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Cardiac depressant activity

Cardiac depressant activity. Tincture of the gland, administered by perfusion to rabbits, produced weak activity on the... [Pg.228]

Cardiac depressant activity. Hot water extract of the dried rhizome, at a concentration of 3 mg/mL, was active on the guinea... [Pg.529]

Reserpine (Serpasil) depletes the store of catecholamine peripherally and centrally and attenuates, but does not abolish, sympathetic reflexes. Reserpine is useful in the management of mild to moderate hypertension. Its onset of action is very slow (2 to 3 weeks) when given orally. The side effects of reserpine are manifested by cholinergic hyperactivity such as diarrhea, bradycardia, and nasal stuffiness. Reserpine can activate a peptic ulcer (cholinergic dominance) and cause depression (depletes norepinephrine stores). Reserpine and propranolol have potential cardiac depressant activity and should not be used together. [Pg.519]

Phenytoin enhances the hypotensive activity of dopamine and the cardiac depressant activity of lignocaine. Care must be taken when treating.196... [Pg.359]

Vasicinone (185) exhibited bronchodilator, - - - weak cardiac stimulant," and potent antianaphylactic activities, whereas vasicine (184) displayed bronchoconstrictor > and cardiac depressant activities. The structure-bronchodilator activity relationship was discussed. Vasicine (184) also had marked respiratory and uterine stimulant activities and a moderate hypotensive activity.Vasicinone (185) was devoid of these activities. ... [Pg.376]

One Eclectic medical text indicates that overdose of grindelia is toxic and may cause paralysis of the respiratory muscles (Ellingwood 1919). Grindelia is reported to have cardiotonic and cardiac depressant activity (BHP 1976 Culbreth 1927). [Pg.427]

The biological activities of vasicine have prompted the synthesis and pharmacological evaluation of vasicine and vasicinone analogues (57). 5,6-Methylenedioxyvasicine possesses uterine stimulant and bronchodilator activities comparable to those of vasicine, but with more marked hypotensive and cardiac depressant activities 192). [Pg.212]

CNS DEPRESSANT Substanccs, e.g. anaesthetics and narcotics, which depress the activity of the central nervous system. Symptoms following exposure include headache, dizziness, loss of consciousness, respiratory or cardiac depression, death. [Pg.12]

Amiodarone (16) has been the center of much interest because of its activity as a cardiac depressant useful in treating ventricular arrhythmia and many analogues have been prepared [4. I he originally patented procedure concludes simply by etherification of benzofuran-containing iodonated phenol 15 with 2-halodiethylaminoethane to give amiodarone (16) [5]. The synthesis t)f 15 is not detailed in the reference but the synthesis of benzbromarone contains closely analo-goii.s steps [6]. [Pg.1475]

In vitro, U-II is a potent constrictor of vascular smooth muscle its activity depends on the type of blood vessel and the species from which it was obtained. Vasoconstriction occurs primarily in arterial vessels, where U-II can be more potent than endothelin 1, making it the most potent known vasoconstrictor. However, under some conditions, U-II may cause vasodilation. In vivo, U-II has complex hemodynamic effects, the most prominent being regional vasoconstriction and cardiac depression. In some ways, these effects resemble those produced by ET-1. Nevertheless, the role of the peptide in the normal regulation of vascular tone and blood pressure in humans appears to be minor. [Pg.390]

The cardiovascular effects of local anesthetics result in part from direct effects of these drugs on the cardiac and smooth muscle membranes and from indirect effects on the autonomic nervous system. As described in Chapter 14, local anesthetics block cardiac sodium channels and thus depress abnormal cardiac pacemaker activity, excitability, and conduction. At extremely high concentrations, local anesthetics can also block calcium channels. With the notable exception of cocaine, local anesthetics also depress myocardial contractility and produce direct arteriolar dilation, leading to systemic hypotension. Cardiovascular collapse is rare, but has been reported after large doses of bupivacaine and ropivacaine have been inadvertently administered into the intravascular space. [Pg.570]

The pressor response to ephedrine is due in part to peripheral constriction and in part to myocardial stimulation. Vasoconstriction can be demonstrated by intra-arterial injection, but compared to epinephrine, ephedrine is only about one thousandth as active. This would imply that the cardiac effect is predominant in increasing the arterial pressure. This, however, is difficult to demonstrate. In perfused hearts, ephedrine produces only minor stimulation and cardiac depression appears if the drug is repeated. [Pg.314]

There have been no recent studies on the pharmacology of samandarine alkaloids. Samandarine is a potent local anesthetic 48). Cardiac depressant effects (48,49) and inhibition of binding of a radiolabeled batracho-toxin analog to sodium channels (50) are consonant with the potent local anesthetic activity of samandarine. Samandarine alkaloids show antimicrobial activity (51 and references therein). [Pg.198]

The properties of these drugs vary widely (3). Nifedipine is said to have little negative inotropic effect and no effect on the atrioventricular node verapamil is a potent cardiac depressant, with a marked effect on the atrioventricular node and diltiazem has less cardiac depressant effect but inhibits atrioventricular nodal activity. [Pg.598]

Renal insufficiency can result in clinically significant accumulation of pharmacologically active opioid metabolites and prolonged narcosis such patients must be monitored for signs of toxicity (SEDA-17, 79) (SEDA-21, 85) (98,99). To date, this effect has only been reported with codeine, morphine, and pethidine. Dextropropoxyphene is not recommended in renal insufficiency, as its metabolite norpropoxyphene, which is eliminated by the kidneys, accumulates, causing cardiac depression (SEDA-17, 79) (SEDA-21, 85). [Pg.2631]

CARDIAC DEPRESSANTS are little used in medicine, however, some are used to slow the heartbeat in tachycardias and a number of these are often analogues or derivatives of other drugs with optimized activity for this purpose in the heart (e.g. procainamide, quinidine) - these are dealt with under antiarrhythmic agents. [Pg.66]

Cibenzoline [ban, inn] (clfenllne [usan]) is a cyclopropyl-imidazole derivative, a hypoglycaemic acting as a pancreatic p-cell potassium-channel blocker. It also is a cardiac depressant and can be used as an ANTIARRHYTHMIC (class la with some class III and class IV properties), cicaprost [inn] is a prostacyclin analogue, an (IP) prostanoid receptor agonist, with platelet aggregation INHIBITOR and vasodilator activity, ciclacillin [ban, inn.ian] (cyclacillin [usan]) is a semisynthetic (penicillin) ANTIBIOTIC. It can be used as an ANTIBACTERIAL to treat certain infections. [Pg.76]

A list of 3-blockers indicating their structure and developmental status and the absence or presence of S-receptor selectivity, partial agonist activity and non-specific cardiac depressant property, is presented in Table I for reference. In addition to propranolol, two new 3-blockers have now been approved for use in man in the U.S. Metoprolol has been approved for use in hypertension, timolol has been approved for use in glaucoma.In other parts of the world, there are at least 17 3-blockers available for use. ... [Pg.81]

The Ca +-entry blockers are heterogeneous with respect both to structure and pharmacologic activity. They differ substantially with respect to their cardiac depressant and vaso-dilatory properties, their activities on different vascular tissues or beds, their onset times and durations of action, their use dependence, the extent to which they inhibit stimulus-secretion coupling processes and tjje extent to which they show antagonism of events other than Ca + entry (9,13,19,71,72). [Pg.35]

Esmolol (No. 14), the first P-blocker pro-drug, has been introduced for IV use when rapid, but not continual, residual blockade is desirable (e.g., acute situations where prolonged cardiac depression must be avoided). Ultrashort duration of activity could solve such a problem. [Pg.435]


See other pages where Cardiac depressant activity is mentioned: [Pg.57]    [Pg.130]    [Pg.67]    [Pg.57]    [Pg.130]    [Pg.67]    [Pg.15]    [Pg.453]    [Pg.237]    [Pg.249]    [Pg.168]    [Pg.171]    [Pg.1504]    [Pg.160]    [Pg.929]    [Pg.550]    [Pg.550]    [Pg.3]    [Pg.149]    [Pg.149]    [Pg.231]    [Pg.244]    [Pg.160]    [Pg.244]    [Pg.1]    [Pg.539]    [Pg.370]    [Pg.558]    [Pg.308]   
See also in sourсe #XX -- [ Pg.212 ]




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