Adrenergic innervation of the cerebral blood vessels in the rabbit

1971 ◽  
Vol 35 (2) ◽  
pp. 148-154 ◽  
Author(s):  
S. John Peerless ◽  
M. Gazi Yasargil

✓ The Hillarp technique of fluorescent staining of monoamines was used to examine the adrenergic fibers in the cerebral vessels of rabbit brains. These fibers were found to lie wholly within the deeper layers of the adventitia and not within muscle layers. Varicosities were interpreted as representing neural transmitter substance. The basilar artery had a sparse innervation; the anterior cerebral, carotid, and middle cerebral arteries were more richly supplied by adrenergic terminals, with the most dense innervation in the superficial vessels between 100 and 300 µ in diameter. Mild trauma to the basilar artery, as well as subarachnoid blood without trauma, caused the catecholamine reaction to disappear. A marked depletion of adrenergic fibers was also noted after administration of alpha methyl tyrosine and subjection of the animals to extremes of blood pressure.

1986 ◽  
Vol 64 (4) ◽  
pp. 594-600 ◽  
Author(s):  
Rolf W. Seiler ◽  
Peter Grolimund ◽  
Rune Aaslid ◽  
Peter Huber ◽  
Helge Nornes

✓ In 39 patients with a proven subarachnoid hemorrhage (SAH), the clinical status, the amount of subarachnoid blood on a computerized tomography scan obtained within 5 days after SAH, and the flow velocities (FV's) in both middle cerebral arteries (MCA's) measured by transcranial Doppler sonography were recorded daily and correlated. All patients had pathological FV's over 80 cm/sec between Day 4 and Day 10 after SAH. The side of the ruptured aneurysm showed higher FV's than did the unaffected side in cases of laterally localized aneurysms. Increase in FV preceded clinical manifestation of ischemia. A steep early increase of FV's portended severe ischemia and impending infarction. Maximum FV's in the range of 120 to 140 cm/sec were not critical and in no case led to brain infarction. Maximum FV's over 200 cm/sec were associated with a tendency for ischemia, but the patients may remain clinically asymptomatic. In cases of no or only a little blood in the basal cisterns, mean FV's in both MCA's increased only moderately whereas, with thick clots of subarachnoid blood, there was a steeper and higher increase of mean FV's.


1971 ◽  
Vol 35 (6) ◽  
pp. 664-671 ◽  
Author(s):  
Takenori Yamaguchi ◽  
Arthur G. Waltz

✓ Bilateral measurements of regional cortical blood flow (CBF) and the diameter of superficial cortical arteries were made before and after puncture of the right middle cerebral arteries (MCA) of 11 cats with bilateral craniectomies. The CBF was decreased in the right cerebral hemispheres before puncture, probably because of manipulation and exposure of the MCA. Decreases of CBF occurred after MCA puncture in the contralateral cerebral hemispheres of five of seven animals without subarachnoid blood over the convexities of the hemispheres. The mean CBF value for the contralateral hemispheres was significantly lower after puncture than before. There was no consistent relationship between CBF and the calibers of surface cortical arteries. Thus, basal subarachnoid bleeding can cause decreases of CBF of the cerebral hemispheres, probably because of basal arterial spasm associated, at times, with vasomotor paralysis and failure of autoregulatory responses. If combined with increases of intracranial pressure, such decreases of CBF may be adequate to produce cerebral ischemia.


1981 ◽  
Vol 55 (5) ◽  
pp. 771-778 ◽  
Author(s):  
Tomio Sasaki ◽  
Sei-itsu Murota ◽  
Susumu Wakai ◽  
Takao Asano ◽  
Keiji Sano

✓ 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.


1980 ◽  
Vol 53 (3) ◽  
pp. 300-304 ◽  
Author(s):  
Toshisuke Sakaki ◽  
Kazuhiko Kinugawa ◽  
Tatsuo Tanigake ◽  
Seiji Miyamoto ◽  
Kikuo Kyoi ◽  
...  

✓ Embolism from an aneurysm is one of the mechanisms involved in the pathogenesis of ischemic symptoms associated with intracranial aneurysms. Four cases are reported in which aneurysms of the internal carotid arteries and middle cerebral arteries were the source of emboli resulting in cerebral infarction. In the treatment of these aneurysms, it is best to clip the neck of the aneurysm with great care to avoid embolism due to extrusion of clot into the distal artery.


2010 ◽  
Vol 299 (2) ◽  
pp. R461-R469 ◽  
Author(s):  
Khodadad Namiranian ◽  
Eric E. Lloyd ◽  
Randy F. Crossland ◽  
Sean P. Marrelli ◽  
George E. Taffet ◽  
...  

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.


2014 ◽  
Vol 59 (No. 7) ◽  
pp. 343-348 ◽  
Author(s):  
W. Brudnicki ◽  
B. Skoczylas ◽  
R. Jablonski ◽  
W. Nowicki ◽  
A. Brudnicki ◽  
...  

The brain arteries derived from 50 adult degu individuals of both sexes were injected with synthetic latex introduced with a syringe into the left ventricle of the heart under constant pressure. After fixation in 5% formalin and brain preparation, it was found that the sources of the brain’s supply of blood are vertebral arteries and the basilar artery formed as a result of their anastomosis. The basilar artery gave rise to caudal cerebellar arteries and then divided into two branches which formed the arterial circle of the brain. The internal carotid arteries in degus, except for one case, were heavily reduced and did not play an important role in the blood supply to the brain. The arterial circle of the brain in 48% of the cases was open from the rostral side. Variation was identified in the anatomy and the pattern of the arteries of the base of the brain in the degu which involved an asymmetry of the descent of caudal cerebellar arteries (6.0%), rostral cerebellar arteries (8%) as well as middle cerebral arteries (12%). In 6% of the individuals double middle cerebral arteries were found. In one out of 50 cases there was observed a reduction in the left vertebral artery and the appearance of the internal carotid artery on the same side. In that case the left part of the arterial circle of the brain was supplied with blood by an internal carotid artery, which was present only in that animal.


1995 ◽  
Vol 83 (3) ◽  
pp. 510-515 ◽  
Author(s):  
Hisashi Onoue ◽  
Nobuyoshi Kaito ◽  
Masahiko Akiyama ◽  
Masato Tomii ◽  
Shogo Tokudome ◽  
...  

✓ 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.


1984 ◽  
Vol 61 (3) ◽  
pp. 494-500 ◽  
Author(s):  
Toshiki Takemae ◽  
P. Josephine Branson ◽  
John F. Alksne

✓ A model of experimental subarachnoid hemorrhage in young pigs has been created using two subarachnoid blood injections. Cerebral arteries of the pig demonstrate intimal proliferation and medial necrosis 10 days after experimental blood injection; this appears to be a reaction to arterial injury. The similarity between the arterial reaction to subarachnoid blood and the general process of atherosclerosis is noted, and steps have been taken to insure that the vasculopathy described is truly a response to the injected blood. The authors conclude that the intimal proliferation observed between 1 and 2 weeks after experimental subarachnoid blood injection is an indicator of arterial injury and is, therefore, a good end point for further studies.


2005 ◽  
Vol 102 (5) ◽  
pp. 918-921 ◽  
Author(s):  
Matthew F. Sanford ◽  
Aquilla S. Turk ◽  
David B. Niemann ◽  
Kari A. Pulfer ◽  
Beverly A. Aagaard-Kienitz

✓ The authors describe the novel use of cerebral perfusion computerized tomography studies to evaluate the effectiveness of internal carotid artery stent placement in a man with symptomatic transient ischemic attacks caused by tandem stenoses of the internal carotid and middle cerebral arteries.


1976 ◽  
Vol 44 (4) ◽  
pp. 513-516 ◽  
Author(s):  
William F. McCormick ◽  
Patrick J. Kelly ◽  
Mohammed Sarwar

✓ A unique case of fatal paradoxical muscle embolism in a patient with a traumatic carotid-cavernous fistula is described. The muscle plug intended to occlude a left-sided fistula passed through the large fistula, bypassed the lungs by way of a patent foramen ovale, and embolized through the right carotid artery to lodge in the internal carotid and middle cerebral arteries producing fatal brain infarction.


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