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)

Primary sleep disorders include narcolepsy, the Pickwickian syndrome, sleep apnea in infants and other rare conditions. Secondary sleep disorders occur in depression, alcoholism, endocrinopathies, heart failure and pregnancy. Medical symptomatology often increases during rapid-eye-movement (REM) sleep, when physiologic activity is high. Insomnia, the most common sleep disorder, requires careful work-up, attempts at environmental manipulation and judicious short-term pharmacotherapy. Pharmacologic manipulation of sleep is beset with complications. A basic understanding of properties and side effects of the sleep-inducing drugs is needed in order to select the optimal agent.
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PMID:Sleep disorders and insomnia. 62 43

Anesthetic indices for methoxyflurane, enflurane, and isoflurane in oxygen and halothane in nitrous oxide and oxygen (50:50), were determined in rats using measurements of heart and brain concentrations of the volatile agents at the endpoints of anesthesia, respiratory arrest and cardiac failure. The indices related respiratory arrest to anesthesia (respiratory index-A1r), cardiac failure to anesthesia (cardiac index-AIc) and respiratory arrest to cardiac failure (cardiorespiratory index-AIcr). Isoflurane had a significantly higher AIr (3.1) and AIc (5.7) than enflurane (AIr 1.8, AIc 3.3), methoxyflurane (AIr 2.2, AIc 3.7) and halothane in nitrous oxide and oxygen (AIr 2.4, AIc 3.7). These indices were also higher than those previously determined for halothane (AIr 2.3, AIc 3.0). Isoflurane had a higher AIcr (1.9) than halothane (1.6). Enflurane had a significantly lower AIr (1.8) than any of the other agents studied. These findings suggested a greater margin of safety for isoflurane, especially with respect to the heart, and a greater potential for respiratory depression for enflurane than for the other agents. Nitrous oxide decreased the amount of halothane necessary to produce anesthesia, but also that needed to produce respiratory arrest or cardiac failure. The addition of nitrous oxide, therefore, did not significantly enhance the overall safety of halothane anesthesia with respect to potential respiratory or cardiac depression.
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PMID:Anesthetic indices--further data. 62 24

Propranolol and practolol were tested in patients with repeated daily occurrence of spontaneous angina. Twenty-one showed ST segment depression (type I) and 15 ST segment elevation (type II) during angina. The efficacy of the treatment was evaluated in subjective (number of reported episodes of pain) and objective terms (number of episodes of electrocardiographic abnormalities documented during periods of continuous recording): practolol was fully effective in 42 per cent and propranolol in 38 per cent of type I cases; in type II angina 73 per cent of the cases fully responded to propranolol, none of the patients in this group given practolol improved. The study also showed that: (a) the effects on angina are strictly dose-dependent, and optimal results are achieved at individualized doses; (b) within the same subject the response may be preferential to one beta-blocker as opposed to the other; (c) propranolol is more effective in type II angina; (d) the occurrence of heart failure is uncommon even with high doses of beta blockers;(e) the relief of angina is due to prevention of ischaemia and not to a placebo or anaesthetic effect; (f) the prevention of ischaemia is not adequately explained by reduction of the mechanical effort and the oxygen need of the myocardium; (g) the antianginal effect is possibly dissociated from the beta blockade of the heart. The hypothesis that beta-blocking agents influence the conronary vasomotion is discussed.
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PMID:Treatment of spontaneous angina pectoris with beta blocking agents. A clinical, electrocardiographic, and haemodynamic appraisal. 77 91

The action of the contrast material over the various contractility indices was assessed five minutes after left ventriculography. There was an increase of the contractility index in normal subjects. On the contrary, in coronary patients, the contractility function remained unchanged or was depressed, related to the presence or not, of signs of cardiac failure. Depression of the various indices was noted in subjects with primary cardiomyopathy. After recalling the mechanism of action of the contrast products on the cardiovascular haemodynamic parameters, the following practical conclusions were drawn in relation with a series of 65 cases of coronary heart disease: the late diastolic left ventricular pressure remained lower than 20 mmHg after ventriculography in the subjects with a normal ejection fraction; it incraeased between 20 and 30 mmHg in most of the subjects with an ejection fraction ranging from 0.4 and 0.6, finally it was constantly found above 35 mmHg in the subjects with severely disturbed ventricular contraction with an ejection fraction lower than 0.4. These results underline the interest of this simple test, easy to perform, consisting in measuring the left ventricular late diastolic pressure before and 5 minutes after left ventriculography.
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PMID:[Modifications of contractility after left ventriculography. A new test in evaluation of myocardial function]. 80 84

The evaluation of left ventricular function in patients with acute myocardial infarction has shown: 1. Limitations in the use and interpretation of central venous pressure. 2. Pulmonary artery end-diastolic pressure reflects left ventricular end-diastolic pressure in the absence of pulmonary vascular or mitral valve disease. 3. Frequent elevations of left ventricular filling pressure in mild or clinically uncomplicated infarction. 4. Anterior infarctions present greater depression of left ventricular function than inferior infarctions. 5. Initial hemodynamic measurements in cardiogenic shock can predict prognosis with medical management. 6. Left ventricular function frequently improves during the early convalescent period. 7. Hemodynamic monitoring can be useful in following changes in left ventricular function and the response to therapy. The assessment of left ventricular performance in patients with chronic heart disease has shown: 1. Resting hemodynamic measurements are often normal but abnormalities can be observed in patients with disease of the left anterior descending coronary artery, diffuse coronary involvement, and after myocardial infarction. 2. Increases in end-diastolic volume or dilatation and left ventricular mass or hypertrophy can develop in severe coronary disease and after myocardial infarction. 3. The size of abnormally contracting segment after myocardial infarction is related to abnormalities in compliance, ventricular end-diastolic pressure, end-diastolic volume, and clinical manifestations of heart failure. 4. Exercise and atrial pacing can produce clinical and hemodynamic abnormalities. 5. The ejection fraction is significantly related to the slope of the ventricular function curve. 6. Angiographic abnormalities of left ventricular wall motion can be increased with atrial pacing and reduced with nitroglycerin or epinephrine.
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PMID:Left ventricular function in acute and chronic coronary artery disease. 80 47

A protein has been isolated from the venom of the western diamondback rattlesnake (Crotalus atrox) which induces acute myocardial depression when administered to experimental animals. Purification was achieved by gel filtration on Sephadex G-100, DEAE- and CM-cellulose ion-exchange chromatography, ultra-filtration, and adsorption chromatography on hydroxyapatite. Amino acid analysis of the highly purified protein indicated N-terminal isoleucine and C-terminal tyrosine residues, and the absence of free sulfhydryl groups. Rabbits were immunized against the myocardial depressor protein (MDP) and a highly specific antiserum prepared which made it possible to study other snake venoms for the presence or absence of MDP. All of the North American Crotalid species of snakes contain MDP in varying degrees of concentration, but none of the Asiatic snake venoms tested reacted with the antiserum to the myocardial depressor protein. Intravenous administration of MDP to experimental animals (dogs, cats) produces an immediate and profound decrease in the cardiac output, the left ventricular systolic and mean pressures, the velocity of shortening of the contractile element, the systemic arterial pressure and an elevation in the left ventricular end-diastolic and pulmonary wedge pressures. These hemodynamic changes indicate that MDP administration induces an acute myocardial failure which is does dependent. The potential use of this protein for the reproducible causation of left ventricular failure, obviating the need for the more commonly used surgical ligation of the coronary arteries, warrants a full investigation into its structure, active site and its mechanism of action on the myocardial cell.
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PMID:Comparative biochemistry and pharmacology of salivary gland secretions. III. Chromatographic isolation of a myocardial depressor protein (MDP) from the venom of Crotalus atrox. 96 63

Eleven elderly patients with idiopathic pericarditis are reported. All but one were older than 60 yr. Evidence of ischemic cardiovascular disease was present in 8 patients. The initial diagnosis was heart failure with pulmonary complications in 4 cases and myocardial infarction in 3. Respiratory infection preceded the onset of pericarditis in 5 cases. Presenting symptoms were typical precordial pain, fever and dyspnea. Pericardial friction was found in 7 cases and transient rhythm disturbances in 5. Four patients had ST elevation and 3 had ST depression in their electrocardiograms. Other findings included an increased sedimentation rate, leukocytosis, elevated venous pressure and normal SGOT levels. Antibiotics were of no avail but prednisone had a dramatic effect. Two patients had a relapsing course lasting 2 yr or more. One patient, who died at the age of 75 from bleeding ulcer, had patent coronary arteries and mild perimyocardial fibrosis. The diagnosis of idiopathic pericarditis in the aged is difficult because the disease simulates ischemic heart disease in patients who frequently have evidence of arteriosclerotic cardiovascular involvment.
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PMID:Acute idiopathic pericarditis in the aged. 114 70

Chronic left ventricular-atrial regurgitation (LVAR) was created in 8 dogs by means of an external conduit so that the effects of acute correction of regurgitation on the mechanics of left ventricular performance could be studied in detail. LVAR of 46 to 77 per cent of the total left ventricular (LV) output was associated with a depression of the LV inotropic state (downward displacement of the stress-velocity relationship, reduction in V max), reduced forward flow, and signs of cardiac failure. Acute occlusion of the shunt (analogous to return of mitral valvular competence) in the anesthetized, open-chest animal resulted in a statistically significant increase in the integrated LV systolic wall stress (afterload), which averaged 18 per cent. In the dog with greatest depression of the LV inotropic state, the increase in afterload was associated with a decrease in forward flow. Occlusion of the shunt had no significant effect on the inotropic state. This model of mitral regurgitation appears to be useful in assessing the effect of chronic LVAR on cardiac performance and may explain the hemodynamic deterioration observed in some patients with severe mitral regurgitation following valve replacement.
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PMID:Experimental mitral regurgitation: effects on left ventricular function before and after elimination of chronic regurgitation in the dog. 116 39

The status of myocardial function in rabbits subjected to cardiac catheterization and infection with Streptococcus viridans was assessed at 3 and 6 days. Sham-operated control animals as well as uninfected catheterized animals were used for comparison. Although left heart hypertrophy and interstitial edema were evident in both uninfected and infected animals, the infected animals exhibited in addition mononuclear cell infiltration and muscle degeneration as well as lung congestion and accumulation of pleural fluid. Both uninfected and infected animals has elevated levels of serum creatine phosphokinase, lactic dehydrogenase and glutamic oxaloacetic transaminase as well as electrocardiographic abnormalities such as increased amplitude of the ORS complex and flattening or inversion of the T wave. Unlike findings in the uninfected animals, the serum calcium, magnesium and sodium levels were slightly but significantly decreased and serum potassium levels were increased in the infected rabbits. Both heart rate and pulse pressure were higher in 6 day uninfected and 3 day infected animals whereas 6 day infected animals showed a decrease in heart rate. In comparison to the sham-operated control rabbits and the uninfected animals, the infected animals exhibited depression in the rates of left ventricular pressure development and relaxation as well as prolongation in time for half relaxation in situ. Relative maximal contractile element velocity extrapolated from intraventricular pressure-velocity curves was decreased by 24, 52 and 76 percent, respectively, of control values in the uninfected hearts and those with 3 and 6 days of infection. The isolated perfused hearts from infected animals also generated less contractile force and showed a decrease in the rates of contraction and relaxation, but half-relaxation time was increased. These results demonstrate myocardial dysfunction during experimental bacterial endocarditis and provide evidence that infective cardiomyopathy is associated with heart failure.
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PMID:Alterations in myocardial function during bacterial infective cardiomyopathy. 125 70

A reproducible tourniquet-shock has been produced in hind limbs of dogs by unilateral and bilateral extremity ischemia. The following parameters have been measured for analysing the function of the cardiovascular system: mean aortic pressure, heart rate, cardiac output, intraventricular pressure and left ventricular pressure. From these data the stroke volume, stroke work, total peripheral resistance and the parameters of heart contractility dp/dtmax, dp/dtmax:IP and t-dp/dtmax were derived. During the ischemic period all circulatory parameters did not change in comparison to the controls. A tourniquet-shock developed upon recirculation of the ischemically stressed extremity which was more pronounced after bilateral than after unilateral hind leg ischemia. After release of the tourniquet all animals with unilateral tourniquet survived an observation period of 5 hours duration, whereas 6 out of 8 dogs with bilateral tourniquet died of heart failure. Upon release of the tourniquet, the cardiac output raised up to 140% of the normal value: the abruptly decreasing aortic pressure was fully compensated by a tachycardia from 100 to 190 (beats/minute). The parameters dp/dtmax:IP and t-dp/dtmax indicated a distinct increase of the left ventricular contractility in the early tourniquet-syndrom. Already after 30 minutes an increasing circulatory depression developed indicative of the decrease in aortic pressure, and enddiastolic pressure. At the same time an increase of heart rate and total peripheral resistance occurred. The parameters of left ventricular contractility did not change markedly during the course of shock except for the final stage.
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PMID:[Hemodynamics and myocardial contractility in experimental tourniquet-shock]. 126 40


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