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Cardiovascular system effects

Cardiotonic steroids, 30 (1993) 135 Cardiovascular system, effect of azides, 31 (1994) 121... [Pg.386]

Jones, R. T. Cardiovascular system effects of marijuana. J Clin Pharmacol 2002 42(11 Suppl) 58S-63S. [Pg.110]

Like the effects on the cardiovascular system, effects on the CNS are also dose-dependent. With moderate doses f 15—45 mg IM), there is little effect on the CNS, but, as the dose increases, or if the drug is given IV in a rapid infusion, CNS effects are prominent. These effects initially include sedation, mental depression, and incoherence, but may progress to more serious effects, such as convulsions. Both the cardiovascular and CNS effects are reversible, however, if the drug therapy is discontinued. [Pg.97]

ACUTE HEALTH RISKS gastrointestinal effects abdominal pain nausea diarrhea vomiting headaches weakness delirium anemia leukopenia decreased production of red and white blood cells cardiovascular system effects abnormal heart rhythm blood vessel damage hypotension liver, kidney and blood effects shock death. [Pg.415]

CHRONIC HEALTH RISKS depressed levels of cholinesterase activity in the semm and erythrocytes anorexia cardiovascular system effects effects on the central nervous system chronic skin disorders. [Pg.837]

Cardiovascular Systemic effects can follow conjunctival application of medications. [Pg.240]

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). [Pg.78]

Side Effects and Toxicity. Adverse effects to the tricycHc antidepressants, primarily the result of the actions of these compounds on either the autonomic, cardiovascular, or central nervous systems, are summarized in Table 3. The most serious side effects of the tricycHcs concern the cardiovascular system. Arrhythmias, which are dose-dependent and rarely occur at therapeutic plasma levels, can be life-threatening. In order to prevent adverse effects, as weU as to be certain that the patient has taken enough dmg to be effective, the steady-state semm levels of tricycHc antidepressant dmgs are monitored as a matter of good practice. A comprehensive review of stmcture—activity relationships among the tricycHc antidepressants is available (42). [Pg.468]

Compounds available in the United States are Hsted in Table 1. Whereas they vary in degree, all of them share similar HabiUties of cardiovascular side effects, the potential for central nervous system (CNS) stimulation, the development of tolerance, and abuse potential. AH, with the exception of ma2indol, are derivatives of phenethylamine. The introduction of an oxygen atom on the -carbon of the side chain tends to reduce CNS stimulant properties without decreasing the anorectic activity. Following the Federal Controlled Dmg Act of 1970, dmgs were classified into one of five schedules according to medical utiUty and abuse potential. [Pg.216]

The Class I agents have many similar side effects and toxicities. The anticholinergic side effects include dry mouth, constipation, and urinary hesitancy and retention. Common gastrointestinal (GI) side effects include nausea, vomiting, diarrhea, and anorexia. Cardiovascular adverse effects are hypotension, tachycardia, arrhythmias, and myocardial depression, especially in patients with congestive heart failure. Common central nervous system (CNS) side effects are headache, dizziness, mental confusion, hallucinations, CNS stimulation, paraesthesias, and convulsions. [Pg.112]

Methyldopa, through its metaboHte, CX-methyInorepinephrine formed in the brain, acts on the postsynaptic tt2-adrenoceptor in the central nervous system. It reduces the adrenergic outflow to the cardiovascular system, thereby decreasing arterial blood pressure. If the conversion of methyldopa to CX-methyl norepinephrine in the brain is prevented by a dopamine -hydroxylase inhibitor capable of penetrating into the brain, it loses its antihypertensive effects. [Pg.142]

At low levels of COHb (0.5-2.0%) the body burden is measurable, but research has not shown any substantive effects at these low levels. When COHb increases to higher levels the body burden of CO is elevated, producing adverse effects on the cardiovascular system and reducing physical endurance. [Pg.103]

Recently, much emphasis has been put on the harmful effects of small particles, i.e., particulate matter (PM), on human health. A number of standards have been established to characterize the PM fractions in the air and their effects on human health. A widely used PM standard in force in both Europe and the United States is based on the mass concentration of particles with a diameter of 10 gm or less (PMjo). However, recently the U.S. Environmental Protection Agency (EPA) proposed a new standard that is based on the aerodynamic diameter of 2.5 gm particles. This new standard emphasizes the significant impact of small particles on human health, especially on the respiratory and cardiovascular systems. 4 ... [Pg.251]

The majority of endogenous prostaglandins tend to exert undesirable effects on the cardiovascular system. These compounds as a rule tend to cause vasoconstriction and promote platelet aggrega-... [Pg.158]

Bazedoxifene is a third generation SERM that displays estrogenic effects in bone and the cardiovascular system, but functions as an antiestrogen in the breast and uterus. [Pg.250]

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. [Pg.295]


See other pages where Cardiovascular system effects is mentioned: [Pg.459]    [Pg.221]    [Pg.459]    [Pg.221]    [Pg.222]    [Pg.243]    [Pg.155]    [Pg.492]    [Pg.516]    [Pg.463]    [Pg.108]    [Pg.643]    [Pg.55]    [Pg.62]    [Pg.19]    [Pg.2]    [Pg.20]    [Pg.204]    [Pg.296]    [Pg.321]    [Pg.364]    [Pg.391]    [Pg.392]    [Pg.573]    [Pg.714]    [Pg.64]   


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Caffeine cardiovascular system effects

Cardiovascular system

Cardiovascular system antidepressant effects

Cardiovascular system antipsychotic effects

Cardiovascular system beta-blocker effects

Cardiovascular system cardiac effects

Cardiovascular system drug-induced effects

Cardiovascular system long-term effects

Cardiovascular system nicotine effects

Cardiovascular system opioid effects

Cardiovascular system reactive oxygen effects

Cardiovascular system xanthine effects

Cardiovascular system, capsaicin effects

Cardiovascular system, effect of azides

Cardiovascular system, serotonin effects

Effects on the Respiratory and Cardiovascular System

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