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The inotropic effects of quinidine and procaine amide : an experimental studyHastings, Elliot P. January 1959 (has links)
Thesis (M.D.)--Boston University
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Studies on the effect of quinidine on cardiovascular hemodynamics and on myocardial nimeral and carbohydrate metabolism /Rod?dan, Pura Norma Suarez January 1962 (has links)
No description available.
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Studies on the relationship of the subcellular distribution of dihydroquinidine to the change in the ventricular conduction velocity in the guinea pig heart /Besch, Henry Roland January 1967 (has links)
No description available.
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Caractérisation de l'interaction entre les antagonistes classiques du récepteur histaminique H¹et les cytochromes P450 /Gauvin, Caroline. January 2001 (has links)
Thèse (M.Sc.)--Université Laval, 2001. / Bibliogr. Publ. aussi en version électronique.
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Pharmacological regulation of c-myc gene expression in human breast cancer cellsMelkoumian, Zaroui K., January 2001 (has links)
Thesis (Ph. D.)--West Virginia University, 2001. / Title from document title page. Document formatted into pages; contains x, 152 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 119-149).
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Atrial and AV-nodal physiology in horses electrophysiologic and echocardiographic characterization and pharmacologic effects of diltiazem /Schwarzwald, Colin C. January 2006 (has links)
Thesis (Ph. D.)--Ohio State University, 2006. / Available online via OhioLINK's ETD Center; full text release delayed at author's request until 2007 Sep 12
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Amelioration of oxidative lung injury by antiarrhythmic agentsDas, Kumuda C. 13 October 2005 (has links)
Class I antiarrhythmic drugs, such as lidocaine, quinidine and procainamide, are known to be effective membrane stabilizers. However, the mechanism of such "membrane stabilization" has not been elucidated. In the present study we found that all three drugs are powerful scavengers of hydroxyl! radical. In addition, lidocaine was found to be a quencher of singlet oxygen. These drugs are also found to inhibit NADPH-dependent lipid peroxidation in bovine lung microsomes in a dose dependent manner. Since oxyradicals are implicated in the lipid peroxidation process and antiarrhythmic drugs were found to scavenge/quench reactive oxygen species, we proposed that the membrane Stabilizing effects of antiarrhythmic drugs may, in part, be due to their antioxidant properties.
Ischemia-reperfusion injury has been studied in many organs. Despite the evidence of functional, metabolic and structural abnormalities during reperfusion, the precise mechanism of reperfusion lung injury remains obscure. Data from the organ models suggest that toxic oxygen metabolites play an important role in the mechanism of reperfusion tissue injury. Lidocaine has also been shown to be clinically valuable for the treatment and prevention of ventricular arrhythmia occurring after surgical correction of myocardial infraction. We found that the class I antiarrhythmic drugs are effective in ameliorating post-ischemic lung reperfusion injury in an ex vivo perfused rat lung model exposed to both normoxic and hyperoxic conditions.
Since phagocytes are known to generate reactive oxygen species and play an important role in causing irreversible oxidative tissue injury during reperfusion of organs, we examined the role of antiarrhythmic agents on macrophage function. We found that these drugs inhibit superoxide and hydrogen peroxide production in stimulated macrophages in a dose dependent manner. The diminished production of superoxide was found to be not due to the inactivation of superoxide generating NADPH-oxidase enzyme but by inhibition of the phagocytosis process by these drugs
The results of these studies indicate that the antiarrhythmic drugs, such as, lidocaine, quinidine and procainamide, are effective antioxidants and can protect biomembranes against lipid peroxidation injury and post-ischemic reperfusion injury of the lung. We have investigated the mechanism(s) of action of these drugs in ameliorating oxidative tissue injury and found that these drugs are not only effective in removing reactive oxygen species but also cause inactivation of pulmonary macrophage from inappropriately generating reactive species of oxygen. The fundamental knowledge derived from these Studies could lead to enhanced functional improvement of patients following cardiopulmonary bypass, pulmonary arterial embolectomy and acute respiratory distress syndrome, all of which undergo a period of elective/induced ischemia and reperfusion or oxidative stress. / Ph. D.
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