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Nifedipine hemodynamics

Kleinbloesem CH, Vanharten J, Wilson JP, Danhof M, Vanbrummelen P and Breimer DD (1986) Nifedipine—Kinetics and Hemodynamic-Effects in Patients with Liver-Cirrhosis After Intravenous and Oral-Administration. Clin Pharmacol TherAd pp 21-28. [Pg.74]

Kleinbloesem CH, van Harten J, Wilson JP, et al. (1986) Nifedipine kinetics and hemodynamic effects in patients with liver cirrhosis after intravenous and oral administration. Clin Pharmacol Ther 40 21-28. [Pg.130]

In pulmonary hypertension, both verapamil and nifedipine increase mean right atrial pressure in association with hypotension, chest pain, dyspnea, and hypoxemia the severe hemodynamic upset resulted in cardiac arrest in two patients after verapamil and death in another after nifedipine (54). A patient with pulmonary hypertension also developed pulmonary edema whilst taking nifedipine (55) and another seems to have developed this as an allergic reaction (56). [Pg.600]

Murakami M, Takeyama Y, Matsubara H, Hasegawa S, Nakamura N, Sekita S, Katagiri T. Effects of intravenous injection of nicorandil on systemic and coronary hemodynamics in patients with old myocardial infarction. A comparison with nifedipine and ISDN. Eur Heart J 1989 10(Suppl) 426. [Pg.2508]

In another study the acute response to inhaled nitric oxide and high doses of oral nifedipine or verapamil was assessed in 33 consecutive patients with primary pulmonary hypertension (2). Ten patients responded acutely to nitric oxide, nine of whom responded acutely to calcium channel blockers, without any complications. The other 23 patients failed to respond to nitric oxide and calcium channel blockers. In these non-responders there were nine serious adverse effects with calcium channel blockers. There was no clinical or baseline hemodynamic feature that predicted the acute vasodilator response. Long-term oral treatment with calcium channel blockers was restricted to the nine acute responders, and there was a sustained clinical and hemodynamic improvement in only six patients. It was concluded that nitric oxide may be used as a screening agent for safely identifying patients with primary pulmonary hypertension who may benefit from long-term treatment with calcium channel blockers. [Pg.2517]

Diamond JR, Cheung JY, Fang LS. Nifedipine-induced renal dysfunction. Alterations in renal hemodynamics. Am J Med 1984 77(5) 905-9. [Pg.2522]

Careful monitoring of the heart and hemodynamic status should be performed. Hypertension and symptoms of CNS stimulation usually resolve spontaneously with only supportive measures. Antiarrhythmic and antihypertensive agents may be necessary in severe exposures. If treatment of hypertension is necessary, a direct vasodilator such as nitroprusside or nifedipine should be utilized. Treat agitation and seizures as necessary with benzodiazepines. Management of concurrently ingested drugs should be appropriate to the agent involved. [Pg.2462]

C. H. Kleinbloesem, P. Van Brummelen, M. Danhof, et al.. Rate of increase in the plasma concentration of nifedipine as a major determinant of its hemodynamics effect in humans. Clin Pharm Ther 41 26-30 (1987). [Pg.363]

Calcium channel antagonists and nitrates also may increase myocardial oxygen supply through coronary vasodilation. Diastolic function also may be improved with verapamil, nifedipine, and perhaps, diltiazem. These effects may vary from those indicated in the table depending on individual patient baseline hemodynamics. [Pg.280]

The hemodynamic effects of verapamil are reportedly more variable than those elicited by nifedipine. Studies conducted in dogs and humans reveal inotropic and vasodilator effects similar to those of nifedipine except that reflex tachycardia... [Pg.70]

Peak effects on mean arterial pressure and heart rate after each dose of nifedipine were -11 3 mm Hg and 44 18 beats/min during the first week of treatment. These effects were transient, values returning to baseline within two hours or less. Hemodynamic effects of nifedipine did not differ significantly between the dietary groups, nor was there a difference in each group between values during the first and last week of treatment. [Pg.181]

Silke B, Verma SP, Guy S. Hemodynamic interactions of a new beta blocker, celiprolol, with nifedipine in angina pectoris. Cardiovasc Drugs Ther (1991) 5,681-8. [Pg.840]

Saltzman LS, Kates RA, Norfleet EA, Corke BC, Heath KS. Hemodynamic interactions of diltiazem-dantrolene and nifedipine and nifed ine-dantrolene. Amsihesiology (1984) 61, All. [Pg.867]

Scardo JA, Vermillion ST, Hogg BB, Newman RB. Hemodynamic effects of oral nifedipine in preeclamptic hypertensive emergencies, Am J Obstet Oynecol( 996) 175, 336-8. [Pg.873]

Kubo SH, Fox SC, Prida XE, Cody RJ. Combined hemodynamic effects of nifedipine and nitroglycerin in congestive heart failure.(1985) 110, 1032-4. [Pg.886]


See other pages where Nifedipine hemodynamics is mentioned: [Pg.152]    [Pg.235]    [Pg.179]    [Pg.583]    [Pg.237]    [Pg.235]    [Pg.312]    [Pg.249]    [Pg.139]    [Pg.599]    [Pg.605]    [Pg.2517]    [Pg.192]    [Pg.621]    [Pg.627]    [Pg.273]    [Pg.283]    [Pg.362]    [Pg.63]    [Pg.70]    [Pg.375]    [Pg.407]    [Pg.66]    [Pg.367]    [Pg.1038]    [Pg.235]   
See also in sourсe #XX -- [ Pg.63 , Pg.64 ]




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