Claims for cordilox

1967 ◽  
Vol 5 (22) ◽  
pp. 85-86

Verapamil (Cordilox - Pfizer; iproveratril*), described by the manufacturers as a mild beta-blocking agent, is promoted as an important new compound for the long-term control of angina pectoris.1 It is claimed that, unlike other beta-blocking agents which reduce the response of the heart to sympathetic stimulation, verapamil induces neither coronary vasoconstriction nor broncho-spasm and is less likely to provoke low-output cardiac failure. These unwanted effects are an unavoidable consequence of intense beta receptor blockade, and (although the manufacturers attribute the advantages to a direct relaxation of plain muscle) their absence suggests that the action of verapamil may depend not on beta receptor blockade but on other mechanisms. The claims for verapamil of advantages over potent beta-blocking agents are clearly aimed at propranolol (Inderal - ICI), the only one available for clinical use. We discussed propranolol in 1965.1

1988 ◽  
Vol 22 (6) ◽  
pp. 484-485 ◽  
Author(s):  
Gopal Das ◽  
Janine C. Ferris

Beta-receptor blocking agents are commonly used to treat patients with heart disease, and generalized seizures due to therapy with these agents are rare. All reported cases of seizures due to beta blocking agents have occurred only in those subjects who ingested large doses of the drugs. We observed generalized convulsions in a patient who was receiving therapeutic doses of an ultrashort-acting beta-blocking agent (esmolol hydrochloride) intravenously. A literature survey and possible mechanisms by which these agents induce seizures are presented.


1974 ◽  
Vol 77 (1_Suppl) ◽  
pp. S6 ◽  
Author(s):  
S. Raptis ◽  
H. Hirth-Schmidt ◽  
K. E. Schröder ◽  
E. F. Pfeiffer

1971 ◽  
Vol 68 (1_Suppla) ◽  
pp. S5-S38 ◽  
Author(s):  
Helmuth Vorherr

ABSTRACT In lactating rats and rabbits the mode of antagonism of sympathomimetics, angiotensin or pain toward oxytocin-induced milk-ejection was investigated. In rats intra-arterial (intrafemoral) doses of 0.01–0.02 μg or intravenous (iv) doses of 0.1–0.5 μg of either epinephrine, isoproterenol, norepinephrine, angiotensin or 10 μg of phenylephrine injected simultaneously with, or 30 seconds before an oxytocin dose (10 μU intrafemoral, 300 μU iv) greatly inhibited or suppressed the oxytocin response. A 15 second pain stimulus caused moderate inhibition. With alpha-receptor blockade pain, epinephrine, isoproterenol, norepinephrine, phenylephrine and angiotensin inhibition were, respectively, 70%, 75%, 100%, 40%, 0% and 100%. Under beta-receptor blockade the corresponding values were 14%, 40%, 0%, 70%, 100% and 100%; with simultaneous intrafemoral injections neither catecholamine was inhibitory toward oxytocin. In corresponding rabbit experiments approximately 10-fold higher iv drug dosages were applied and similar results were observed. In both species, combined alpha and beta-receptor blockade nearly eliminated the antagonistic actions of sympathomimetics toward oxytocin, whereas angiotensin inhibition persisted unchanged. The results indicate: 1) Mammary myoepithelial cells contain beta-adrenergic receptors but no alpha-receptors; 2) Inhibition of oxytocin-induced milk-ejection by isoproterenol and phenylephrine is meditated through stimulation of myoepithelial beta-receptors (myoepithelial relaxation) and vascular alpha-receptors (vasoconstriction), respectively; 3) Epinephrine and norepinephrine inhibition of milk-ejection is due to stimulation of vascular alpha-receptors and myoepithelial beta-receptors; 4) Angiotensin effects are unrelated to adrenergic receptor mechanisms; 5) Administration of both alpha and beta-adrenergic blockers is desirable for stabilizing the sensitivity of the oxytocin milk-ejection assay preparation against interference from endogenous or exogenous catecholamines; 6) Other than using adrenergic blockers, pharmacologic doses of oxytocin can correct nursing difficulties in animals and man with hyperfunction of the adrenal-sympathetic system.


1985 ◽  
Vol 13 (4) ◽  
pp. 187-193 ◽  
Author(s):  
Olov Fagerström ◽  
Kenneth Hugdahl ◽  
Nils Lundström

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