Drugs online research references
Kardiologiia. 1991 Mar;31(3):13-6.
[Various aspects of the anti-aggregatory action of diltiazem and cordaphene in patients with ischemic heart disease]
[Article in Russian]
Leonova MV, Rumiantsev DO, Belousov IuB.
Some aspects of the antiaggregatory action of calcium antagonists were studied in 50 patients with stable angina pectoris. Dilzem (diltiazem) and cordaphene (nifedipine) were tested for their effects on the erythrocytic component of hemostasis, taking into account their capability of suppressing hemolysis, which made ADP, an important thrombocytic activator, enter the blood flow. The two agents significantly reduce the concentration of plasma ADP, free hemoglobin, diminish mechanical erythrocytic resistance, and block platelet aggregation to a varying degree. A relationship was established between the levels of blood nifedipine and the magnitude of rheological effects. With this, the patients with coronary heart disease showed a good antianginal effect.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1875587&dopt=Abstract
Life Sci. 1994;54(16):PL271-5.
Kainic acid and 4-aminopyridine seizure models in mice: evaluation of efficacy of anti-epileptic agents and calcium antagonists.
Cramer CL, Stagnitto ML, Knowles MA, Palmer GC.
Biology Department, Fisons Pharmaceuticals, Rochester, NY 14603.
Seizures may be induced in mice in response to stimulation of subtypes of glutamate receptors by kainic acid or inhibition of certain voltage-dependent potassium channels by 4-aminopyridine (4-AP). The anti-seizure efficacy of intraperitoneally administered anticonvulsants and Ca++ antagonists to CF-1 mice was tested using these models. The order of potency for prevention of kainate convulsions and the subsequent lethality was: dihydropyridine Ca++ antagonists (nicardipine, nisoldipine > nitrendipine > nifedipine > nimodipine) followed by verapamil > prenylamine > diltiazem > flunarizine > remacemide HCl > ethosuximide > valproate. In the 4-AP model the order of potency to prevent hind limb tonic extension was: MK801(+/-) > lamotrigine > phenytoin, phenobarbital > carbamazepine > FPL 12495AA (the desglycine metabolite of remacemide HCl), remacemide HCl > flunarizine > prenylamine >>> valproate. Therefore, compounds that limit activation of kainate receptors and voltage-operated linked calcium channels are active in the kainate model. Agents effective against maximal electroshock appear to be effective in the 4-AP model.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8152336&dopt=Abstract
J Pharmacol Exp Ther. 1991 Jul 1;258(1):332-8.
Effects of KT-362, a new antiarrhythmic agent with vasodilating action on intracellular calcium mobilization of atrial muscle.
Kodama I, Shibata S.
Department of Pharmacology, University of Hawaii School of Medicine, Honolulu.
Effects of KT-362 (5-[3[2-3, 4-dimethoxyphenyl) ethyl]amino]-1-oxopropyl]-2,3,4,5- tetrahydro-1,5-benzothiazepine fumarate; 3-100 microM) on the twitch contraction of isolated rabbit left atria were examined to elucidate the influence of this substance on the intracellular calcium mobilization of cardiac muscles. A 30-sec rest period interrupting the conditioning stimulation at rates greater than 0.5 Hz caused positive inotropy of the first postrest (B1) contraction (rest potentiation). The potentiated B1 contraction was much more resistant to the negative inotropic effect of nifedipine (1 and 3 microM) than the steady-state contraction. The nifedipine-resistant B1 contraction was abolished by ryanodine (30 nM) or caffeine (5 mM). Single treatment of the muscle with KT-362 much greater than or equal to 10 microM resulted in a concentration-dependent decrease in the steady state beat as well as in B1 contraction. In preparations pretreated with 1 microM nifedipine, KT-362 had greater inhibitory action against B1 contraction (IC50 = 7.8 microM). KT-362 (3 and 10 microM) reduced the late plateau amplitude of transmembrane action potential associated with the B1 contraction. Tetrodotoxin (1 and 3 microM) and quinidine (3 and 10 microM) caused a rightward shift of the force-frequency relationship for the B1 contraction but, unlike KT-362, they caused no or minimal reduction of the maximal B1 values. In the presence of 1 microM nifedipine, B1 contraction showed biphasic response to a prolongation of the preceding rest period, an initial rapid increase up to 30 sec was followed by a gradual decrease.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2072305&dopt=Abstract
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