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At least 19 recordsLinked to original sources

Feline cerebral veins and arteries: comparison of autonomic innervation and vasomotor responses.

1. The innervation of feline cerebral (pial) vessels by nerve fibres containing noradrenaline, substance P or vasoactive intestinal polypeptide (VIP) has been examined using the Falck-Hillarp histo-fluorescence method and immunohistochemical techniques. Cerebral veins were shown to be innervated by nerve fibres containing noradrenaline, substance P or VIP. Nerve fibres containing noradrenaline were the most numerous, while fibres containing substance P were observed least frequently in both types of vessel. For each putative neurotransmitter, the density of the innervation of the cerebral veins was less than that of cerebral arteries.2. The vasomotor responses of individual pial arteries and veins on the convexity of the cerebral cortex to perivascular micro-injection of noradrenaline, substance P and VIP were examined in twenty-five cats anaesthetized with alpha-chloralose.3. The perivascular micro-application of noradrenaline resulted in pronounced dose-dependent reductions in the diameter of pial veins (maximum calibre reduction: 32+/-3% noradrenaline 10(-5) M) and arteries (22+/-3% noradrenaline 10(-5) M). Pial veins were more sensitive to noradrenaline than were pial arteries tested under similar conditions. The reductions in the diameter of cerebral veins and arteries resulting from the administration of noradrenaline could be attenuated by the concomitant micro-application of phentolamine (10(-6) M).4. The perivascular micro-application of substance P effected significant dose-dependent increases in the calibre of pial veins (maximum calibre increase: 16+/-4% substance P 10(-7) M) which were of a similar magnitude to those observed in pial arteries in response to this peptide (21+/-4% substance P 10(-6) M).5. The perivascular micro-application of VIP resulted in small increases in the calibre of pial veins (maximum calibre increase: 9+/-2% VIP 10(-8) M) which were proportionately smaller than those observed in pial arteries in response to this peptide (23+/-5% VIP 10(-7) M).

Animals↗

Effects of dihydroergotamine and sumatriptan on isolated human cerebral and peripheral arteries and veins.

BACKGROUND: Pharmacological cerebral vasoconstriction has recently been suggested as treatment for patients with increased intracranial pressure (ICP) after severe traumatic brain lesions. Hypothetically, a moderate constriction of precapillary resistance vessels might be advantageous since it decreases intracapillary blood pressure, and a contraction of cerebral veins might effectively reduce intracranial blood volume and ICP. This report examines the in vitro effects of two vasoconstrictors, dihydroergotamine (DHE) and sumatriptan, which may be considered for treatment of increased ICP. METHODS: The reactivity of isolated small human cerebral subcutaneous and omental arteries and veins were studied during exposure to different concentrations of DHE and sumatriptan. RESULTS: Both sumatriptan and DHE induced concentration-dependent contractions in human cerebral arteries and veins and 50% of maximum contractions were obtained at significantly lower concentrations of DHE than of sumatriptan. The maximum contraction of cerebral arteries was significantly higher with sumatriptan than with DHE. Both drugs caused contractions of subcutaneous arteries at concentrations of 10(-7)-10(-6)M, which is within the therapeutic concentration range of sumatriptan, while no effect was obtained in omental vessels. CONCLUSIONS: Both DHE and sumatriptan cause contraction of isolated human cortical arteries and veins at very low concentrations. The differences observed between the two drugs may be explained by the fact that DHE is an alpha-adrenergic as well as a 5-HT agonist while sumatriptan acts specifically on 5-HT receptors. The study supports the hypothesis underlying the use of DHE for the treatment of increased ICP in patients with severe traumatic brain lesions.

Cerebral Arteries↗

Accumulation and release of [3H]-5-hydroxytryptamine in saphenous veins and cerebral arteries of the dog.

Experiments were performed to examine whether isolated canine blood vessels have the ability to accumulate [3H]-5-hydroxytryptamine ([3H]-5-HT) and if so, whether the 3H-amine can be released from the tissues by stimuli known to evoke release of norepinephrine. Helical strips of saphenous veins and cerebral arteries obtained from dogs were incubated with [3H]-5-HT and mounted for superfusion. Both blood vessels take up [3H]-5-HT in a concentration-dependent manner; this accumulation is markedly reduced in veins and arteries denervated with 6-hydroxydopamine and in veins pretreated with cocaine. In saphenous veins and cerebral arteries labeled with [3H]-5-HT, a basal efflux of 3H, consisting mainly of [3H]-5-hydroxyindole-acetic acid, was observed. Electrical stimulation of the preparations evoked a frequency-dependent overflow of tritium due in part to an overflow of intact [3H]-5-HT. This stimulation-induced 3H-overflow was inhibited by tetrodotoxin and was nearly absent in denervated tissues and in veins pretreated with cocaine. In saphenous veins the overflow of 3H evoked by electrical stimulation was markedly augmented by phentolamine but not influenced by methiothepin. In the veins, both K+ and tyramine caused an overflow of [3H]-5-HT which was absent after denervation or after pretreatment of the preparations with cocaine. Our results show that the major part of the [3H]-5-HT which is taken up by the isolated blood vessels accumulates in the adrenergic nerves and that the indoleamine can be released from these nerves as a "false" transmitter, together with norepinephrine.

Animals↗

[Activation mechanisms of the contractile cells of cerebral arteries and veins].

In isolated strips of internal carotid artery and middle cerebral artery in humans, spontaneous electric and contractile activities were revealed. Low (35 degrees C) and high (40--41 degrees C) temperatures inhibited the development of spontaneous contractions. Under depolarization of the cells' membranes by potassium ions, no development of spontaneous electric or contractile waves occurred, while contractions of the tonic type were observed in arterial preparations. No spontaneous contractions were found in the cerebral veins.

Acetylcholine↗

Distribution of cGMP-dependent and cGMP-independent Ca(2+)-activated Cl(-) conductances in smooth muscle cells from different vascular beds and colon.

In the present patch-clamp study we have, for the first time, shown the tissue distribution of a recently characterized cGMP-dependent Ca(2+)-activated Cl(-) conductance [18] in smooth muscle cells freshly isolated from different regions: aorta, pulmonary artery, tail artery, femoral artery, femoral vein, middle cerebral artery, renal artery, portal vein, superior mesenteric artery, mesenteric small artery and colon. The cGMP-dependent Cl(-) conductance has properties distinct from those of the 'classical' Ca(2+)-activated Cl(-) conductances; their different sensitivities to niflumic acid and zinc were here utilized to distinguish them. They were found to be co-expressed in different patterns in smooth muscle cells of different origins. The cGMP-dependent conductance was greater in myocytes from cerebral artery and femoral vein and was greater in the renal artery, aorta, mesenteric small artery, femoral artery and the superior mesenteric artery. The presence of the cGMP-dependent Ca(2+)-activated Cl(-) current in smooth muscle cells isolated from the colon demonstrates that this conductance is not limited to the vasculature. The 'classical' Ca(2+)-activated Cl(-) conductance was strongly expressed in smooth muscle cells from the portal vein and the tail artery, and noticeably higher in the pulmonary artery.

Animals↗

Subclavian to middle cerebral artery saphenous vein bypass graft.

A variation of an extracranial-intracranial arterial bypass is presented. The subclavian artery is used as the donor vessel and the saphenous vein as the graft; thus, a bypass to a cortical branch of the middle cerebral artery can be accomplished. The advantage of this modification is that the saphenous vein, when tunneled subcutaneously behind the ear, is positioned in a straight line from the donor to the recipient vessel. Since the vein lies in the axis of head rotation, turning of the head causes little displacement of the graft, as opposed to a graft from the common carotid artery to the middle cerebral artery. An additional advantage over the superficial temporal artery to middle cerebral artery bypass is the large flow obtained immediately after anastomosis.

Aged↗

Efficacy of bypass between extracerebral artery and cerebral vein with retrograde verapamil infusion into focal cerebral ischemic tissue in rats.

We examined the efficacy of a bypass from an extracerebral artery to a cerebral vein (EA-CV) with retrograde verapamil infusion on acute focal cerebral ischemia in 35 rats. In 12 rats, within 1 hour after occlusion of the middle cerebral artery (MCAO), changes in blood-brain barrier permeability were examined by [14C]alpha-aminoisobutyric acid autoradiography after EA-CV bypass surgery; there were no significant changes during a period of 2 hours after EA-CV bypass. The other 18 rats having MCAO were divided into three groups of six each. Group A rats (control) underwent only cannulation of the cerebral vein. Group B rats had an EA-CV bypass. Group C rats received verapamil (0.1 mg/kg every 2 h) by transvenous perfusion of the brain (TVPOB) through the EA-CV bypass. In all rats in Groups A and C, local cerebral blood flow (LCBF) and quantitative measurement of early cerebral infarct volume were performed by autoradiography using [14C]iodoantipyrine and histochemical staining methods. Group B rats were examined only with the LCBF measurement. Group B (EA-CV bypass only) showed a nonsignificant improvement (18-40%) of LCBF in the ischemic cerebral cortical areas as compared with control Group A. Group C (EA-CV bypass with TVPOB with verapamil) showed an extensive and significant improvement in LCBF in the ischemic cortical areas (115-140%; P less than 0.05) and a slight increase in LCBF in the subcortical areas (17-29%), with a significant reduction (greater than 35%; P less than 0.05) in a total cerebral infarct volume in the ischemic cerebral hemisphere as compared with the control Group A.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Comparison of the effects of potassium and pH on the calibre of cerebral veins and arteries.

The vasomotor response of individual pial veins and arteries on the convexity of the cerebral cortex to perivascular microinjection of mock cerebrospinal fluid (CSF) containing various concentrations of potassium (K+) and of various pH (achieved by altering the bicarbonate, HCO-3 concentration) have been examined in cats anaesthetised with alpha-chloralose. Microapplication of CSF containing 0 mM HCO-3 (pH 4.80) effected significant increases in calibre of pial veins and arteries of 9.3 +/- 2.4% and 38.2 +/- 4% respectively (mean calibre change +/- SE), whereas CSF containing 22 mM HCO-3 (pH 7.45) which constricted pial arteries significantly (-18.5 +/- 2.9%) minimally altered venous calibre (-4.3 +/- 2.2%). Microapplication of CSF containing 0 mM potassium resulted in a significant reduction in pial arterial calibre (-11.4 +/- 2.8%) but failed to alter pial venous calibre (-0.3 +/- 0.6%). Perivascular microapplication of CSF containing moderately elevated potassium concentrations (10 mM) which effected marked, significant increases in pial arterial calibre (49.3 +/- 3.9%) did not significantly alter the calibre of the pial veins (mean response -1.6 +/- 2.4%). The perivascular administration of CSF containing a high concentration of potassium (40 mM) resulted in the significant constriction of both pial veins (-13.5 +/- 0.9%) and pial arteries (-47.2 +/-6.3%). The magnitude of the response was significantly smaller in the pial veins. The relative insensitivity to K+ and pH of the pial veins as compared to pial arteries suggests that alteration in the chemical composition of of the perivascular fluid are of lesser importance in the control of cerebrovascular capacitance than for the regulation of cerebrovascular resistance.

Animals↗

Interaction of histamine with noradrenergic constrictory mechanisms in cat cerebral arteries and veins.

We examined responses of pial arteries and veins in situ to noradrenergic stimuli in the presence of histamine. Electrical stimulation of sympathetic nerves and perivascular microapplication of norepinephrine in mock cerebrospinal fluid produced constriction of arteries and veins in anesthetized cats. During simultaneous perivascular injection of histamine, these noradrenergic responses were attenuated or reversed. In both arteries and veins, constriction from sympathetic nerve stimulation was prevented by simultaneous application of the histamine receptor agonists, pyridylethylamine (H1) or impromidine (H2), results that suggest interference involving both types of histamine receptors. In arteries, impromidine, but not pyridylethylamine, inhibited constriction resulting from exogenous norepinephrine. Our findings indicate that histamine may have an inhibitory influence, exerted through both receptor types, on noradrenergic mechanisms in cerebral vessels.

Animals↗

Arterialization of cerebral veins on dynamic MDCT angiography: a possible sign of a dural arteriovenous fistula.

OBJECTIVE: MDCT angiography allows fast imaging of the cerebral vessels, and its potential as a noninvasive technique to detect vascular abnormalities on the basis of morphologic changes is well established. We analyzed vascular enhancement patterns of cerebral venous structures on MDCT angiography, which enabled us to diagnose dural arteriovenous fistula. CONCLUSION: MDCT angiography performed during an early arterial phase showed asymmetrically higher contrast intensity in the transverse or sigmoid sinus, or both, in five patients. In all patients, digital subtraction angiography confirmed the presence of a dural arteriovenous fistula on the side on which the higher contrast intensity appeared. Radiologists should actively look for this sign in the imaging workup of patients presenting with nonspecific symptoms that might be related to a dural arteriovenous fistula.

Aged↗