Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium channel blockers reduce the arterial smooth muscle tone and lower blood pressure. They may be regarded as left ventricular unloading agents. Left ventricular unloading efficacy of nifedipine (15 cases) and verapamil (14 cases) was tested in hypertensive decompensated patients, through one-month treatment period. Nifedipine persistently reduced systemic vascular resistance, mean arterial pressure, mean pulmonary wedge pressure and left ventricular diastolic diameter and improved cardiac index and velocity of circumferential fiber shortening. All of the patients had relief from dyspnea and reduction in heart size. The only side effect was ankle edema in 6 cases. Verapamil reduced systemic vascular resistance and mean arterial pressure and was not effective on mean pulmonary wedge pressure, left ventricular diastolic diameter and velocity circumferential fiber shortening. The drug was discontinued in 2 patients who developed severe dyspnea at rest after a 3-4 day continued oral treatment. Clinical symptoms and signs did not improve in the remaining subjects despite persistent pressure reduction. A less potent vasodilating action of verapamil and a prominent depression in cardiac contractility may account for the different results with the two compounds, in spite of a shared vasodilating antihypertensive effect. These findings prove that functional changes in the failing hypertensive heart may differ from one calcium blocker to another as a result of interaction and relative preponderance of influences on afterload and contractility.
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PMID:Left ventricular unloading with calcium antagonists. 623 2

Calcium binding to fragmented sarcolemma isolated from dog heart was measured by an ultracentrifugation technique. Two classes of binding sites with dissociation constants of 4.2 x 10(-5) M and 1.2 x 10(-3) M were identified. The maximum number of high and low affinity sites were 15 and 452 nmol/mg, respectively. The effects of various cations and drugs on calcium binding were studied in the presence of 0.1 mM total calcium. All cations tested inhibited calcium binding to a certain degree. La3+ (1 mM) and Mn2+ (1 mM) abolished calcium binding to the sarcolemma. The other divalent cation, Mg2+, used at a concentration of 1 mM, produced a partial inhibition Na+ and K+ also depressed calcium binding, with Na+ being the more potent inhibitor. Verapamil produced a depression at concentrations as low as 10(-7) M and abolished calcium binding at 10(-3) M. The effects of these cations and drugs on fragmented sarcolemma appear different from those reported for the isolated sarcoplasmic reticulum. Thus it is unlikely that the calcium binding observed was caused by a contamination of the sarcolemmal preparation by the fragmented sarcoplasmic reticulum. In addition, the calcium binding seems to be on the sarcolemma itself, rather than to the remaining fragments of the basement membrane, because the calcium binding was not significantly modified by pretreatment with purified neuraminidase (0.25 U/g of sarcolemma).
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PMID:Influence of cations and agents on sarcolemmal calcium binding. 624 41

Effects of electrolyte concentrations on atrioventricular (AV) conduction were studied in isolated, perfused rabbit hearts by recording the His bundle electrogram. Initial calcium (Ca++), sodium (Na+), and potassium (K+) concentrations were 2.4, 144.8, and 4.5 mM, respectively. Lowering of Ca++ to 0.8 mM slightly prolonged the AH interval, whereas elevation of Ca++ to 4.8 or 7.2 mM more markedly prolonged this interval, often causing intranodal block. High Ca++-induced depression of intranodal conduction was antagonized by high K+ (7.5 mM). Verapamil (0.5 to 1.0 mg/L) produced second-degree intranodal block. High Na+ (172 mM) restored 1:1 conduction, whereas high Ca++ did not. These results suggest that: (1) an optimal Ca++ concentration for intranodal conduction exists; (2) high K+ counteracts high Ca++-induced intranodal block; (3) verapamil effect on AV node is antagonized by high Na+; and (4) slow Na+ current may play a role in AV nodal action potentials.
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PMID:Effects of calcium and sodium concentrations on atrioventricular conduction: experimental study in rabbit hearts with clinical implications on heart block and slow calcium channel blocking agent usage. 627 62

The interaction of halothane anesthesia and intravenous verapamil (0.15 mg/kg over 10 min) was investigated in eight patients scheduled for coronary artery bypass surgery. All patients had a normal left ventricular (LV) function at rest and were on chronic beta-blocker therapy. Halothane produced a marked reduction in mean arterial pressure (MAP), cardiac index, and in LV contractility as documented by a decrease in LV peak positive dP/dt. Verapamil caused an additional depression (16%) of LV peak positive dP/dt accompanied by a small increase (3 mm Hg) in LV end-diastolic pressure. The combined negative inotropic propensities of halothane and verapamil did not produce any overt untoward effects even in the presence of chronic low dose beta-blocker therapy. The predominant hemodynamic effect of verapamil was a systemic vasodilation resulting in a further reduction in MAP (12%) while heart rate remained unaffected. Despite reducing myocardial oxygen demand, caution must be exercised in dose selection in each drug to avoid regional myocardial ischemia due to the combined hypotensive effects of halothane and verapamil.
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PMID:Combined effects of halothane anesthesia and verapamil on systemic hemodynamics and left ventricular myocardial contractility in patients with ischemic heart disease. 633 75

Calcium channel blockers reduce arterial smooth muscle tone and lower blood pressure. They may be regarded as left ventricular (LV) unloading agents. LV unloading efficacy of nifedipine (15 patients) and verapamil (14 patients) was tested in hypertensive decompensated patients, during a 1-month treatment period. Nifedipine persistently reduced systemic vascular resistance (SVR), mean arterial pressure, mean pulmonary wedge pressure (PWP), and LV diastolic diameter, and improved cardiac index and velocity of circumferential fiber shortening (Vcf). All of the patients had relief from dyspnea and reduction in heart size. The only side effect was ankle edema in six. Verapamil reduced SVR and mean arterial pressure and was not effective on PWP, LV diastolic diameter, and Vcf. The drug was discontinued in two patients who developed severe dyspnea at rest after 3 to 4 days of continuous oral treatment. Clinical symptoms and signs did not improve in the remaining patients despite persistent pressure reduction. A less potent vasodilating action of verapamil and a prominent depression in cardiac contractility may account for the differential results with the two compounds, in spite of a shared vasodilating antihypertensive effect. These findings indicate that functional changes in the failing hypertensive heart may differ from one calcium blocker to another as a result of interaction and relative preponderance of influence on afterload and contractility.
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PMID:Disparate unloading efficacy of the calcium channel blockers, verapamil and nifedipine, on the failing hypertensive left ventricle. 637 29

1. The chronotropic and inotropic effects of the anti-anginal agent SG-75 (2-nicotinamidoethyl nitrate) and 1-verapamil were investigated in isolated blood-perfused canine atrial preparations. The compounds were administered via the cannulated sinus node artery. 2. SG-75 induced a selective negative inotropic as opposed to a chronotropic effect. Verapamil showed no selective negative chronotropic or inotropic activity. 3. Effects of SG-75 and 1-verapamil on the frequency-force relationship were studied. SG-75 produced a uniform depression of the developed tension at all frequencies tested which the depression with 1-verapamil was greater at higher than at lower frequencies.
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PMID:Differential chronotropic and inotropic effects of 2-nicotinamidoethyl nitrate (SG-75) in the dog isolated atrium. 644

In a patient with ischaemic heart disease chronic atrial flutter reverted to sinus rhythm during treatment with oral Verapamil, given at dosage of 240 mg once a day in order to prevent spontaneous angina. Such an unexpected event was accompanied by a remarkable sinus node depression and by a transient complete a-v block, that gradually subsides leaving a slight permanent a-v conduction delay. Either a higher bioavailability of the drug or an extremely increased sensitivity of the receptors can explain such a marked electrophysiological effect at a moderate drug dosage.
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PMID:Conversion of longstanding atrial flutter to sinus rhythm and transient complete A-V block following oral administration of verapamil. Report of a case. 650 Feb 21

To study the value of 4-aminopyridine as an antidote to verapamil intoxication, we subjected 12 adult cats to verapamil poisoning by administering doses of 4.0-25.0 mg/kg verapamil by intravenous infusion. Six animals were given 4-aminopyridine 2 X 0.5 mg/kg i.v. after the verapamil infusion was stopped and the other six animals (the control group) were not. Verapamil caused profound cardiovascular depression and also partial neuromuscular block, both of which were completely reversed by 4-aminopyridine within 50 min, in spite of extremely high serum verapamil concentrations (ranging between 3,700 and 13,500 ng/ml). The six animals that received 4-aminopyridine survived the verapamil intoxication, whereas four of the six animals in the control group died. The results suggest that 4-aminopyridine may be useful in the treatment of verapamil intoxication.
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PMID:Effective treatment of verapamil intoxication with 4-aminopyridine in the cat. 653 84

The effects on indirectly elicited muscle twitch amplitude associated with the calcium (slow) channel blocker, verapamil, with or without pancuronium were investigated using isolated bullfrog sciatic nerve-sartorius muscle preparations. Verapamil (2-8 mM) produced a dose-related depression of indirect muscle twitch height (P less than 0.05). Twitch response was depressed 11% below control by the lowest concentration employed and 86% by the highest concentration. Pancuronium (0.07 mM) depressed neuromuscular function 35% below control (P less than 0.05). The combination of 5 mM or 8 mM verapamil with 0.07 mM pancuronium caused significantly greater degrees of depression than either drug alone. Verapamil produced significant depression of twitch height in vitro in relatively high concentrations. The mechanism of action remains unknown. Verapamil possesses pharmacologic properties that may be unrelated to slow (calcium) channel inhibition. The reduction of muscle twitch height caused by verapamil alone (5 mM) could not be antagonized by neostigmine, calcium, or frequent washings.
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PMID:Effects of verapamil on indirect muscle twitch responses. 660 98

We evaluated the effects of intravenous verapamil, a calcium antagonist, on hemodynamics and regional left ventricular (LV) performance in patients with acute myocardial infarction (AMI). Twenty patients having uncomplicated infarction or moderate heart failure were randomized to receive either verapamil or placebo and were studied a mean of 12 hours after onset of symptoms. Verapamil, 7.5 mg intravenously, acutely reduced systolic arterial pressure (p less than 0.0005), systemic vascular resistance, and LV stroke work (p less than 0.005) and rate-pressure product (p less than 0.05); the heart rate did not alter. The Frank-Starling relationship by Swan-Ganz catheter did not change for 1 hour. Segmental wall motion amplitudes were recorded from eight standardized segments around the left ventricle by a multidirectional M-mode echocardiographic technique. The systolic wall motion of the uninvolved LV segments and LV cavity size did not change after verapamil. Verapamil improved mechanical performance in the ischemic segments (p less than 0.005). Therefore, the overall regional contractile function of the left ventricle improved as well (by 11% to 13%, p less than 0.05). This echocardiographic improvement continued after the acute vasodilatory response of intravenous verapamil subsided and was preserved for 1 week, the patients having had oral verapamil, 240 mg daily. Chest pain was relieved in five of the six patients having ongoing slight pain before verapamil injection. No sequential hemodynamic or echocardiographic changes occurred in the placebo-treated patients. Thus, in patients with uncomplicated AMI, verapamil improve contractile function of the acutely ischemic LV segments by hemodynamic unloading and/or by direct myocardial effect, without manifest depression of the uninvolved myocardium.
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PMID:Effects of verapamil in patients with acute myocardial infarction: hemodynamics and function of normal and ischemic left ventricular myocardium. 669 58


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