Drugs online research references
Cardiovasc Res. 1986 Apr;20(4):282-5.
Reversal of depressant effects of propranolol on the left ventricular pump function by nifedipine in dogs with chronic ischaemia.
Tani M, Yamazaki H, Noma S, Ohnishi S, Handa S, Nakamura Y.
The aim of this study was to clarify the combined effects of propranolol and nifedipine on the regional wall motion and haemodynamic variables of the heart in dogs with chronic ischaemia. After an injection of propranolol the heart rate and stroke volume significantly decreased (from 128(18) beats X min-1 to 113(12) beats X min-1 and from 15.1(3.1) ml to 12.2(2.6) ml respectively) and the left ventricular end diastolic pressure and systemic vascular resistance in systole increased significantly (from 7.3(1.5) mmHg to 10.0(1.8) mmHg and from 8.61(1.42) kPa X litre-1 X min-1 to 11.80(1.59) kPa X litre-1 X min-1 respectively). In the regional myocardium the end diastolic length increased significantly in both border and normal zones (7(3)% and 4(2)% respectively) and the percentage systolic shortening in the normal zone decreased significantly from 18.0(3.1)% to 15.1(2.9)%. In the border and infarcted zones the percentage systolic shortening or systolic lengthening did not change. The administration of nifedipine resulted in significant decreases in left ventricular systolic pressure and in systemic vascular resistance (from 122(17) mmHg to 105(14) mmHg and from 11.80(1.59) kPa X litre-1 X min-1 to 6.63(1.24) kPa X litre-1 X min-1 respectively) and stroke volume increased to 18.2(4.4) ml. The percentage systolic shortening in the border and normal zones improved significantly to 9.8(3.2)% and 19.2(3.7)% respectively without any change in end diastolic length and left ventricular end diastolic pressure. In the infarcted zone no significant change in systolic lengthening or end diastolic length was seen. Thus impaired left ventricular pump function induced by propranolol was reversed by nifedipine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3719608&dopt=Abstract
Am Heart J. 1985 Mar;109(3 Pt 1):529-32.
The electrophysiologic effects of nisoldipine in the conscious dog.
Schwartz JB, Herre JM, Lewis RM.
The electrophysiologic effects of nisoldipine, 10 to 100 micrograms/kg, were studied in eight conscious nonsedated chronically instrumented dogs. No change in blood pressure or electrophysiologic measurements followed 10 micrograms/kg nisoldipine. Following 30 micrograms/kg, the mean arterial pressure was decreased from 116 +/- 9 to 105 +/- 10 mm Hg (means +/- SD) and the sinus cycle length decreased from 536 +/- 101 to 428 +/- 75 (msec) without changes in PR, AH, HV intervals, atrioventricular (AV) nodal conduction, or sinus node recovery times. After 100 micrograms/kg, the mean blood pressure was further reduced (87 +/- 17 mm Hg), the sinus cycle length further decreased (378 +/- 71 msec), and the AV nodal effective and functional refractory periods shortened (178 +/- 59 to 148 +/- 43 and 178 +/- 59 to 148 +/- 43 msec, respectively), as did the sinus node recovery time (corrected and uncorrected) and the QT and QTc intervals. No significant changes in atrial or ventricular pacing thresholds, atrial or ventricular refractory periods, or in the HV interval were observed. Nisoldipine, a nifedipine derivative, did not significantly change electrophysiologic parameters in intact conscious animals when given in doses which did not alter blood pressure. When nisoldipine produced significant vasodilatation, the enhancement of AV nodal conduction observed probably reflects a balance of the direct effect of nisoldipine and opposing autonomic activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3976479&dopt=Abstract
Cephalalgia. 1985 May;5 Suppl 2:181-3.
Pupillary and vascular effects of calcium antagonists in migraine.
Fanciullacci M, Boccuni M, Pietrini U, Cangi F, Gatto G, Marabini S, Fusco BM.
In migraine patients the effect of calcium antagonists (flunarizine, verapamil and nifedipine) on both venous and pupillary neuromuscular functions, as well as on blood pressure have been evaluated. A single oral dose of flunarizine (10 mg) and verapamil infusion (50 micrograms/ml/min) increased venous compliance. Verapamil also counteracted dose-dependent dopamine induced venoconstriction. Nifedipine (10 mg orally) reduced mean arterial pressure in upright position in migraineurs but not in controls. In addition, chronic treatment with flunarizine (10 mg for 2 weeks) induced a transient miotic effect and a reduction of tyramine induced mydriasis. These findings demonstrated that calcium antagonists affect vascular and extravascular structures. It is postulated that, in migraine, calcium entry blockers may prevent exaggerated responses to catecholaminergic stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=4016932&dopt=Abstract
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