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Vascular hyperactivity

The pathogenesis of rosacea is multifactorial. Vascular hyperactivity is the primary phenomenon that is complicated by inflammatory changes. Endocrine, psychological, pharmacological, immunological, infectious, thermal and alimentary factors contribute to produce vascular instability and tissue damage (Fig. 17.1). The role of Helicobacter pylori is still being discussed. [Pg.185]

SUR2B/Kir6.2 Efforts have also focused on the development of selective KAXP channel openers for vascular and nonvascular indications including angina, airway hyperactivity, bladder overactivity, and erectile... [Pg.996]

Antipyretic activity. Ethanol (50%) extract of the plant, administered intraperito-neally to guinea pigs, was inactive " . Anti-thrombotic effect. Olive oil extract of the fmit, administered intragastrically to male rabbits at a dose of 150 g/kg, was active. Lipid profile was improved with decreased platelet hyperactivity and subendot-helial thrombogenicity and less severe morphological lesion of the endothelium and vascular wall . [Pg.383]

Acute poisoning is manifested by excitement and peripheral sympathomimetic effects convulsiorrs may occur also, in acute or chronic overuse, a state resembling hyperactive paranoid schizophrenia with hallucinations develops. Hyperthermia occurs with cardiac arrhythmias, vascular collapse and death. Treatment is chlorpromazine with added antihypertensive, e.g. labetalol, if necessary these provide sedation and a- and P-adrenoceptor blockade (not a P-blocker alone), rendering unnecessary the enhancement of elimination by urinary acidification. [Pg.193]

Clonidine is used in the management of hypertension, attention-deficit hyperactivity disorder, opiate or nicotine withdrawal, vascular headache prophylaxis, and as an aid in the diagnosis of pheochromocytoma. It is also used as an epidural infusion for pain management. [Pg.623]

ADHD, attention-deficit/hyperactivity disorder AV, atrioventricular BPH, benign prostatic hypertrophy CAD, coronary artery disease CHF, congestive heart failure COPD, chronic obstructive pulmonary disease CV, cardiovascular DA, dopamine Dl, subtype 1 dopamine receptor Epi, epinephrine FFA, free fatty acids 5-HT, serotonin ISA, intrinsic sympathomimetic activity MI, myocardial infarction NE, norepinephrine NO, nitric oxide PVR, peripheral vascular resistance. [Pg.184]

An abnormal, general elevation of sympathetic activity (termed either hyperactivity, hyper-reactivity or overreactivity) as the major cause of Raynaud s phenomenon in vibration-exposed workers has been advocated by Olsen (1990). In a recent paper, however, the same author (Olsen 1991) sees this as only one of several possible mechanisms leading to vibration-induced Raynaud s phenomenon. The active mechanism of digital artery closure mediated by central sympathetic reflexes is seen as predominant, but other active and passive mechanisms - such as abnormal adrenergic receptor activity of the smooth muscle cell or hypertrophy of vascular smooth muscle cells - are also envisaged as possible etiologic factors. An imbalance between the parasympathetic and sympathetic parts of the autonomic nervous system has been suggested to contribute to the development of VWF (Heinonen et al. 1987 Bovenzi 1990 Farkkila et al. 1990). [Pg.164]


See other pages where Vascular hyperactivity is mentioned: [Pg.240]    [Pg.320]    [Pg.167]    [Pg.221]    [Pg.221]    [Pg.1331]    [Pg.242]    [Pg.1508]    [Pg.165]    [Pg.463]    [Pg.605]    [Pg.324]    [Pg.496]    [Pg.339]    [Pg.319]    [Pg.422]    [Pg.329]    [Pg.731]    [Pg.58]    [Pg.31]    [Pg.45]   
See also in sourсe #XX -- [ Pg.185 ]

See also in sourсe #XX -- [ Pg.185 ]




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Hyperactive

Hyperactivity

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