Hypotensive


Sedative, analgesic, antipyretic, hypotensive 87  [c.147]

H H CO,H Me Slight hypotensive action 949  [c.153]

Combined Hj /H2 receptor stimulation by histamine is responsible for vasodilation-related symptoms, such as hypotension, flushing, and headache, as well as for tachycardia stimulated indirecdy through vasodilation and catecholamine secretion.  [c.139]

Morphine has certain undesirable side effects. Among these are respiratory depression, nausea, and vomiting, depression of the cough reflex, cardiovascular depression and hypotension, smooth muscle contraction (constipation), and histamine release (93). Morphine s onset of action, duration, and low therapeutic indices have prompted a search for a more effective opiate iv anesthetic. Extreme simplification of the complex morphine molecule has resulted in anilido —piperidines, the fentanyl class of extremely potent opiate iv anesthetics (118,119).  [c.411]

Agent or class CNS effects Orthostatic hypotension Arrhythmias Anticholinergic effects Weight change  [c.468]

Toxic effects of propranolol are related to its blocking P-adrenoceptor blocking actions. They include cardiac failure, hypotension, hypoglycemia, and bronchospasm. Propranolol is lipophilic and crosses the blood—brain barrier. Complaints of fatigue, lethargy, mental depression, nightmares, hallucinations, and insomnia have been reported. GI side effects include nausea, vomiting, diarrhea, and constipation (1,2).  [c.119]

Because of its brief half-life and minimal hpid solubihty, the side effects of esmolol are transient and include hypotension, cold extremities, dyspnea (from bronchospasms), bradycardia, nausea, vomiting, and headaches (41).  [c.119]

Mention must be made of the u.se of o- or p-hydroxystyryl thiazolo dyes as indicators for protolytic titrations in nonaqueous media (145). and of the hypotensive action of some neotrinuclear thiazolo cyanines in experiments on animals (146).  [c.80]

The resuspended and formulated Fraction II precipitate normally contains some aggregated IgG and trace substances that can cause hypotensive reactions in patients, such as the enzyme prekail ikrein activator (186). These features restrict this type of product to intramuscular adininistration. Further processing is required if products suitable for intravenous adininistration are required. Processes used for this purpose include treatment at pH 4 with the enzyme pepsin [9001-75-6] being added if necessary (131,184), or further purification by ion-exchange chromatography (44). These and other methods have been fiiUy reviewed (45,185,187,188). Intravenous immunoglobulin products are usually suppHed in the freeze-dried state but a product stable in the solution state is also available (189).  [c.532]

During the 1970s, hypotensive reactions with plasma protein fraction were associated with the presence of prekail ikrein activator (PKA) (191), a potent vasodilator generated from Factor XII [9001-30-3] (Hageman Factor) by surface activation during processing. Operating conditions can be controlled to  [c.532]

Dorex is very toxic (see Table 2) and must be handled with extreme care. Because it may produce severe dermatitis on moist skin, it is difficult to use in hot, humid climates inhalation of the dust or spray may irritate the mucous membranes. Whereas symptoms may include a flushed face, tachycardia, headache, vertigo, and hypotension, it does not produce the typical cyanide effect.  [c.424]

Adrenocorticotropic Hormone. Adrenocorticotropic hormone [9002-60-2] is required for maintenance and function of the adrenal cortex, which secretes potent steroid hormones regulating metaboHsm, ie, glucocorticoids. Insufficient secretion of the steroid hormones of the adrenal cortex, as in Addison s disease, may result in insulin hypersensitivity, inabiUty to maintain blood sugar levels during food deprivation, hypotension, general weakness, fatigue, and psychological disturbances. Glucocorticoids regulate their own production by suppressing the synthesis and secretion of POMC-derived hormones, ie, negative feedback. Removal of the pituitary gland induces a pronounced physical atrophy of the adrenal cortex, which accompanies loss of function including a reduction in steroid hormone secretion. The size and functional integrity of the adrenal gland can be restored by the administration of ACTH. The sequence of the first 24 N-terminal amino acids of ACTH cosyntropin [16960-16-0] confers hiU bioactivity at the adrenal gland and is highly conserved among species. Across species, the ACTH molecule differs slightly in stmcture and retains similar biologic function. It is a single-chain peptide, 39 amino acids in length (Fig. 1). Adrenocorticottopic hormone is not generally used for the treatment of adrenal insufficiency, because the adrenal steroids can be easily synthesized and administered. Clinically, ACTH is used for diagnostic testing of adrenal function. Commercial preparations of ACTH are available from Armour Pharmaceutical, Ciba Pharmaceutical, Hoechst-Roussel, Organon Inc., and Wyeth-Ayerst Laboratories.  [c.175]

Biologica.1 Activities. Substance P was first isolated for its hypotensive action and stimulation of rabbit jejunum contraction and later for following its ability to produce salivation in rats. It also stimulates glucagon secretion and produces hyperglycemia in rats, stimulates smooth muscle contraction in the guinea pig vas deferens and ileum, and elevates growth hormone and prolactin secretion in humans (48). In the brain, one of the most commonly discussed roles of substance P is the mediation of pain information, where this peptide acts as one of the primary neurotransmitters in the sensory afferent fibers which conduct pain information (49,50). Thus compounds which increase substance P release, eg, capsaisin, tend to increase pain, while potential substance P antagonists are sought-after analogues for analgesic purposes.  [c.202]

Neurotensin. This hormone has been isolated and characterized from acid—acetone extracts of bovine hypothalamus (118) on the basis of its hypotensive activity. Immunoreactive neurotensin is present in mammalian gut and is distributed throughout the central nervous system its highest concentration is in the hypothalamus and in the substantia gelatinosa of the spinal cord (119). Its overall brain distribution is not unlike that of enkephalin ( )  [c.204]

Biologica.1 Activities a.ndAna.logues, The many pharmacological actions of neurotensin include hypotension, increased vascular permeabihty, hyperglycemia, increased intestinal motility, and inhibition of gastric acid secretion (120). In the brain, it produces analgesia at remarkably low doses (121).  [c.204]

Acute intoxication with DHBs occurs mainly by the oral route symptoms are close to those induced by phenol poisoning including nausea, vomiting, diarrhea, tachypnea, pulmonary edema, and CNS excitation with possibiUty of seizures followed by CNS depression. Convulsions are more frequent with catechol as well as hypotension due to peripheral vasoconstriction. Hypotension and hepatitis seem more frequent with hydroquinone and resorcinol. Methemoglobinemia and hepatic injury may be noted within a few days after intoxication by DHBs.  [c.494]

Ethanol [64-17-5] C2H OH (1) is a potent sleep inducing agent that in the form of wine (qv), Hquor (see Beverage spirits, distilled), and beer (qv) has been in recreational use since prehistory. Ethanol (qv) is a sedative, anxiolytic, and hypnotic agent. It can prove fatal in excess both acutely, owing to CNS depressive actions, and chronically as the result of progressive alcohol-induced tissue atrophy, most notably cirrhosis of the Hver and neurological damage. Whereas ethanol is typically viewed as a CNS stimulant, this perceived effect results from a depression of tonic inhibitory neurotransmission processes. Chlorinated alcohols such as ethchlorvynol [113-18-8] C H CIO (2) and chloral hydrate [302-17-0], C2H2CI2O2 (3) are also useful hypnotics. The latter compound also possesses anticonvulsant and muscle relaxant activities. Both ethanol derivatives are associated with nausea, vomiting, dizziness at high doses and a typical hangover effect reflecting a residual depression of the CNS. Chloral hydrate irritates the gastrointestinal tract and can cause ataxia, nightmares, and allergic reactions. Ethchlorvynol has many properties in common with chloral hydrate and in addition has hypotensive actions.  [c.530]

The largest single class of naturally occurring iadoles are the plant alkaloids. These occur with a wide range of stmctural diversity and are typically derived from tryptophan and terpenoid stmctural units. Several of these compounds are pharmacologically significant. Reserpiae [50-55-5] (15) acts as a tranquilizer and hypotensive agent. Although not widely used at present, it was one of the first dmgs to be iatroduced for the treatment of mental illness (38). The dimeric vinca alkaloids vincristine [57-22-7] and vinblastine [865-21-4] are used ia the treatment of Hodgkia s disease, leukemia, and other forms of cancer (39). Derivatives of the ergot alkaloid lysergic acid are used ia the treatment of migraine (40) and the diethylamide is lysergic acid diethylamide (LSD) (see Alkaloids).  [c.88]

Lead is poisonous in all forms, but to different degrees, depending on the chemical nature and solubiUty of the lead compound. Exposure maybe acute or chronic. Because the symptoms of lead poisoning may be similar to those of other ailments, they should be checked with blood and urine tests. Lead is one of the most hazardous toxic metals because the poison is cumulative, and its toxic effects are many and severe. Prolonged absorption of lead or its inorganic compounds can cause the onset of lead poisoning symptoms or plumbism, including weakness, lassitude, weight loss, insomnia, hypotension, and anemia. Associated with these may be gastrointestinal disturbances. Physical signs are usually facial pallor, malnutrition, abdominal tenderness, and pallor of the eye grounds. On gingival tissues, a line or band of blue-black pigmentation (lead line) may appear, but only in the presence of poor dental hygiene.  [c.73]

SRIF acts as an excitatory neuromodulator in the CNS inhibiting the release of TRH, corticotropin-releasing hormone (CRH), growth hormone releasing factor (GHRH), and NE. It produces general arousal and hypotension. It inhibits the release of a number of peptides and modulators in the GI tract.  [c.575]

Isoflurane is a respiratory depressant (71). At concentrations which are associated with surgical levels of anesthesia, there is Htde or no depression of myocardial function. In experimental animals, isoflurane is the safest of the oral clinical agents (72). Cardiac output is maintained despite a decrease in stroke volume. This is usually because of an increase in heart rate. The decrease in blood pressure can be used to produce "deHberate hypotension" necessary for some intracranial procedures (73). This agent produces less sensitization of the human heart to epinephrine relative to the other inhaled anesthetics. Isoflurane potentiates the action of neuromuscular blockers and when used alone can produce sufficient muscle relaxation (74). Of all the inhaled agents currently in use, isoflurane is metabolized to the least extent (75). Unlike halothane, isoflurane does not appear to produce Hver injury and unlike methoxyflurane, isoflurane is not associated with renal toxicity.  [c.409]

Propanidid. Propanidid [1421-14-3] (Epontol), C gH2yNO, (7) a derivative of the propyl ester of homo vanillic acid, has been in clinical use in Europe for a number of years. Its main advantage is rapid onset of action and a fast recovery which, like etomidate, is because of rapid metaboHsm by esterases rather than redistribution (108). Excretion is rapid 75 to 90% of the dmg is eliminated as metaboUtes within two hours. Propanidid side effects include hypotension, tachycardia, and hyperventilation followed by apnea, as well as excitatory side effects such as tremor and involuntary muscle movement (109).  [c.411]

One approach taken to the treatment of chronic alcoholism rehes on a form of aversion therapy involving prophylactic adrninistration of inhibitors of aldehyde dehydrogenase, such as disulfiram [97-77-8] (62) and calcium carbimide [156-62-7] CaCN2. Any consumption of alcohol then results in an accumulation of acetaldehyde yielding flushing hypotension, tachycardia, nausea, and vomiting. However, it has been reported that the efficacy of disulfiram in reducing relapse is only modest, primarily owing to noncompliance (235). Mote recendy, the. -opiate antagonist naltrexone [16590-41 -3] (63) was approved in the United States for the treatment of alcohol abuse. Clinical results suggest that relapse rate in alcohoHcs may also be reduced by SSRIs, dopaminergic agents, lithium salts, P-adrenergic blockers, carbama2epine, and hydroxy2ine.  [c.237]

Clinical studies of WR-2721 using XRT for certain types of cancer show promise, but toxicity remains a concern. Although systemic WR-2721 is generally well tolerated as a single iv infusion, the achievable concentration of WR-2721 is stiU limited by toxic side effects. These include nausea, vomiting, sneezing, a warm or flushed feeling, mild somnolence, a metallic taste in the mouth, transient hypocalcemia, and allergic reactions (4). Emesis may be moderately severe, but can be reduced by antiemetics such as ondansetron and dexamethasone. The potentially dose-limiting toxicity is hypotension, which is rapidly reversed by discontinuing the dmg.WR-2721 shows promise for patients with inoperable, unresectable, or recurrent rectal adenocarcinoma who receive pelvic irradiation (48). In these studies there is no evidence of tumor protection. Some acute reactions are less frequent in the WR-2721-treated group. There are no moderate or severe late effects in the WR-2721-treated group, compared to 14% in the XRT-only group. Patients receiving WR-2721 15 min before each fraction show no significant hypotension or hematologic toxicity up to 18 months. Mild to moderate emesis occurred in 80% of the courses. These encouraging results are being extended worldwide, and trials are plaimed for patients having head and neck or lung cancer, with and without concomitant antiemetics (5,48). WR-2721 also shows promise for protecting the BM of patients receiving total body irradiation (TBI) for lymphoma or chronic lymphocytic leukemia (CLL) (49,50).  [c.489]

Normally, dietary tyramine is broken down in the gastrointestinal tract by MAO and is not absorbed. In the presence of MAOI, however, all of its potent sympathomimetic actions are seen. Other side effects of MAOI include excessive CNS stimulation, orthostatic hypotension, weight gain, and in rare cases hepatotoxicity. Because the monoamine oxidase inhibitors exhibit greater toxicity, yet no greater therapeutic response than other, newer agents, clinical use has been markedly curtailed. The primary use for MAOIs is in the treatment of atypical depressions, eg, those associated with increased appetite, phobic anxiety, hypersomnolence, and fatigues, but not melancholia (2).  [c.466]

Doridosine. Doridosine, AJ -methyhsoguanosine, (35) was isolated from the dorid nudibranchs of Anisodoris nobilis and the sponge, Tedania (106,107). The injection of (35) into the saphenous vein of anesthetized rats produces hypotension and bradycardia almost immediately. The observed changes in the electrocardiograms are minor and indicate Httie interference with conduction of the impulse within the heart (see Cardiovascularagents).  [c.122]

The early stages of African trypanosomiasis, ie, before central nervous system involvement and the sleeping sickness take effect, can be best treated with intravenous suramin sodium (92), a compound with a dyelike stmcture (Table 10). Suramin is most effective against T. b. rhodesiense but has also been used against T. b. gambiense infection. The compound causes side effects such as nausea, photophobia, and peripheral neuropathy which disappear shortly after conclusion of adruinistration. Because the dmg is unable to pass the blood-brain barrier, prompt treatment of patients is essential. Suramin in combination with tryparsamide (93, Tryparsone [554-72-3]) is an alternative that has been investigated. Pentamidine (26), as the isethionate or methanesulfonate salt, has been used successfliUy against T. b. gambiense but the compound also does not enter the central nervous system and is not effective in advanced disease. It can cause severe side effects such as syncope, hypotension, hypoglycemia, vomiting, abdominal pain, and a peripheral neuropathy. Pentamidine (26) has been administered to large populations prophylacticaHy against T. b. gambiense. This probably accounts for the appearance of resistant strains.  [c.276]

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.  [c.112]

The cardiovascular adverse effects associated with quinidine therapy are hypotension and tachycardia, both of which are related to its a-adrenoceptor blocking actions. The tachycardia may be a reflex adjustment to the fall in blood pressure or may also be a direct action of the dmg on sympathetic nerve terminals leading to an increased release of NE. Quinidine also produces ringing in the ears (cinchonism) (1,2).  [c.113]

The side effects and toxic reactions to verapamil iaclude upper GI upset, constipation, di22iaess, headaches, flushing and burning, edema, hypotension, bradycardia, and various conduction disturbances. Verapamil has negative iaotropic activity and may precipitate heart failure ia patients having ventricular dysfunction (1,2).  [c.120]

Isoproterenol is given sublingually or by iv. It is metabolized by monoamine oxidase and catechol-0-methyltransferase in brain, Hver, and other adrenergically innervated organs. The pharmacological effects of isoproterenol are transient because of rapid inactivation and elimination. About 60% is excreted unchanged. Adverse effects using isoproterenol therapy include nervousness, hypotension, weakness, dizziness, headache, and tachycardia (86).  [c.120]

Adenosine in large doses produces vasodilation resulting in facial flushing, Hghtheadedness, dizziness, and hypotension. Shortness of breath and  [c.120]

Amiodarone dilates arteriolar vascular smooth muscle, especiady coronary arteries, and thus exhibits antianginal effects. Its effects on the peripheral vasculature to decrease resistance leads to a decrease in left ventricular stroke work and a decrease in myocardial oxygen consumption. The dmg rarely produces hypotension that requires discontinuation of the dmg (1,2).  [c.121]

Adverse effects with bretylium include hypotension, nausea, vomiting, parotid gland tenderness, and arrhythmogenesis (1,2).  [c.121]

Sotalol is rapidly and almost completely (>90%) absorbed. Bioavahabhity of absorbed dmg is 89—100%. Peak plasma levels are achieved in 2—4 h. Sotalol is 50% bound to plasma proteins. Plasma half-life of the compound is about 5.2 h. No metabolites of sotalol have been identified indicating littie metabolism. The dmg is excreted mainly by the kidneys (80—90%) and about 10% is eliminated in the feces. The plasma half-life is prolonged in patients having renal failure. Kinetics of the compound are not affected by changes in liver function (1,2). Sotalol has ah the adverse effects of -adrenoceptor blockers including myocardial depression, bradycardia, transient hypotension, and proarrhythmic effects (1,2).  [c.121]


See pages that mention the term Hypotensive : [c.66]    [c.147]    [c.545]    [c.550]    [c.338]    [c.435]    [c.272]    [c.388]    [c.155]    [c.230]    [c.469]    [c.118]    [c.274]   
The organic chemistry of drug synthesis Vol.4 (1990) -- [ c.13 , c.149 ]