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)

The purpose of this investigation was to examine the effects of norepinephrine cardiomyopathy (NE-CM) on left ventricular (LV) performance in diabetic rabbits. Diabetes mellitus was produced in 11 rabbits by giving them alloxan monohydrate, 120 mg/kg. Cardiomyopathy was produced in five animals by a 90-min infusion of norepinephrine (2 micrograms/min/kg). Left ventricular contractility and pump function (VF) were examined 2 days later. The effects of hypercapnia and inotropic responsiveness to NE were also determined. VF was assessed by means of left ventricular function curves obtained with constant mean aortic pressure and heart rate and quantified by determining stroke volume (SV) at a left ventricular pressure of 10 cm H2O (SV10). Mean SV10 was 1.22 +/- 0.08 ml in control diabetics but averaged only 0.95 +/- 0.08 ml in diabetics with NE-CM (P less than 0.05). NE-CM markedly reduced LV dP/dt max responses to NE infusion but the increments in SV10 did not differ. Hypercapnia caused significantly greater ventricular depression in NE-CM than in control diabetic rabbits (P less than 0.001). The depressive effect of hypercapnia can be countered in part by the administration of NE in both groups, but differential depression in VF to hypercapnia was persistent between the two groups.
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PMID:Ventricular performance in diabetic rabbits with norepinephrine cardiomyopathy. 394 45

Seventeen clinically normal adult English Cocker Spaniels from a kennel population with a history of cardiomyopathy were assessed, using M-mode echocardiography, to establish reference values for left ventricular (LV) dimensions for this breed of dog. Echocardiographic measurements were compared with postmortem measurements in 10 of 17 dogs. The LV weight calculated from the echocardiographic measurements correlated significantly with LV weight at postmortem (P less than 0.05). Echocardiographic measurements of end diastolic and end systolic diameters for the 17 dogs correlated significantly with body surface area (P less than 0.01). Measurements of the interventricular septum were in close agreement with values in clinically normal dogs and were significantly correlated with postmortem measurements (r = 0.94, P less than 0.01). However, 76% of the measurements for LV caudal wall thickness in this group of dogs were above the normal range. Calculation of fractional shortening values identified a group of 5 dogs with reduced fractional shortening (mean +/- SD, 20.97 +/- 3.66%), which indicates that a depression in contractility may be present in some apparently healthy dogs of this kennel population. The remaining 12 dogs had fractional shortening values of mean +/- SD, 34.26 +/- 4.54%.
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PMID:Echocardiographic assessment of left ventricular dimensions in clinically normal English cocker spaniels. 395 6

The ultrastructural changes in the left ventricles of rabbits with alloxan (100 mg/kg i.v.)-induced diabetes were examined. Injection of alloxan resulted in a diabetic state characterized by increased hemoglobin glycosylation, blood and urine glucose and a significant depression of serum insulin levels. Electron microscopic examination of 10-week diabetic hearts revealed a spectrum of abnormalities ranging from mild to severe. Cardiac muscle cells in diabetic hearts showed some myofibrillar damage and varying degrees of contraction. The most prominent findings, however, were alterations in the mitochondria. Swollen and fragmented mitochondria containing amorphous dense bodies were evident upon electron microscopic examination. The cristae in the mitochondria appeared distorted and in some cases were completely lysed. A marked increase in lipid droplets and glycogen granules was also apparent. In addition, the sarcoplasmic reticulum was dilated and contained varying degrees of electron-dense material. These ultrastructural alterations suggest that the cardiomyopathy observed in alloxan-induced diabetic rabbits could be due to alterations in the vasculature or may be secondary to a number of metabolic alterations previously reported in this model.
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PMID:Myocardial ultrastructural changes in alloxan-induced diabetes in rabbits. 396 81

Aortic input impedance and hydraulic power were derived from simultaneous catheter recordings of ascending aortic pressure and velocity in eight normal subjects and 11 age-matched subjects with clinical heart failure secondary to idiopathic congestive cardiomyopathy. Resting data revealed the characteristic depression of cardiac output and elevation of systemic vascular resistance in patients with heart failure. The pulsatile component of vascular hydraulic load, characteristic impedance (Zc), was similar in both groups (Zc normal: 85 +/- 30 dyne-sec-cm-5; Zc cardiomyopathy: 93 +/- 33 dyne-sec-cm-5). The oscillatory fraction of aortic input power in patients with heart failure (14 +/- 4%) was also similar to that of normal subjects (11 +/- 2%). The transition from rest to exercise in patients with heart failure was marked by a decrease in the steady component of arterial hydraulic load, although characteristic impedance did not change. A similar qualitative response occurred in normal subjects, although the systemic vascular resistance during exercise remained above normal in patients with heart failure. The modulus of the first harmonic of impedance significantly decreased during exercise in normal subjects but did not change significantly in patients with heart failure. Furthermore, the modulus of the first harmonic of the reflection coefficient decreased significantly during exercise in normal subjects but did not change in patients with heart failure in spite of systemic vasodilation. Exercise appears to impose no additional increase in vascular hydraulic load on the ejecting left ventricle. The similar aortic characteristic impedances in patients with heart failure and in normal subjects, at rest and during exercise, are consistent with a constant oscillatory fraction of input power.
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PMID:Characteristics of vascular hydraulic load in patients with heart failure. 400 37

Changes of T waves and ST segments in normally conducted beats are frequently seen in patients treated with ventricular demand pacing. The alteration in the sequence of ventricular activation is accompanied by inversion of T waves and sometimes a depression of ST segments in several leads. These changes have a close resemblance to those often seen in ischaemic heart disease. Some of the clinical implications are illustrated in four case stories. The slow regression of changes after cessation of pacing is particularly emphasised. The time required for complete disappearance of changes was directly related to the duration of ventricular pacing. In contrast to this finding a quickly developed, though temporary, regression was observed during exercise. The development of repolarisation changes requires a certain duration and extent of pacing. Therefore changes are not present in all ventricular paced patients. Consequently, recording of the spontaneous rhythm is proposed as a routine in the pacemaker clinic. The recordings might prove valuable for future comparison in case of suspected myocardial disease.
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PMID:T wave inversion and ST segment depression in normally conducted beats in patients treated with ventricular demand pacing. 400 27

We have previously described a subpopulation of patients with septic shock who had a reversible depression of radionuclide-determined left ventricular ejection fraction (EF). To investigate the mechanism of this myocardial depression, an in vitro model of mammalian myocardial cell performance was established employing primary spontaneously beating rat myocardial cells. The contraction of a single cardiac cell was quantitated by recording the changes in area occupied by the cell during contraction and relaxation. In 20 septic shock patients during the acute phase, the mean left ventricular EF was decreased (mean = 0.33, normal mean = 0.50), and serum obtained during this acute phase induced a mean (+/- standard error of the mean) 33 +/- 4% decrease in extent and 25 +/- 4% decrease in velocity of myocardial cell shortening during contraction (P less than 0.001). In contrast, serum obtained from 11 of these same patients before shock (n = 2) or after recovery (n = 9) of the left ventricular EF (mean = 0.50) showed a return toward normal in extent and velocity of shortening (P less than 0.001). Sera from 17 critically ill nonseptic patients, from 10 patients with structural heart disease as a cause for a depressed EF, and from 12 healthy laboratory personnel, induced no significant changes in in vitro myocardial cell performance. In 20 patients during the acute phase of septic shock, the decreased EF in vivo demonstrated a significant correlation (r = +0.52, P less than 0.01) with a decrease in the extent of myocardial cell shortening in vitro. The quantitative and temporal correlation between the decreased left ventricular EF and this serum myocardial depressant substance argues for a pathophysiologic role for this depressant substance in producing the reversible cardiomyopathy seen during septic shock in humans.
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PMID:A circulating myocardial depressant substance in humans with septic shock. Septic shock patients with a reduced ejection fraction have a circulating factor that depresses in vitro myocardial cell performance. 405 39

Controversy exists over the nature of the abnormality in cardiac sympathetic nerves in heart failure. In the cardiomyopathy of the Syrian hamster, reduction in tissue stores and increased turnover of norepinephrine is clearly associated with excessive sympathetic stimulation but in animal models and humans with heart failure secondary to mechanical overload there is evidence for depression of neuronal uptake. Because norepinephrine is both released and taken up by sympathetic fibers it is impossible to assess norepinephrine kinetics in an intact heart without separating these two functions. A technique for doing so has recently been developed in normal dogs and we therefore acquired similar data in humans with heart failure secondary to chronic pressure and volume overload. The technique involves the combination of transient norepinephrine tracer coronary sinus outflow in relation to intravascular and interstitial references after simultaneous injection into the left coronary artery and the measurement of endogenous norepinephrine concentrations in artery and coronary sinus. We found a marked reduction in cardiac norepinephrine release and uptake in a group of patients with clinical left ventricular failure secondary to mechanical overload, relative to a group of patients with no failure. Norepinephrine balance and overflow across the heart were not significantly different. We conclude that there is hypofunction of the cardiac sympathetic nerves in heart failure secondary to mechanical overload and that traditional methods are inadequate in assessing cardiac norepinephrine kinetics when there are simultaneous changes in neuronal uptake and release.
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PMID:Tracer norepinephrine kinetics in coronary circulation of patients with heart failure secondary to chronic pressure and volume overload. 405 51

It is known that the heart will adapt to actual demand by increasing or decreasing its size through different mechanisms. In this presentation, the possible role of catecholamines in regulating heart protein synthesis and developing cardiac hypertrophy and cardiomyopathy is discussed. Injecting animals with catecholamines has been found to induce cardiac hypertrophy. In vitro perfusion of rat heart in the presence of catecholamines has been found to induce a time-dependent and dose-dependent stimulation of amino acid transport and incorporation into proteins. Acute haemodynamic effects of catecholamines increase cardiac performance while long-term treatment seems to cause depression of cardiac function, especially during ischaemic conditions. Chronic beta-blockade in patients with primary congestive cardiomyopathy improved both cardiac function and clinical condition in more than half the patients. Furthermore, a beneficial effect on survival was also found, when compared with a matched control group. It is hypothesised that catecholamines may play a role in developing cardiac hypertrophy as well as congestive cardiomyopathy.
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PMID:Possible adrenergic effects on heart protein metabolism. 613 40

Mitral valve prolapse ( MVP ) , responsible for most of the symptoms which had previously been interpreted as being due to neurocirculatory disorders or cardiac neurosis , is being recognised more often and has an incidence of about 6-8 % in an unselected population . Although this condition was considered for a long time to be a benign auscultatory abnormality , it may be the cause of serious cardiac complication . Arrhythmias predominate with an incidence of 60 to 80 % on continuous electrocardiography . In a series of 245 patients with mitral valve prolapse confirmed on echocardiography , 52 patients chosen at random were studied to determine the incidence pf ST changes , disturbances of heart rate , QT interval , changes of QRS , arrhythmias with resting , exercise and continuous ECG over 24 hours ( HMS = Holter Monitoring System ) . Abnormalities of ventricular repolarisation , especially flattening of the T wave and , less commonly , St depression were observed in about one third of the patients . These changes were more common in the inferior but were also found in the left precordial leads . 73 % of the 52 patients had a heart rate of 75/mn and their QT intervals showed the following changes : 30.7 % Had a duration greater than the 120 th percentile ; 19.2 % had a duration greater than the upper limit of normal . The other 50 % had a QT interval of around the 100 th percentile . None had a duration of less than the 90 th percentile . In 22.5 % patients , QRS changes due to conduction defects were recorded ( 15 % right bundle branch block - RBBB - , 7.5 % incomplete RBBB ) . HMS is the method of choice for detection of arrhythmias . Resting ECG only showed premature ventricular contractions ( PVCs ) in 12.5 % , compared to 32.5 % on exercise ECG and 62.5 % on HMS . 50 % PVCs were monomorphic , 5 % polymorphic , 7.5 % in salvos and 7.4 % supraventricular in origin . The circadian variation of PVC was striking with a high incidence during periods of activity . There was no statistical correlation between the incidence of PVCs , age , sex , type of MVP and the symptoms and auscultatory findings . The theories on the pathogenesis of the arrhythmias are divided between that based on an underlying cardiomyopathy ( confirmed by the presence of degenerated myocytes on electron microscopy ) and the mechanical hypothesis ( chordae tendinae irritating the endocardium or traction on the papillary muscle with resulting ischaemia ) which provide a better explanation of the clear predominance of monomorphic PVCs . The treatment of Barlow's syndrome is discussed . In our opininon , therapy is only required for ventricular arrhythmias detected by a sufficiently sensitive method such as HMS . Most authors use beta blockers , eventually in association with quinidine Therapeutic successes have also been observed with mexiletine , amiodarone , aprindine and less commonly with disopyramide .
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PMID:[Electrocardiographical changes and rhythm disorders in Barlow's syndrome]. 615 62

The hemodynamic and contractile effects of acute cigarette smoking were analyzed in 35 patients with normal cardiac and coronary function as well as with cardiac failure and with coronary artery disease. In normal patients (normal ventricular function, normal coronary arteriogram) cigarette smoking exhibited no contractile depressant effects. Moderate increase in global and in regional wall motion and contractility was found. Likewise, in patients with compensated hypertensive hypertrophy (normal ventriculogram, significant left ventricular hypertrophy, normal coronary arteriogram) cigarette smoking increased global and regional contraction function. In cardiac disease patients (dilatative cardiomyopathy, advanced coronary artery disease, decompensated hypertensive heart disease) cigarette smoking was associated with depression in the overall and regional contraction behavior of the left ventricular myocardium. In patients with coronary artery disease, cigarette smoking was accompanied by marked depression of the regional contraction pattern in hypokinetic, akinetic, and dyskinetic zones. Moreover, contractile depression also occurred in the non-ischemic zones, without pre-existing coronary artery stenoses. In conclusion, acute cigarette smoking may not cause contractile depressant effects in normal patients and patients with compensated hypertensive hypertrophy. However, in coronary patients, significant negative inotropic effects are present not only in the ischemic zones, but also in the non-ischemic myocardium.
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PMID:Global and regional wall motion and contractility of the left ventricle following cigarette smoking. 623 23


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