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)

To assess the relationship between left ventricular (LV) response to exercise and myocardial ischaemia, 40 patients with coronary artery disease (CAD) and 17 control subjects underwent radionuclide ventriculography at rest and during semiupright exercise. In 14 of the 40 patients with CAD, radionuclide exercise studies were repeated 20 min after 20 mg of sublingual nifedipine. Patients with CAD had increases in both LV end-diastolic and end-systolic volumes and no change in ejection fraction during exercise. End-systolic volume increased and ejection fraction decreased significantly more in patients with multivessel disease, exercise-induced angina and/or ischaemic ST segment depression. Nifedipine reduced angina and ST-segment depression during exercise, attenuated exercise-induced increase in end-diastolic and end-systolic volumes and improved ejection fraction. This study suggests that in patients with CAD, the response of LV volumes and ejection fraction to exercise is related to the degree of exercise-induced myocardial ischaemia and nifedipine improves exercise LV performance.
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PMID:Left ventricular response to exercise in coronary artery disease: relation to myocardial ischaemia and effects of nifedipine. 383 Jul 8

The cardiac, pulmonary vascular, and systemic vascular effects of bolus injections (2.5, 25, 50 micrograms/kg) and 5-min infusions of 50 micrograms/kg/min of Nifedipine were tested in conscious, chronically instrumented newborn lambs. While breathing room air, bolus injections of 50 micrograms/kg into the pulmonary artery caused the cardiac index and left ventricular dp/dt to fall as did systemic arterial pressure and calculated resistance (all changes significant p less than 0.05). Pulmonary artery, pulmonary vein, and left atrial pressure all tended to increase and there was a shift in flow away from the injected lung (14 +/- 0.05%). Pulmonary arteriolar resistance in the injected lung increased significantly (p less than 0.05). Nifedipine failed to prevent hypoxia-induced pulmonary vasoconstriction, and when given during hypoxia, caused a further rise in pulmonary artery pressure with a marked fall in left ventricular dp/dt and systemic vascular resistance. These acute effects peaked 30 s to 2 min after injection and all hemodynamic variables returned to baseline by 10 min. Five-min infusions caused similar effects which completely reversed 20 min after the infusion was stopped. Nifedipine causes significant cardiac depression combined with systemic vasodilatation and pulmonary arteriolar constriction in conscious newborn lambs. Assuming similar actions in humans, it seems quite unsuitable for the therapy of pulmonary hypertensive problems of newborn infants.
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PMID:The circulatory effects of nifedipine in the conscious newborn lamb. 394 11

The short-term effect of oral nifedipine on effort tolerance was tested in 10 patients with effort angina pectoris and a positive effort test (GXT). The patients had four symptom-limited GXTs, using the Bruce protocol, on each day of the study at 0800, 1000, 1400, and 1800 hours. They received four doses of 10 mg oral nifedipine on one day and four doses of placebo on the other, each dose given half an hour prior to each GXT. Values with nifedipine were compared to values with placebo at the same time during each day. Nifedipine improved effort tolerance by 0.5 +/- 0.6 min (p = NS) on the first GXT (mean +/- SEM), by 1.2 +/- 0.6 min (p = NS) on the second GXT, by 1.0 +/- 0.3 min (p less than 0.01) on third GXT, and by 1.3 +/- 0.3 min (p less than 0.01) on the fourth GXT. Improvement of effort tolerance was associated with a fall in resting blood pressure and less ST depression; these changes were statistically significant only on the fourth GXT, which may indicate a cumulative effect of subsequent doses of nifedipine.
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PMID:Short-term effect of nifedipine on effort tolerance in patients with angina pectoris. 394 42

Nifedipine, a slow calcium-channel blocker, has been used to preserve myocardial function in the ischemic heart. To quantitatively evaluate the effectiveness of nifedipine as a cardioplegic agent during moderate hypothermia (28 degrees C), 15 pigs were evaluated on total and right heart bypass with measurement at normothermia and after 1 hour of hypothermic ischemia of stroke volume, coronary blood flow, myocardial oxygen consumption, and lactate extraction. Myocardial tissue gases (oxygen and carbon dioxide) were continuously monitored. Animals were divided into three groups: hypothermic ischemia, hypothermic ischemia with infusion of nifedipine carrier without nifedipine, and hypothermic ischemia with nifedipine and its carrier. A significant decrease in stroke volume was seen in all three groups; however, the depression was significantly greater following hypothermic ischemia than following cardioplegia with either nifedipine or its carrier. The mean recovery value of stroke volume was highest in the nifedipine group, but this difference between nifedipine and its carrier alone did not reach statistical significance. Coronary blood flow, myocardial oxygen consumption, lactate extraction, and tissue gases failed to substantiate a significant benefit when nifedipine was compared with its carrier alone. We conclude that under these hypothermic conditions, no proven statistically significant advantage was noted in the nifedipine group when compared with the nifedipine carrier group in swine. However, both nifedipine and the carrier were superior as a myocardial preservative when compared with hypothermic ischemic arrest alone.
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PMID:Quantitative evaluation of the myocardial preservative characteristics of nifedipine during hypothermic myocardial ischemia. 406 42

The effects of intravenous (iv) nifedipine (7.5 micrograms/kg over 10 min) on systemic hemodynamics and myocardial contractility were investigated under steady state conditions of halothane anesthesia (0.5 MAC) in 8 patients scheduled for elective coronary artery bypass surgery. All patients received long-term medication in the form of beta adrenergic receptor blockers and had a normal global left ventricular function at rest. Halothane produced a marked reduction in left ventricular contractility as documented by a considerable fall in LV max dP/dt. Nifedipine caused a small additional depression of LV max dP/dt without affecting LVEDP significantly. The slight myocardial depressant effect of nifedipine was counterbalanced by a concomitant reduction in left ventricular afterload due to a decrease in the systemic vascular resistance resulting in unchanged or even improved cardiac output. The results indicate that iv nifedipine in the doses used here is safe for patients with ischemic heart disease, even in the presence of already compromised myocardial contractility due to halothane anesthesia and chronic low-dose beta blocker therapy.
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PMID:Cardiovascular interactions of halothane anesthesia and nifedipine in patients subjected to elective coronary artery bypass surgery. 619 57

Calcium channel blockers relax the arterial smooth vasculature and lower blood pressure when it is elevated because of excessive vasoconstriction. They may be regarded as ventricular unloading agents. Nifedipine (11 cases, Group 1) and verapamil (12 cases, Group 2) were tested in hypertensive patients with cardiac enlargement (LV diastolic diameter greater than or equal to 60 mm), ECG signs of LV strain, lung congestion and dyspnea at rest, in an acute (nifedipine 20 mg; verapamil 160 mg) and 1-month (nifedipine 20 mg q.i.d.; verapamil 160 mg t.i.d.) therapeutic evaluation. In the acute study nifedipine reduced systemic vascular resistance (SVR), mean arterial pressure (MAP), mean pulmonary wedge pressure (PWP) and LV diastolic diameter (DD) and improved cardiac index (CI) and Vcf. In Group 2 verapamil reduced SVR and MAP, improved CI and was not effective on PWP, LV DD and Vcf. Verapamil was discontinued in 2 patients who developed severe dyspnea at rest after 3-4 days of continued oral treatment. At the end of the trial Vcf, PWP and LV DD were unchanged in the remaining subjects in Group 2 despite persistent pressure reduction. In Group 1 all of the patients had relief of dyspnea and lung congestion, reduction of heart size, persistent decrease of MAP and PWP, and improvement in Vcf. The only side effect was ankle edema in 4 cases. A less potent vasodilating action of verapamil and a predominant depression in cardiac contractility may account for the different results with the two drugs, in spite of a shared antihypertensive effect. These findings prove that functional changes in the failing hypertensive heart may differ after nifedipine compared to verapamil as a result of interaction and relative preponderance of influences on afterload and contractility.
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PMID:Clinical use of calcium channel blockers as ventricular unloading agents. 622 Aug 95

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

The comparative efficacy of diltiazem, a new calcium-antagonist drug, and nifedipine were evaluated with computerized treadmill exercise test in 12 patients with stable effort angina. The drugs were administered in a random single-blind fashion in divided doses (diltiazem 60 mg three times daily and nifedipine 10 mg four times daily) over 3 weeks. Maximal exercise tests were performed before and at the end of each 3-week treatment period. Both diltiazem and nifedipine increased the total duration of exercise (p less than 0.001) and the time to appearance of 1.5 mm of ST depression (p less than 0.001). Both drugs reduced resting systolic and diastolic blood pressure; however the effect was greater with nifedipine. Nifedipine, but not diltiazem, caused a significant increase of resting heart rate (p less than 0.05). Both drugs blunted the blood pressure and heart rate response to exercise: nifedipine had a greater effect on the former (p less than 0.001), diltiazem on the latter (p less than 0.05). The rate-pressure product was significantly reduced at rest (p less than 0.01) and submaximal (p less than 0.001), but not maximal exercise with both drugs. The reduction of rate-pressure product is possible as the mechanism by which calcium-antagonist drugs enhance the duration of exercise in the coronary patients. Our results documented a comparable therapeutic efficacy of the two drugs, but side effects were more common with nifedipine.
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PMID:[Evaluation of the effects of a new calcium antagonist, diltiazem, in patients with stable effort angina and a therapeutic comparison with nifedipine]. 635 30

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

The effects of intracoronary nifedipine on myocardial performance were studied in the absence and presence of beta-blockade with propranolol (0.5 mg X kg-1 i.v. bolus + infusion). In anaesthetized pigs nifedipine (0.025, 0.05 and 0.5 microgram X kg-1 X min-1) produced dose-dependent increases in coronary flow (up to 65% from base line, 39 +/- 4 ml X min-1) and decreases in myocardial O2-consumption (MO2-cons, up to 50%, base line 3.10 +/- 0.34 ml X min-1). The two lower doses caused a negligible depression of systemic haemodynamics (cardiac output, CO smaller than 8%, base line 2.70 +/- 0.14 l X min-1; mean arterial pressure, MAP smaller than 10%, base line 10.9 +/- 0.4 kPa), but after the highest dose MAP and CO decreased by 20%. Following pretreatment with propranolol, the effects of nifedipine on cardiac output and mean arterial pressure were additive for the two lower doses, but with 0.5 microgram X kg-1 X min-1 the superimposed effects were less pronounced. Nifedipine alone was able to increase cardiac efficiency, defined as (MAP X CO)/MO2-cons, by 10-20%, but failed to improve cardiac efficiency when this was previously reduced by administration of propranolol. Our data indicate that intracoronary infusion of nifedipine can be performed safely when beta-blockade is already instituted, but that nifedipine alone decreases MO2-consumption to the same level as the combination, with less depression of global myocardial function.
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PMID:Nifedipine and myocardial performance in the presence and absence of beta-blockade with propranolol. 666 65


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