Drugs online research references
Cardiovasc Drugs Ther. 1989 Jan;2(6):815-21.
Comparative study on the enhancement of ischemic tolerance by intracoronary pretreatment with three calcium antagonists in pig hearts.
Klein HH, Pich S, Lindert S, Nebendahl K, Kreuzer H.
Department of Cardiology, University of Gottingen, Federal Republic of Germany.
The effect of intracoronary (IC) pretreatment with different calcium antagonists (diltiazem, nifedipine, verapamil) on the development of infarcts was investigated in two experimental series including 35 open-chest pigs. The left anterior descending coronary artery (LAD) was distally ligated for 75 minutes (series A) or for 45 minutes (series B) and was reperfused for 24 hours. Infarct size was determined as the ratio of infarcted myocardium (tetrazolium stain) to the risk region (dye technique). In series A, 20 pigs were pretreated immediately before occlusion with either IC diltiazem (n = 5, 4 mg/2 min), IC nifedipine (n = 5, 0.4 mg/2 min), IC verapamil (n = 5, 1 mg/2 min), or isotonic sodium chloride solution (n = 5). In series B, IC diltiazem (n = 5, 4 mg/2 min), IC verapamil (n = 5, 1 mg/2 min), or isotonic saline solution (n = 5) were administered 8 minutes prior to ischemia. The IC infusion of all calcium antagonists (series A) depressed left ventricular peak pressure, diastolic blood pressure, and dp/dt max and increased heart rate and coronary venous oxygen saturation. The development of infarcts was significantly delayed by IC diltiazem and IC verapamil. Mean infarct sizes (series A) amounted to 62% in the diltiazem group, 88% in the nifedipine group, 40% in the verapamil group, and 94% in the control group. In series B, where a time period of 8 minutes elapsed between pretreatment and induction of ischemia, mean infarct sizes after 45 minutes of ischemia and 24 hours of reperfusion amounted to 47% in the diltiazem group, 4% in the verapamil group, and 76% in control experiments.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2488097&dopt=Abstract
Am J Physiol. 1986 Apr;250(4 Pt 2):F695-701.
Calcium channel blockers enhance extrarenal potassium disposal in the rat.
Sugarman A, Kahn T.
The effect of calcium channel blockers on the extrarenal disposition of an acute potassium load was examined in acutely nephrectomized rats infused with KCl (0.75 meq X kg-1 X h-1 for 60 min) alone or in combination with either verapamil or nifedipine. The increment in plasma potassium concentration during the potassium infusion (delta PK) with either verapamil or nifedipine was less than control (P less than 0.05 and 0.01, respectively). Studies were repeated in acutely adrenalectomized rats (ADX) to evaluate whether the changes in plasma potassium were consequent to the enhanced activity of epinephrine and other adrenal hormones. delta PK with ADX was higher than control (P less than 0.01). Verapamil or nifedipine with ADX resulted in a lower delta PK than ADX alone (P less than 0.05). Further studies were then conducted with the selective beta 2-adrenergic blocker butoxamine hydrochloride to rule out enhanced peripheral sympathetic activity of the beta 2-adrenergic system in facilitating the potassium disposal. delta PK with butoxamine was greater than control (P less than 0.01) but not significantly different from ADX. Verapamil or nifedipine in conjunction with butoxamine resulted in a lower delta PK than butoxamine alone (P less than 0.01). Changes in arterial pH and plasma bicarbonate were similar in all groups. In conclusion, during potassium infusion the delta PK is lower in the presence of calcium channel blockers. The alteration in potassium transport produced by calcium channel blockers does not appear to be dependent on adrenal function or peripheral sympathetic activity. Impaired calcium entry into cells may alter potassium transport in the intact animal.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3083698&dopt=Abstract
Eur J Pharmacol. 1993 Nov 16;249(3):317-24.
Ca2+ channel antagonists enhance tension in skinned skeletal and heart muscle fibres.
Schiereck P, De Beer E, Van Heijst B, Janssen P, Van Andel A, Jennekens F, Sontrop A, Bavinck A.
Department of Medical Physiology and Sports Medicine, University Utrecht, Netherlands.
Striated muscle fibres, both skeletal and cardiac of different species including human, skinned by freeze-drying, were activated in solutions strongly buffered for Ca2+. The single fibres were immersed in solutions with different [Ca2+]. Sarcomere length was set and controlled by laser diffraction. Fibre type was determined by Sr2+ activation. The relation between the negative logarithm of the Ca2+ concentration and the normalized tension, the Ca2+ sensitivity curve, was investigated. The effect on the contractile machinery of three different Ca2+ channel antagonists (verapamil, diltiazem and nifedipine) in a therapeutic concentration (10(-6) M) was investigated. The possible effects on the Ca2+ sensitivity curve were quantified by: (1) the change in maximal tension developed at pCa2+ = 4.4; (2) the change in pCa2+ value at which 50% of the tension induced at pCa2+ = 4.4; (3) the steepness of the Ca2+ sensitivity curve in this point. The three drugs tested, at a therapeutic concentration of 1 microM, all enhanced maximal induced tension by respectively 25, 20 and 7%. The sarcomere length dependency of the effect proved to be dependent upon the drug, but also slightly on fibre type (skeletal or cardiac), or on species. It is concluded that the drug influences the cooperativity of the two different types of binding sites on troponin-C (low- and high-affinity sites). Tension enhancement was due to increased stiffness of the actin-myosin interaction site.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8287918&dopt=Abstract
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