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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injection of meglumine diatrizoate (Renografin-76) into the selectively perfused sinus node artery of the dog produces bradycardia which is unaltered by autonomic blockade or by changes in sinus node artery pressure. Contrast agents and other hyperosmolar substances prolong the R-R interval in proportion to their osmolarity. Selective injection of contrast media into other cannulated segments of the coronary tree produces no change in heart rate. Transfemoral arteriography, however, produces bradycardia with both right and left coronary injections. Both direct and reflex sinus node depression occur with coronary arteriography in the dog. Direct effects are mediated by hyperosmolarity.
Cardiovasc Res 1976 Mar
PMID:Effects of angiographic contrast media on sino-atrial nodal function. 0 55

Cardiac toxicity due to anthracycline therapy is dose related, and congestive failure is a major limiting factor to therapy. Radionuclide cardiac evaluation provides a sensitive noninvasive method for detecting changes in cardiac function. Fifteen patients receiving either doxorubicin or daunomycin were evaluated with radionuclide ejection fractions (EFrn). The data indicate that the EFrn can detect an acute depressant cardiac action of these drugs as early as 24 hr after drug administration. In addition, a cumulative or chronic cardiac depression was noted; cumulative dosage of doxorubicin or daunomycin correlated with a reduced EFrn (p less than 0.001). We conclude that (1) the EFrn can noninvasively detect significant changes in cardiac function at low cumulative doses of doxorubicin or daunomycin and (2) the EFrn may be useful in evaluating cardiac function in patients during doxorubicin or daunomycin therapy.
J Cardiovasc Pharmacol
PMID:Time- and dose-dependent changes in ejection fraction after anthracycline therapy. 9 17

We have investigated the effects of quinidine on the force of contraction and the intracellularly recorded action potential in papillary muscles isolated from human hearts. All preparations were obtained from patients undergoing corrective open heart surgery. The following results were obtained: (1) quinidine had a depressant effect on myocardial contractile force; (2) quinidine reduced the maximal upstroke velocity of the action potential; (3) quinidine shortened the plateau phase and prolonged the terminal repolarization of the action potential; (4) at higher concentrations quinidine reduced the resting potential; and (5) the depression by quinidine of both the plateau and the force of contraction was antagonized by isoprenaline. It is concluded that quinidine reduces the membrane conductances for sodium, calcium, and potassium ions. All of these actions of quinidine may contribute to the antiarrhythmic effects of the drug. The negative inotropic effect of quinidine can be explained by a depression of the calcium conductance at the myocardial cell membrane. The results show that earlier findings in laboratory animals regarding the effects of quinidine on the upstroke velocity and repolarization phase of the action potential are applicable to the human heart.
J Cardiovasc Pharmacol
PMID:Electrophysiological study of human ventricular heart muscle treated with quinidine: interaction with isoprenaline. 9 19

The antiarrhythmic activity of flecainide acetate (R-818), 2 mg/kg, was investigated in anesthetized, open-chest pigs. Ventricular arrhythmias were provoked by reducing the flow in the left anterior descending coronary artery (LAD) to 25% of control during 30 min. During this period ventricular fibrillation occurred in 33% (11 out of 33) of control animals against 12.5% (1 out of 8) of animals treated with flecainide. Ventricular tachycardias were seen in 42% (14 out of 33) of the untreated animals as compared to none of the animals previously treated with flecainide. Total number of ventricular arrhythmias was significantly lower in the treated than in the untreated animals (p less than 0.05). However, when the LAD was occluded completely at its distal part, ventricular fibrillation occurred in all animals (5 untreated and 6 pretreated with flecainide). Time to onset of ventricular fibrillation was the same for both groups of animals, despite a lower incidence of preceding ventricular arrhythmias in the pretreated group. Flecainide depressed myocardial contractility (LVdP/dt max), caused hypotension, and increased QRS width. Both myocardial depression and widening of QRS are related to arterial plasma levels of flecainide. Therefore, a slower infusion rate than the 1 mg/kg per minute used in this study is advisable when myocardial function is impaired.
J Cardiovasc Pharmacol
PMID:Antiarrhythmic and hemodynamic actions of flecainide acetate (R-818) in the ischemic porcine heart. 9 25

Intraoperative hypertension is a common problem in patients undergoing myocardial revascularization. Twenty patients who developed acute hypertension after sternotomy were studied. Ten patients received three doses of intravenous nitroglycerin (32, 64, and 96 mcg. per minute), and 10 patients received nitroprusside, (20, 40, and 60 mcg. per minute). All patients were anesthetized with morphine, diazepam, nitrous oxide, oxygen, and pancuronium bromide. Five patients in each group also received enflurane. The study compared the effects of nitroglycerin and nitroprusside on systemic hemodynamics, myocardial oxygen supply/demand relationships, and ischemic changes on the electrocardiogram. Both drugs decreased preload and afterload in a dose-related manner. Heart rate increased significantly only with the largest dose of each drug. Myocardial oxygen demand was decreased significantly by both drugs, while the coronary perfusion pressure was decreased more by nitroprusside. Both nitroglycerin and nitroprusside improved left ventricular performance. Nitroglycerin improved ST-segment depression in eight of 10 patients; while nitroprusside improved the ST segments in six patients, and worsened the ST segments in three patients. None of the nitroglycerin group had worsening of the electrocardiographic ST segments. These findings demonstrate that both drugs can control intraoperative hypertension and can decrease myocardial oxygen demand. Nitroglycerin was shown to improve ischemic changes on the electrocardiogram more often than nitroprusside.
J Thorac Cardiovasc Surg 1979 Feb
PMID:Vasodilator therapy during coronary artery surgery. Comparison of nitroglycerin and nitroprusside. 10 11

Electrocardiograms of 90 patients with arteriographically documented acute submassive or massive pulmonary embolism and no associated cardiac or pulmonary disease were studied. Patients were derived from the Urokinase-Pulmonary Embolism Trial National Cooperative Study. In massive embolism, the electrocardiogram was normal in 6 per cent (3 of 50) of patients. With submassive embolism, 23 per cent of patients (9 of 40) had a normal electrocardiogram. Since one or more of the traditional manifestations of acute cor pulmonale (S1Q3T3, right bundle branch block, P pulmonale, or right axis deviation) occurred in only 26 per cent of patients, one could not rely exclusively upon these electrocardiographic abnormalities for the diagnosis of pulmonary embolism. The most common electrocardiographic abnormalities were nonspecific T wave changes which occurred in 42 per cent of patients and nonspecific abnormalities (elevation or depression) of the RST segment which occurred in 41 per cent of patients. Left axis deviation occurring in 7 per cent of the patients was as frequent as right axis deviation. Low voltage QRS complexes, previously undescribed in pulmonary embolism, occurred in 6 per cent of patients. None of the patients had atrial flutter or atrial fibrillation, which appears to occur more typically in patients with pulmonary embolism who have preexistent cardiac disease. All of the varieties of electrocardiographic abnormalities disappeared in some of the patients by 2 wk. Inversion of the T wave was the most persistent abnormality. Larger defects on the lung scan or pulmonary arteriogram occurred in patients with various abnormalities on the electrocardiogram than in patients with normal electrocardiograms. The pulmonary arterial mean pressure and/or right ventricular end-diastolic pressure was significantly higher in patients with several varieties of abnormal electrocardiograms, although the partial pressure of oxygen in arterial blood, in general, did not differ from that in patients with normal electrocardiograms. These hemodynamic correlations, made for the first time in patients, suggest that acute ventricular dilatation, possibly in combination with hypoxemia, is a causative factor of the electrocardiographic changes in acute massive or submassive pulmonary embolism.
Prog Cardiovasc Dis
PMID:The electrocardiogram in acute pulmonary embolism. 12 74

A two-dimensional framework can be used for considering the characteristics of left ventricular ejection in terms of the appropriateness of the matching between afterload and the level of inotropic state, as modulated by the preload reserve. An afterload mismatch (reduced velocity and extent of shortening) can be induced acutely in the normal heart under controlled conditions if the preload is not allowed to compensate for an increased afterload, or if the limit of preload (Frank-Starling) reserve has been reached. In the intact circulation the normal heart is sensitive to some degree to acute changes in afterload, perhaps due to impaired venous return; but under basal resting conditions the ejection phase measures (such as the ejection fraction and the mean velocity of circumferential fiber shortening or VCF, corrected for heart size) encompass a relatively narrow range. This finding, and the lack of change in ejection phase measures after the normal heart has adapted to a chronic pressure or volume overload, provides justification for the use of ejection phase indices for detecting depressed inotropic state under basal conditions. When there is mild depression of myocardial inotropic state, with or without accompanying mechanical overload, enhanced preload may allow full compensation, but acute pressure loading may allow early detection of a less than normal preload reserve. When the inotropic state is substantially reduced, however, a mismatch between afterload and contractility (a reduction in mean VCF) will become evident even in the basal state (venous return being presumed to be adequate under these conditions). The concept of afterload mismatch with limited preload reserve provides an explanation for the value of ejection phase indices compared to isovolunic phase measures in assessing the basal level of inotropic state: the former may be more reliable because they are sensitive to afterload. The effects and implications of therapeutic afterload reduction as modulated by the preload also are understood within this framework.
Prog Cardiovasc Dis
PMID:Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function. 12 34

Using a silicone elastometer sheath, wrapped around the portal vein, with an external probe for electromagnetic flowmetry, and with the aid of an outside depression, the authors succeeded in measuring portal vein blood flow with great precision, both under normal conditions and during vasoconstriction induced by drug administration. The above system allows variations synchronous with respiration and cardiac contractions to be seen. The reproducibility of a "no flow" point further enables registrations to be continued for hours for physiological and pharmacological studies. The sheath probe system described for the registration of portal vein blood flow is applicable to all other veins.
J Cardiovasc Surg (Torino)
PMID:A new method for measuring venous blood flow with the aid of an electromagnetic flowmeter. 13 13

Myocardial levels of ammonia, glutamate, and glutamine and the release of glutamate and glutamine were studied in the isolated perfused rat heart during perfusion with ammonium chloride, epinephrine, and conditions of anoxia or ischaemia. Perfusion for 15 min with effective ammonium chloride concentrations of 0.53, 0.71, and 2.06 mmol/l resulted in glutamine production of 1.34, 0.95, and 4.41 mmol with 15 min-1/200 dry weight compatible with the presence of glutamine synthetase in rat myocardium. Myocardial ammonium content was unchanged by perfusion with 0.53 and 0.71 mmol/l ammonium chloride, but was increased by 1.36 mumol with 15 min-1/200 mg dry weight by perfusion with 2.06 mmol/l ammonium chloride. Increased myocardial contents of ammonia and glutamine were not accompanied by depression of left ventricular pressure. Perfusion with epinephrine (0.20 mug/ml) resulted in an increased myocardial content of glutamine. Anoxia or ischaemia resulted in no changes in ammonia content, and no changes in glutamine or glutamate production. The net release of glutamine into the perfusate was about 10 times the net release of glutamate.
Cardiovasc Res 1975 May
PMID:Glutamine production by the isolated perfused rat heart during ammonium chloride perfusion. 24 May 5

In a 66-year-old patient with chronic obstructive pulmonary disease (COPD) complicated by arterial hypoxemia and repeated episodes of respiratory and right ventricular failure, a satisfactory level of oxygenation could not be maintained despite controlled oxygen therapy. To enable oxygen to be administered without depression ventilation, artificial respiration by means of phrenic nerve stimulation (diaphragm pacing) has been employed. Evidence of clinical improvement since pacing was begun 32 months ago include fewer episodes of respiratory failure and better control of congestive heart failure despite a gradual worsening of pulmonary function.
J Thorac Cardiovasc Surg 1978 Feb
PMID:Diaphragm pacing. Application to a patient with chronic obstructive pulmonary disease. 30 48


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