel function is a principle mechanism of NO induced modulation of cerebrovascular reactivity and whether the variability of findings in the literature concerning a modulatory role of NO can be explained by different levels of vascular NO/cGMP concentrations within the cerebrovascular tree.

scholarly journals Impaired Vascular Reactivity of Isolated Rat Middle Cerebral Artery after Cortical Spreading Depression in Vivo

2004 ◽  
Vol 24 (5) ◽  
pp. 526-530 ◽  
Author(s):  
Iris Seitz ◽  
Ulrich Dirnagl ◽  
Ute Lindauer
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cortical Spreading Depression ◽  
Vascular Reactivity ◽  
Spreading Depression ◽  
Cerebral Arteries ◽  
Cerebrovascular Reactivity ◽  
Middle Cerebral Arteries ◽  
Isolated Rat

Cortical spreading depression (CSD) is accompanied by hyperemia followed by long-lasting hypoperfusion and impaired cerebrovascular reactivity. The authors show that vasodilation to extraluminal acidosis (pH 7.0) and increased concentrations of extraluminal potassium (12, 20, 40 mmol/L) was significantly reduced in isolated rat middle cerebral arteries after CSD in vivo before the artery was isolated, compared with sham-operated controls. Application of 80-mmol/L potassium induced vasoconstriction after CSD. Therefore, the impairment of vascular reactivity after CSD in vivo occurs, at least in part, at the vascular level itself.

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