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)

Clinical measurements were made of the effects of various drugs on the stimulation threshold of human heart [right ventricle]. Of antiarrhythmic drugs, a marked and prolonged elevation of the stimulation threshold was produced by procainamide, quinidine, and aimaline. Relatively short-lasting elevation was elicited by local anaesthetics [trimecaine, lidocaine]. Beta-blockers were little effective. No detectable effect on the stimulation threshold was produced by phenytoin and digitalis glucosides from the group of antiarrhythmics. The deepest and most prolonged depression of the stimulation threshold was achieved with anabolics [nandrolone phenylpropionate, nandrolone decanoate] and with high doses of prednisone and of 6-methylprednisolone sodium succinate. Hydrocortisone was ineffective. A slight and brief depression was produced by atrophine. The effects of sympathomimetics were complicated: at stimulation with short pulses the threshold was always raised. At stimulation with long pulses the effects were variable, mostly biphasic [occasionally triphasic]: a transitory depression of the stimulation threshold was followed by a marked elevation. The I-t curve's slope altered. In exit block, sympathomimetics are indicated because of their chronotropic effect, not because of their questionable effect on the stimulation threshold. A number of drugs, often administered to stimulated patients, produced no effect on the stimulation threshold: antibiotics, nitrites, purine compounds, opiates, and others.
Cor Vasa 1978
PMID:Effect of drugs on the stimulation threshold of the human heart. 2 97

The effects of premature atrial depolarizations (PADs) on the sinus node function were studied in isolated rabbit atria by using simultaneous intracellular recordings in the sinus node and adjacent regions. Late PADs (test cycle 85% or more of the basic cycle) did not capture the sinus node, blocking somewhere between this structure and the crista terminalis, inducing however a shortening of action potential, an increased rate of rise (Vmax) and amplitude of phase 0, and a variable depression of phase 4 depolarization on sinus node fibres. These effects were attributed to electrotonic interactions. Earlier PADs (test cycle 45--85% of the basic cycle) penetrated and captured the sinus node, changing its action potential shape, depending on the prematurity of the response. Two major effects were demonstrated: 1) a reduction in the maximum diastolic potential; 2) a linearly-related (p less than 0.001) decrease of the slope of phase 4 depolarization. These effects resulted in a depression of sinus node automaticity that was inversely-related to the test cycle length. Dominant pacemaker shifts within the sinus node were frequently observed with early as well as with late PADs resulting in a change of the basic cycle by as much as 90 msec. It is concluded that the use of the technique of premature atrial stimulation may not permit precise evaluation of sinoatrial conduction time.
Cor Vasa 1978
PMID:Effects of atrial premature stimulation on sinus node function in isolated rabbit atria. 74 26

The fall in the ventricular fibrillation threshold during the first half an hour following ligation of the descending branch of the left coronary artery in dog was not influenced by the i.v. injection of trimecain (Mesokain Spofa). On the other hand, an i.v. injection of methypranol (Trimepranol Spofa) given prior to ligation increased the level of ventricular fibrillation threshold 3 to 4 times compared to control value before occlusion in all 10 studied dogs. Depression of the beta-blocking adrenergic activity may thus prevent the occurrence of ventricular fibrillation in acute myocardial ischaemia.
Cor Vasa 1977
PMID:Prevention of ventricular fibrillation in experimental myocardial infarction. 92 60

Fifty-three men with significant obliterative arteriosclerosis of coronary arteries were examined at rest, during and after pacing. Pacing induced both angina pectoris and depression of the ST segment in 38% of the patients; either angina pectoris or depression of ST segment, in 32% of the patients; the remaining 30% of patients were without symptoms or ECG signs of coronary insufficiency. Haemodynamic findings at rest, or during and after cessation of pacing were not different between these groups. Pacing increased heart rate, cardiac index remained unchanged, the stroke volume decreased, the left ventricular ejection time shortened. In both systemic and pulmonary arteries the systolic pressures decreased, the diastolic and mean pressures rose. The left ventricular end-diastolic pressure decreased. In 28 of the patients the myocardial metabolism was investigated. A close correlation was found between positive symptoms and ECG signs of myocardial ischaemia on the one hand, and metabolic signs on the other hand. Absence of angina pectoris and depressions of the ST segment during pacing does not exclude the presence of metabolic signs of ischaemia; an opposite finding is about three times less frequent. The study offers objective information about haemodynamics and myocardial metabolism before, during and after pacing, and represents an attempt of a simple classification of symptoms and signs of induced ischaemia.
Cor Vasa 1976
PMID:Haemodynamics and myocardial metabolism in patients with obliterative coronary arteriosclerosis and tachycardia induced by pacing. 100 Sep 81

The authors evaluate the coronary risk factor changes in middle-aged men from the point of view of changed nutritional habits of the whole population (yearly per capita consumption of different food). They compared 3,754 men aged 40-50 years when screened in 1976-77 (Skoda I Study) and 568 men aged 40-50 years when screened in 1986-88 (Skoda II Study). During the 10-year period, a significant decrease of smoking habits was observed, hypertension prevalence remained unchanged and hypercholesterolaemia prevalence increased significantly. The estimated yearly per capita consumption of meat and fat remained unchanged in the years 1975-1985, however, the structure of consumption revealed a gradual change towards food containing high amounts of animal fat. Education efforts during the 10-year period (1976-1986) led to a decrease in smoking habits in middle-aged men leaving hypertension control unchanged. The observed increase of cholesterol levels may be attributed to inappropriate nutritional habits gradually worsening in the whole population probably due to a socio-economic depression.
Cor Vasa 1991
PMID:Serum cholesterol increase in a middle-aged male industrial population during ten years (1976-1986) and general food consumption changes in Czechoslovakia. 188 8

The study was designed to clarify the clinical and angiographic attributes of patients with exercise induced silent myocardial ischaemia. The sample consisted of 102 patients who had ischaemic exercise electrograms (greater than or equal to 1 mm ST segment depression) and had a significant angiographic stenosis (greater than 50% diameter stenosis), in at least one of the major coronary arteries. In 61 patients (60%) painful ischaemia was observed during exercise (group A) while in 41 patients (40%) only ST depression (silent ischaemia) occurred (group B). The groups were similar with respect to age, sex, history of diabetes and all angiographic parameters including the Gensini coronary score. A history of prior myocardial infarctions was observed more frequently (p less than 0.01) in patients with silent ischaemia (group B). Prior myocardial infarction may be a factor causing silent myocardial ischaemia.
Cor Vasa 1988
PMID:Painful and silent myocardial ischaemia during exercise testing. 297 59

Anoxic stress is accompanied by activation of the central and peripheral sympathetic nervous system resulting in a high local catecholamine concentration. The authors studied how myocardial cells cope with the high level of catecholamines under ischaemic conditions. The beta-adrenoceptor-adenylate cyclase system (AC) was investigated in different models of ischaemia and anoxia (global ischaemia, low-perfused hearts, coronary artery ligation) in rat hearts. It was shown that beta-receptor function is not changed up to 40 min of ischaemia. Myocardial AC function was depressed in the total ischaemic myocardium but not in the low-perfused hearts indicating a non-uniform alteration of AC function. Reduced AC activity was completely reversible by aerobic perfusion as long as the ischaemic period did not exceed 20 min. Depression of AC function during severe ischaemia was avoided by reducing Ca2+ in the extracellular fluid and by pretreatment with Ca2+ channel blockers (verapamil). Depression of AC function during severe ischaemia is caused mainly by increased intracellular Ca2+ which inhibits AC at its catalytic site. Myocardial ischaemia alters the response of myocardial cells to catecholamines and other activators of the AC system. This alteration is time-limited and turns damage to AC function from reversible to irreversible after prolongation of ischaemia to more than 30 min.
Cor Vasa 1986
PMID:Adrenergic regulation of the acute ischaemic myocardium: facts, interpretations and consequences. 301 89

Twenty men with coronary heart disease underwent the following exercise tests: a) bicycle ergometry, b) 5 kilometre walk and c) short march with a 5 kilogram weight carried in one hand. In each performed test during maximal work the following parameters were determined: oxygen uptake (VO2), plasma noradrenaline (NA) and lactate (LA) concentrations. ECG was monitored continuously and blood pressure was measured. It was found that a supplementary static load added to the dynamic work during short march with a weight resulted in the highest NA concentration. In that test, the rate-pressure product (HR X BPs) also increased and a greater ST segment depression and aggravation of arrhythmia were noted as compared to the findings obtained during the 5 kilometer march and also in the classic ergometric test.
Cor Vasa 1988
PMID:Supplementary static effort during dynamic exercise. Its influence on electrocardiogram, haemodynamic and metabolic adaptation of circulation in coronary patients. 323 8

In 70 consecutive patients (pts) with acute transmural inferior infarction, 58 had significant precordial ST depression (group A) and the remaining 12 had no ECG changes in precordial leads (group B) on admission. At the time of hospital discharge, the persistence of anterior ST depression was observed in 13 pts (group A1), normalization in 45 (group A2). Infarct size was significantly greater (p less than 0.05) in group A than in group B (37.6 vs. 23.8 CK-MB gEq). The largest infarct (51.5 CK-MB gEq) and the most serious clinical course was observed in group A1. No significant differences were noticed in the frequency of reinfarction and episodes of acute coronary insufficiency during hospitalization and one-year follow-up between groups. Persistent precordial ST depression is a simple ECG marker of extensive infarction, left ventricular dysfunction and a worse clinical course.
Cor Vasa 1987
PMID:Significance of anterior precordial ST-segment depression in acute inferior myocardial infarction. 359 51

15 patients with intact coronary arteries (control group) and 49 patients with coronary stenosis were for the purpose of differential diagnosis of ischaemic heart disease [IHD] subjected to coronarography, left ventriculography and transesophageal atrial pacing. The possibility of using the sum R wave amplitude as a criterion of IHD was assessed, as well as the relation between the R wave amplitude and the left ventricular function indicators--the ejection fraction and the end-diastolic volume. It was found that the increase of the R wave amplitude has distinctly lower specificity (40%) and sensitivity (29%) than the ischaemic depression of the ST segment (73 and 74% respectively). No correlation was found between R wave amplitude changes and indicators of the left ventricular function. The increase in the R wave amplitude cannot be therefore regarded as a reliable criterion of IHD and is not a reflection of the functional state of the left ventricle.
Cor Vasa 1987
PMID:R wave amplitude changes during transoesophageal atrial pacing in patients with chronic ischaemic heart disease. 362 47


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