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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After an intravenous injection of 0.1 mg Verapamil per kg body weight and during an infusion of 0.007 mg Verapamil per kg body weight and minute the heart rate increased, P,Q,-time increased, pulmonary vascular pressures increased. Aortic pressures decreased. No change in maximum dp/dt of the aortic pressure. The word maximum is still missing. Pre-ejection period decreased. During an exercise on a load of 650 kpm/min on average heart rate after Verapamil was increased, aortic pressures decreased, stroke work decreased and there were no signs of any negative inotropic effect.
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PMID:[The hemodynamic effect of verapamil by intravenous administration in middle-aged, subjectively healthy subjects at rest and during exercise]. 112 28

The effect of the antiarrhythmic drug verapamil (Isoptin) on circulatory dynamics and myocardial contractility was studied in six patients in sinus rhythm: three patients were control subjects and three had underlying rheumatic valvular disease. The drug was given as an intravenous bolus (10 mg) and measurements made in the control state and repeated 1, 3, 5 and 10 min after administration of verapamil. Left ventricular (LV) systolic pressure fell by 18% 1 min after intravenous verapamil (p less than 0.01) and returned twoards the range of normal after 10 min. Heart rate increased and cardiac and stroke index were not altered 5 and 10 min after administration of the drug. Peak LVdp/dt and Vmax were reduced while LV end-diastolic pressure increased reflecting a decrease in LV contractility. The hemodynamic effects were similar in digitalised and nondigitalised patients.
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PMID:Immediate haemodynamic effects of verapamil in man. 123 67

To assess the hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration [Ca2+] and enflurane (2.5%), halothane (1.2%) or isoflurane (1.6%), seven dogs were chronically instrumented to measure heart rate (HR), aortic, left atrial and left ventricular (LV) pressures, and cardiac output (CO). [Ca2+] was lowered 0.35 mmol.l-1 by citrate infusion and then increased 0.35 mmol.l-1 above control level by CaCl2 infusions. Verapamil was infused at 3 micrograms.kg-1 x min-1 (loading dose 200 (awake), 150 (isoflurane) or 100 (enflurane and halothane) micrograms.kg-1), giving mean verapamil concentrations around 75 (range of means: 66-84 ng.ml-1). Verapamil produced mostly minor changes in the cardiovascular effects of changing [Ca2+] in both awake and anesthetized dogs, indicating mostly additive effects. Verapamil induced a decrease in HR at high [Ca2+] and abolished an increase in mean aortic pressure at both low and high [Ca2+] awake. Verapamil exaggerated the decrease in CO and stroke volume (SV) induced by low [Ca2+] during enflurane anesthesia and abolished the increase in CO induced by low [Ca2+] and exaggerated the increase in SV and LV dP/dtmax induced by high [Ca2+] during halothane anesthesia.
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PMID:Hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration and enflurane, halothane or isoflurane in chronically instrumented dogs. 146 19

Adjustment of myocardial mass to work load is a fundamental characteristic of the heart. We studied the effect of verapamil, a calcium channel blocker, on growth and function of chick embryonic ventricle. We treated stage 18 chick embryos with verapamil delivered to the extraembryonic vascular bed by a miniosmotic pump and compared them with saline-treated control and untreated embryos. At stages 24, 27, and 29, we measured ventricular pressure and dP/dt by a servo-null system, dorsal aortic stroke volume and dV/dt by pulsed-Doppler, and ventricular and embryo wet weights. Mean myocyte profile area was measured by digital planimetry technique, and cell growth response by DNA and protein assay. Verapamil treatment decreased ventricular pressure in experimental (P less than 0.05) compared with saline control and normal embryos; at stage 27, 1.59 +/- 0.21 vs. 2.17 +/- 0.05 and 2.35 +/- 0.08 (SE) mmHg, respectively. Mean dorsal aortic blood flow decreased in experimental (P less than 0.05) vs. control and normal embryos; at stage 27, 0.98 +/- 0.07 vs. 1.54 +/- 0.10 and 1.56 +/- 0.07 mm3/s, respectively. Stroke volume remained the same in all experimental, normal, and control embryos except at stage 29. Ventricular weight decreased in experimental (P less than 0.05) vs. control and normal embryos; at stage 27, 1.09 +/- 0.07 vs. 1.51 +/- 0.08 and 1.54 +/- 0.11 mg, respectively. Embryo weights, myocyte size, and cytoplasmic fractional volume were similar in all groups. Morphology of ventricles was normal. DNA was lower in experimental (P less than 0.05) compared with control and normal embryos.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of chronic verapamil treatment on ventricular function and growth in chick embryos. 185 17

Representative calcium antagonists from proposed class I (nifedipine), class II (verapamil) and class III (flunarizine) have been examined for effects on blood pressure, heart rate, ventricular pressures, ECG, cardiac output and regional blood flow in pentobarbitone-anaesthetized rats. Flow was measured by the microsphere technique. Low and high infusion rates of each drug were chosen to decrease mean arterial pressure by 25 and 40 mmHg, respectively. At equi-depressor infusion rates, all drugs equally decreased total peripheral resistance and slightly increased cardiac output and stroke volume. Heart rate was decreased by verapamil and flunarizine, but increased by nifedipine. Verapamil markedly decreased dP/dtmax of ventricular pressure and prolonged the PR-interval. Flunarizine was similar. Nifedipine decreased dP/dtmax and had no effect on the PR-interval of the ECG. Similar effects on regional blood flow were seen with the three drugs; flow to lungs, heart, liver, skeletal muscle and stomach increased. Correction for blood pressure changes, i.e. conductance, showed that vasodilatation occurred in all regions, with all drugs, except for the skin. Therefore, representatives from three sub-classes of calcium antagonists had similar effects on blood flow but different effects on the heart.
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PMID:Effects of verapamil, nifedipine and flunarizine on haemodynamics and regional blood flows in pentobarbitone-anaesthetized rats. 197 79

Impaired diastolic function of the hypertrophied and stiffened left ventricle is a characteristic feature of hypertrophic cardiomyopathy (Figure 1). Altered left ventricular filling dynamics and reduced left ventricular distensibility or increased left ventricular diastolic chamber stiffness are associated with reduced left ventricular stroke volume, increased left ventricular filling pressures and compressive effects on the coronary microcirculation. These factors contribute importantly to the clinical presentation of many patients, including symptoms of fatigue, dyspnea and angina pectoris. Reduced distensibility results both from factors determining the passive elastic properties of the ventricular chamber (including severity of hypertrophy, fibrosis and cellular disarray) and from factors influencing the rate and extent of active left ventricular relaxation (Figure 2). The factors contributing to impaired relaxation in hypertrophic cardiomyopathy are mediated via either inactivation dependent or load-dependent mechanisms. In laboratory animals, compromise of myocardial inactivation results in a persistent increase in intracellular calcium concentration and in prolonged interaction of the contractile proteins. Additionally, there is evidence for an increased number of active receptors for calcium antagonists and, lastly, for myocardial ischemia (Figure 3). Load-dependent mechanisms include diminished wall tension at the opening of the mitral valve, changes in afterload, contractility and coronary flow. Other factors are nonuniform and asynchronous regional ventricular function due to differing increases in thickness of the ventricular walls and ischemia (Figure 4). Calcium channel blockers exert a favorable influence on left ventricular relaxation and filling (Figure 5); verapamil and diltiazem are preferable to nifedipine. Verapamil increases left ventricular stroke volume without an increase in the end-diastolic pressure (Figure 6), reduces regional asynchrony if present, and leads to a more homogeneous regional diastolic filling (Figure 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular diastolic function in hypertrophic cardiomyopathy. 202 81

The effects of i.v. administration of the calcium channel blockers--verapamil (0.045 and 0.45 mg.kg-1) and Mepamil (2-methylphenyl-derivative of verapamil; 0.0445 and 0.445 mg.kg-1) on the cardiovascular system of rabbits in vivo under the paced and non-paced heart conditions were investigated. Verapamil induced--in the dose-dependent manner--a decrease in blood pressure (max. 65.2%), a significant decrease in dP/dtmax. (max. 46.0%), a bradycardia (max. 79.4%), a decrease in minute blood flow (max. 63.9 %) and stroke blood flow (max. 71.5%). The administration of Mepamil did not induce important changes in heart rate; changes in other parameters were--again in the dose-dependent manner--of a similar qualitative character as after verapamil administration, but they were quantitatively less expressed (especially marked in the effect on dP/dtmax, where the maximum decrease was only to 71.5%). The results show a less pronounced cardiodepressive activity of Mepamil compared to verapamil in rabbits.
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PMID:The effects of calcium channel blockers on the cardiovascular system of rabbits in vivo. 209 7

1. The effects of hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis or hypercarbia with acidosis on the blood pressure and pulse rate responses to verapamil were studied in chloralose-anaesthetized rats. 2. At a fixed stroke volume (10 mL/kg) and rate (80 strokes/min; except for the hypocarbic group at 160 strokes/min), hypoxaemia, hyperoxaemia, hypercarbia with acidosis, or hypocarbia with alkalosis was induced by artificial ventilation with gas mixtures containing 17% O2, 28% O2, 23% O2, with 5% CO2, or 17% O2, without CO2 respectively. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3 respectively, in animals artificially ventilated with room air. 3. Changes in individual blood gas/pH parameters had no significant effect on blood pressure except for acidosis which caused a significant decrease. Effects on pulse rate were significant increases in the alkalosis and hypercarbia groups, decrease in the acidosis group, while in other conditions no significant changes were recorded. 4. In the controls, intravenous injections of verapamil 20-320 micrograms/kg caused dose-dependent increases in mean blood pressure, while effects on pulse rate were not marked. 5. The hypotensive responses to verapamil were significantly alleviated or enhanced in the presence of alkalosis or acidosis respectively. Verapamil also caused greater falls in pulse rate during acidosis. Effects of Po2 changes were not statistically significant. The influence of PCO2 changes remained unclear. 6. The present findings suggest that changes in blood pH may play a more important role than Po2 alterations in affecting the cardiovascular responses to verapamil in the presence of blood gas abnormalities.
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PMID:Effects of blood gas/pH abnormalities on the cardiovascular actions of verapamil in rats. 212 29

Left ventricular (LV) diastolic function is often impaired in coronary artery disease (CAD). To assess whether verapamil could improve LV diastolic properties, 12 patients with CAD undergoing right- and left-sided cardiac catheterization, as well as simultaneous radionuclide angiography, were studied before and during intravenous administration of verapamil (0.1 mg/kg as a bolus followed by 0.007 mg/kg/min). The heart rate was kept constant by atrial pacing in both studies. LV pressure-volume relations were obtained. Verapamil decreased LV systolic pressure (130 +/- 22 to 117 +/- 16 mm Hg, p less than 0.01) and the end-systolic pressure/volume ratio (2.4 +/- 1.3 to 1.6 +/- 0.5 mm Hg/ml, p less than 0.05), and increased LV end-diastolic (13 +/- 4 to 16 +/- 4 mm Hg, p less than 0.02) and pulmonary capillary pressures (10 +/- 5 to 12 +/- 5 mm Hg, p less than 0.005). Despite such negative inotropic effects, cardiac index increased (3.4 +/- 0.7 to 3.9 +/- 0.6 liters/min/m2, p less than 0.02). The time constant of isovolumic relaxation shortened (63 +/- 14 to 47 +/- 9 ms, p less than 0.02); peak filling rate increased (370 +/- 155 to 519 +/- 184 ml/s, p less than 0.001; 2.6 +/- 1.1 to 3.3 +/- 0.9 end-diastolic counts/s, p less than 0.02; and 4.1 +/- 1.6 to 5.5 +/- 1.5 stroke counts/s, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intravenous verapamil on left ventricular relaxation and filling in stable angina pectoris. 222 May 79

Treatment of hypertension may prevent many of the complications attributable to blood pressure elevation, particularly those that are "pressure-related," such as stroke. However, the atherosclerotic complications of hypertension, e.g., coronary artery disease manifested as coronary morbidity and mortality, have not been reduced significantly with antihypertensive therapy. This disappointing outcome may reflect the adverse metabolic effects of the traditional therapies, diuretics and beta blockers, and their lack of specific vasoprotective properties. Increasing attention is thus being paid to the newer antihypertensive agents, which typically have fewer adverse effects and perhaps more physiologic mechanisms of antihypertensive action. Since calcium plays a key role in the genesis of atherosclerosis, calcium antagonists may positively affect the course of vascular disease. Investigators have observed that calcium antagonists display clear antiatherosclerotic properties in experimental as well as clinical studies. In one recently published clinical study, coronary artery disease was shown to develop more slowly, with a slower progression of individual stenoses, higher regression rate and less frequent occurrence of new lesions in patients treated chronically with verapamil compared to those receiving conventional therapies. Other similar investigations are currently under way to evaluate the antiatherogenic properties of calcium antagonists, including the Frankfurt Isoptin Progression Study (FIPS), the Multicenter Isradipine Diuretic Atherosclerosis Study (MIDAS), the International Nifedipine Trial on Atherosclerosis Coronary Therapy (INTACT), and the large-scale Montreal Heart Institute Study. Results of these studies, which use precise end points such as myocardial infarction, cerebral infarction and peripheral vascular disease, may revolutionize the treatment of hypertension by identifying therapeutic approaches that control both the pressure-related and atherosclerotic complications of the disease.
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PMID:Anti-atherosclerotic and vasculoprotective actions of calcium antagonists. 225 66


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