Disease relevance of Cerebral Veins

• Efficacy of retrograde perfusion of the cerebral vein with verapamil after focal ischemia in rat brain [1].
• Focal (1-2 mm) occlusion of the MCA at its origin, at the olfactory tract, or lateral to the inferior cerebral vein produced infarction in 13%, 67%, and 0% of rats, respectively (N = 38) and produced variable neurologic deficits [2].
• The vein of Galen malformation is a midline arteriovenous fistula with aneurysmal dilatation of the vein of Galen [3].
• BACKGROUND: This study investigates the association between cerebral vein thrombosis (CVT) and the mutations FV 1691A (factor V Leiden), PT 20210A and MTHFR 677TT and acquired factors including oral contraceptive (OC) use [4].
• The use of thrombolysis in venous thrombosis has included deep venous thrombosis of the upper and lower extremities and vena cava, mesenteric veins, cerebral veins, and central access catheters [5].

High impact information on Cerebral Veins

• Sumatriptan (0.01-10 microM), when microinjected perivascularly, caused a decrease in pial artery diameter (maximum change of -19 +/- 9%; mean +/- SD) but had no effect on the diameter of pial veins [6].
• In unrelated subjects the doses of norepinephrine constricting basal vein diameter by 50% (ED50) ranged from 3.9 to 120.5 ng/min [7].
• In the cerebral veins, the abundant SP fibers innervated the cortical veins, deep cerebral veins, and dural sinuses [8].
• The concentration of endothelin inducing half-maximal response was in the nanomolar range, with pial veins being slightly more sensitive to the peptide than pial arterioles [9].
• The formation of platelet thrombi after occlusion was significantly (p less than 0.05) inhibited in the pial veins of cilostazol-treated compared with solvent-treated cats [10].

Biological context of Cerebral Veins

• Endothelin (3 x 10(-10) -3 x 10(-6) M) induced marked vasoconstriction of pial arterioles (-33.5 +/- 3.8% at 3 x 10(-6) M) and pial veins (-35.1 +/- 2.7% at 3 x 10(-6) M) [9].
• Nitric oxide is the predominant mediator for neurogenic vasodilation in porcine pial veins [11].
• The propensity to develop cerebral vein and sinus thrombosis in PNH may be due to release of thromboplastin material from hemolyzed red blood cells, the interaction of complement with red blood cells and platelets, or from increased sensitivity to platelet aggregation [12].

Anatomical context of Cerebral Veins

• We report on the effect of calcium channel blocker verapamil administered into the inferior cerebral vein in rats 1 hour after occlusion of the middle cerebral artery [13].
• The distribution of nerve fibers in the cerebral veins was studied by catecholamine fluorescence simultaneously with acetylcholinesterase (AChE) histochemistry [14].
• Attention is drawn to the capacity for Purkinje cell dendrites and Bergmann glia to extract materials from the CSF, and to the close anatomical relationships of the susceptible lobules I-II, IX and X to the roof of the IVth ventricle and to the cistern of the great cerebral veins [15].
• Immunohistochemistry revealed that CYP1A1 was preferentially induced in endothelial cells (EC) in the choroid plexus, in veins in the leptomeninges, and in cerebral veins of AhR agonist-pretreated mice [16].
• These results provide evidence indicating that perivascular nerves in pial veins like cerebral arteries can convert L-citrulline to L-arginine for synthesizing nitric oxide [17].

Associations of Cerebral Veins with chemical compounds

• Cerebral circulation and histamine: 2. Responses of pial veins and arterioles to receptor agonists [18].
• The alpha 1 and alpha 2 adrenoceptor antagonists, prazosin and yohimbine, had only minor effects on pial veins [19].
• Pial veins exhibited only minor reaction, i.e. a 6% (statistical n.s.) dilatation of large veins during nimodipine, and an 8% dilatation of small veins 20 minutes after stopping nimodipine [20].
• Serotonin 5-HT(7) receptors mediate relaxation of porcine pial veins [21].
• 5-carboxamidotryptamine, which is a potent but nonselective agonist at 5-HT(7) receptors, has been shown to be the most potent inhibitor of RC in porcine pial veins [21].

Gene context of Cerebral Veins

• Nineteen published cases of cerebral vein thrombosis and a deficiency of either anti-thrombin III, protein C, or protein S were reviewed [22].
• In addition the role of prothrombotic risk factors, including PAI-1 4G/5G promoter polymorphism, in cerebral vein thrombosis should be clarified in a multicentre study [23].
• We describe a patient with defective tissue plasminogen activator (t-PA) release who developed internal cerebral vein thrombosis [24].
• In vitro tissue bath studies demonstrated that porcine pial veins in the presence of active muscle tone relaxed on applications of exogenous 5-HT, CGRP, SP, VIP, and sodium nitroprusside, whereas exogenous norepinephrine and neuropeptide Y induced only constrictions [11].
• In addition, basal vein size was smaller, and plasma endothelin concentrations greater, in the hypertensive CRF group [25].

Analytical, diagnostic and therapeutic context of Cerebral Veins

• The pial veins of solvent-treated cats showed significant (p less than 0.05) constriction during occlusion, whereas cilostazol-treated cats exhibited only mild constriction of the pial veins [10].
• Therefore, the present study was designed to determine if the 5-HT-mediated inhibition of RC in pial veins is mediated by 5-HT(7) receptors and if 5-HT(7) receptor mRNA is expressed in endothelium-denuded pial veins; the study was done with the use of an in vitro tissue bath and RT-PCR techniques [21].
• In Group A (n = 10), one dorsal cerebral vein was occluded; in Group B (n = 10), two adjacent dorsal cerebral veins were occluded; and in a sham-operated group (n = 5), the rats also underwent craniotomy and light exposure but received injections of saline rather than the rose bengal dye [26].

References