Ionamin online research references
Virchows Arch B Cell Pathol. 1975;18(1):51-60.
Lipidosislike renal changes in rats treated with chlorphentermine or with tricyclic antidepressants.
Lullmann-Rauch B.
Histological, histochemical and ultrastructural examinations were performed on renal tissues of rats after prolonged oral administration of the anorectic drug chlorphentermine or of the tricyclic antidepressants iprindole, imipramine and clomipramine. All drugs caused the formation of multilamellated cytoplasmic inclusions throughout the nephron and the collecting duct system, and in interstitial cells. The cytological alterations were most prominent in the glomerular podocytes, in the proximal convoluted tubules, and in the collecting duct system. In view of the histochemical properties (staining with Baker's acid hematein) and the ultrastructural appearance of the cytoplasmic inclusions the cellular alterations are interpreted as a renal manifestation of a generalized lipidosis induced by drugs of amphiphilic character.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=167510&dopt=Abstract
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Res Commun Chem Pathol Pharmacol. 1976 Aug;14(4):677-87.
The protective effects of methysergide, 6-hydroxydopamine and other agents on the toxicity of amphetamine, phentermine, MDA, PMA, and STP in mice.
Lopatka JE, Brewerton CN, Brooks DS, Cook DA, Paton DM.
The ability of various drugs to prevent the lethal effects of 4-methoxyamphetamine (PMA) and 3, 4-methylenedioxyamphetamine (MDA) were reduced by pretreatment with phentolamine and 6-hydroxydopamine suggesting that release of norepinephrine from peripheral adrenergic nerves contributed to their toxicity. Pretreatment with methysergide reduced the lethal effects of (+)- and (-)-amphetamine, MDA, PMA and 2, 5-dimethoxy-4-methylamphetamine (STP) suggesting that an action on serotonergic receptors contributed to their toxicity. Pretreatment with 4-chloroamphetamine, practolol and haloperidol did not alter the lethal effects of the agents studied.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=989173&dopt=Abstract
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J Pharmacol Exp Ther. 1975 May;193(2):317-26.
Effects of verapamil on myocardial contractility, cardiac adenosine 3,'5'-monophosphate and heart phosphorylase.
Shanfeld J, Hess ME, Levine NR.
The effects of verapamil on myocardial isometric force on contraction, cardiac adenosine 3,'5'-monophosphate (cyclic AMP) and heart phosphorylase alpha activity were studied in the isolated perfused rat heart. When hearts were perfused with verapamil (5.98 times 10- minus 8 M), force of contraction was reduced approximately 50% within 4 to 5 minutes; at this point, the concentration of cyclic AMP was significantly lower than control but phosphorylase alpha activity was unchanged. In hearts perfused continuously for 60 minutes with verapamil, force of contraction and cyclic AMP levels returned to normal within 20 minutes after administration of verapamil was begun. Isoproterenol (0.355 nmol/min) reversed the depressant effect of verapamil on cardiac contractility and restored heart cyclic AMP levels to normal. Methoxamine (35.5 nmol/min) given to verapamil-depressed hearts, caused contractile force to return to normal, but cardiac cyclic AMP levels remained low. Mephentermine (23.0 nmol/min) had no effect on cardiac contraction, cyclic AMP or phosphorylase alpha activity in hearts depressed by verapamil. It was concluded that with the concentration of verapamil used in these experiments, the drug caused a transient decrease in force of contraction and myocardial cyclic AMP. Both the depression in myocardial contractility and in cardiac cyclic AMP caused by verapamil were reversed promptly by isoproterenol, whereas methoxamine overcame acutely only the negative inotropic effect of verapamil. Mephentermine had no effect on hearts depressed by verapamil.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=167148&dopt=Abstract
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