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Cerebral blood vessels

Destmction of the aluminum complex with ammonia then permits hydrocarbon extraction of the alkaloid. The alkaloid is subsequently both isolated and used as its tartrate salt. This nonnarcotic dmg, for which tolerance may develop, is frequently used orally with caffeine (16) for treatment of migraine it acts to constrict cerebral blood vessels, thus reducing blood flow to the brain. [Pg.549]

Caffeine is a mild to potent CNS stimulant, with the degree of its stimulating effect dependent on the dose administered. Caffeine stimulates the CNS at all levels, including the cerebral cortex, die medulla, and the spinal cord. Caffeine has mild analeptic (respiratory stimulating) activity. Other actions include cardiac stimulation (which may produce tachycardia), dilatation of coronary and peripheral blood vessels, constriction of cerebral blood vessels, and skeletal muscle stimulation. Caffeine also has mild diuretic activity. [Pg.246]

Thymic hemorrhage and congested cerebral blood vessels occurred in rats exposed to a 1-hour LC50 of methyl parathion described in Section 3.2.1.1 (EPA 1978e). These are probably nonspecific agonal lesions. [Pg.44]

In contrast to the deleterious effects of arginine described by Buisson, L-arginine was shown to decrease infarct size caused by middle cerebral artery occlusion in spontaneously hypertensive rats. L-Arginine is a precursor for NO synthesis by NOS. The authors attributed the protection to dilation of cerebral blood vessels by NO (Morikawa et 1992). These examples illustrate the difficulty that the NO villain/protector paradox presents to us. [Pg.267]

The often severe headaches, common in caffeine withdrawal, appear to be caused by vasodilation of cerebral blood vessels. This action is probably mediated by the action of the methylxanthines on adenosine receptors. [Pg.234]

Sympathetic nerves are distributed to most vascular beds. They are most abundant in the renal, gastrointestinal, splenic, and cutaneous circulations. Recall that these tissues receive an abundant blood flow, more than is necessary simply to maintain metabolism. Therefore, when blood is needed by other parts of the body, such as working skeletal muscles, sympathetic vasoconstrictor activity reduces flow to the tissues receiving excess blood so that it may be redirected to the muscles. Interestingly, there is no sympathetic innervation to cerebral blood vessels. In fact, these vessels do not have a.j-adrenergic receptors, so they cannot be affected by circulating catecholamines. No physiological circumstance exists in which blood should be directed away from the brain. [Pg.203]

The role of CuZnSOD on oxygen radical production in cerebral vessels has been studied. Didion et al. [28] demonstrated that endogenous CuZnSOD diminished superoxide levels in rabbit cerebral blood vessels and affected nitric oxide- and cyclooxygenase-mediated responses in cerebral microcirculation. A subsequent study by the same group [29] showed increased superoxide production and vascular dysfunction in CuZnSOD-deficient mice. Chang et al. [30] suggested that superoxide induced cytokines, which activated microglial... [Pg.909]

Yamada, M., Lamping, K. G., Duttaroy, A. etal. Cholinergic dilation of cerebral blood vessels is abolished in M5 muscarinic acetylcoholine receptor knockout mice. Proc. Natl Acad. Sci. U.S.A. 98 14096-14101,2001... [Pg.209]

Methyixanthines relax smooth muscle, and have a bronchodilating effect in the lungs. Theophylline is used as a treatment for asthma. Methyixanthines dilate coronary arteries, increasing cardiac blood flow, but an opposite effect occurs on cerebral blood vessels (see below). [Pg.100]

NIOSH-recommended exposure limits for NG, EGDN, or a mixture of the two were set at a level to prevent significant changes in the diameter of cerebral blood vessels during initial exposure, as indicated by the occurrence of headache or by decrease in blood pressure, thereby preventing the development of compensatory vasoconstrictive mechanisms that may eventually result in more serious effects. ... [Pg.528]

Like many volatile halocarbons and other hydrocarbons, inhalation exposure to carbon tetrachloride leads to rapid depression of the central nervous system. Because of its narcotic properties, carbon tetrachloride was used briefly as an anesthetic in humans, but its use was discontinued because it was less efficacious and more toxic than other anesthetics available (Hardin 1954 Stevens and Forster 1953). Depending on exposure levels, common signs of central nervous system effects include headache, giddiness, weakness, lethargy, and stupor (Cohen 1957 Stevens and Forster 1953 Stewart and Witts 1944). Effects on vision (restricted peripheral vision, amblyopia) have been observed in some cases (e.g., Johnstone 1948 Smyth et al. 1936 Wrtschafter 1933), but not in others (e.g., Stewart and Wtts 1944). In several fatal cases, microscopic examination of brain tissue taken at autopsy revealed focal areas of fatty degeneration and necrosis, usually associated with congestion of cerebral blood vessels (Ashe and Sailer 1942 Cohen 1957 Stevens and Forster 1953). [Pg.33]

Xanthines (usually caffeine) are frequently combined with aspirin in the treatment of headaches. In combination with an ergot derivative, methylxanthines have been used to treat migraine. These effects are likely due to their ability to produce vasoconstriction of cerebral blood vessels. Aminophylline is useful in the rehef of pain due to acute biliary colic. [Pg.352]

Contrast-enhanced MRI with Gd-DTPA has been applied to the evaluation of several compounds in man, some focusing on the hemodynamic effects of the drugs on cerebral blood volumes. Kolbtisch and others compared the anesthetic agents nitrous oxide and sevofhirane, noting them to produce compound-specific patterns of diffuse increases in cerebral blood volume (Kolbitsch et al., 2001). Intravenous cocaine, on the other hand, was observed to produce dose-dependent vasoconstriction of cerebral blood vessels (Kaufman et ul., 1998). [Pg.218]

Important differences in vascular selectivity exist among the calcium channel blockers. In general, the dihydropyridines have a greater ratio of vascular smooth muscle effects relative to cardiac effects than do diltiazem and verapamil. Furthermore, the dihydropyridines may differ in their potency in different vascular beds. For example, nimodipine is claimed to be particularly selective for cerebral blood vessels. Splice variants in the structure of the cq channel subunit appear to account for these differences. [Pg.262]

Nimodipine, a member of the dihydropyridine group of calcium channel blockers, has a high affinity for cerebral blood vessels and appears to reduce morbidity after a subarachnoid hemorrhage. Nimodipine was approved for use in patients who have had a hemorrhagic stroke, but it has recently been withdrawn. Nicardipine has similar effects and is used by intravenous and intracerebral arterial infusion to prevent cerebral vasospasm associated with stroke. Verapamil as well, despite its lack of vasoselectivity, is used by the intra-arterial route in stroke. Some evidence suggests that calcium channel blockers may also reduce cerebral damage after thromboembolic stroke. [Pg.262]

NPY produces a variety of central nervous system effects, including increased feeding (it is one of the most potent orexigenic molecules in the brain), hypotension, hypothermia, respiratory depression, and activation of the hypothalamic-pituitary-adrenal axis. Other effects include vasoconstriction of cerebral blood vessels, positive chronotropic and inotropic actions on the heart, and hypertension. The peptide is a potent renal vasoconstrictor and suppresses renin secretion, but can cause diuresis and natriuresis. Prejunctional neuronal actions include inhibition of transmitter release from sympathetic and parasympathetic nerves. Vascular actions include direct vasoconstriction, potentiation of the action of vasoconstrictors, and inhibition of the action of vasodilators. [Pg.389]

Migraine headaches that do not respond to analgesics may be relieved by the use of an agonist of the 5-HT receptor, since these receptors are known to mediate vasoconstriction. Though the causes of migraine are not clear, they are characterized by dilation of cerebral blood vessels. 5-HTi agonists based on the 5-HT structure in current use include the sulphonamide derivative sumatriptan, and the more recent agents naratriptan, rizatriptan,... [Pg.347]

Patients really should not smoke, not only for the sake of their kidneys, but also for the sake of their heart and cerebral blood vessels. Smokers die earlier than non-smokers, but diabetic smokers die much earlier and often develop serious circulation problems at a young age. [Pg.382]

Q7 The mechanisms which trigger migraine remain controversial. The underlying pathophysiology could be due to vasoconstriction of the cerebral arteries, causing transient ischaemia. This would be followed by compensatory vasodilation of the cerebral blood vessels to protect the ischaemic areas. This vasodilation may lead to an increase in intracranial pressure, which causes a severe headache. These events may be followed by changes in nerve activity and neurotransmitter levels. Inflammatory components are also likely to be involved in the pathology of this condition. [Pg.137]

A compensatory vasodilation of the cerebral blood vessels may lead to an increase in intracranial pressure, which causes a severe headache. Serotonin (5-HT) has been implicated in the pathogenesis of migraine. [Pg.138]

Flow to the brain tissue is precisely regulated by a process of autoregulation, according to local chemical conditions. Cerebral blood vessels dilate and so increase blood flow in response to decreased pH and arterial PO2 and to increased arterial PCO2, conditions associated with increased metabolic activity. The neurones are very sensitive to changes in cerebral blood flow interruption of flow for a few seconds causes unconsciousness. [Pg.187]

Amyloid associated with cerebral blood vessels is called ... [Pg.638]


See other pages where Cerebral blood vessels is mentioned: [Pg.274]    [Pg.315]    [Pg.816]    [Pg.110]    [Pg.447]    [Pg.22]    [Pg.326]    [Pg.50]    [Pg.60]    [Pg.10]    [Pg.434]    [Pg.817]    [Pg.502]    [Pg.279]    [Pg.475]    [Pg.326]    [Pg.64]    [Pg.372]    [Pg.104]    [Pg.22]    [Pg.380]    [Pg.429]    [Pg.245]   


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