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 the present study was to investigate the effect of the dose of nitroglycerin (NTG) on myocardial ischemic injury. In 20 closed chest dogs the anterior descending branch of the left coronary artery was occluded by inflating a balloon in its lumen. Compared with the untreated control group the sigma ST elevation was significantly lower when NTG was applied at a rate of 0.02 mg/min, but significantly higher when NTG was administered at a rate of 0.10 mg/min. In 12 patients with acute myocardial infarction NTG was infused at a rate of 3 mg in the first hour (0.05 mg/min) and 6 mg in the second hour (0.1 mg/min). Sigma ST elevation and sigma ST depression decreased during the lower infusion rate (p less than 0.001). When the rate of NTG infusion was raised to 6 mg/hr, the improvement in ST segment deviation was partially reversed. This effect, particularly evident in patients not in heart failure, was associated with a significant rise in heart rate (p less than 0.05) and a fall in diastolic arterial pressure (p less than 0.025). Patients with left ventricular failure were less sensitive to higher doses of NTG than those without failure. Thus, the effect of NTG on myocardial ischemic injury depends on the NTG dose and on the functional state of the injured left ventricle.
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PMID:Nitroglycerin in acute myocardial infarction. X. Effect of small and large doses of nitroglycerin on sigma ST segment deviation -- experimental and clinical results. 12 66

Indirect measures of left ventricular function were studied in seven patients with respiratory failure secondary to chronic obstructive pulmonary disease to determine if there were a relationship between left ventricular function and treatment of the pulmonary disease. All patients were studied during acute episodes while in respiratory failure having arterial Pco2 (Paco2) values greater than 49 torr with no clinical evidence of left ventricular failure. Indirect methods to evaluate left ventricular function included the use of the Swan-Ganz catheter for pulmonary capillary wedge pressure measurement, systolic time intervals, and cardiac output. There was improvement in left ventricular function with treatment of the respiratory failure manifested by decreases in the wedge pressure and pre-ejection period/left ventricular ejection time ratio, and an increase in the dp/dt/pulmonary capillary wedge pressure with treatment of the chronic obstructive pulmonary disease. The improvement in left ventricular function suggests that there is a depression of left ventricular function in respiratory failure. The depressed function improved with therapy of the lung disease without additional medication directed at cardiac function.
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PMID:Left ventricular function during respiratory failure. 87 4

The effects of carbon monoxide on ventilation were studied in unanesthetized goats. Responses to single breaths of 10-25% CO in O2, which rapidly raised carboxyhemoglobin (COHb) from 5 to 60%, were considered to reflect peripheral chemoreceptor-mediated reflexes whereas responses to continuous inhalation of 1% CO in O2, which slowly raised COHb from 0 to 60%, were considered to reflect both peripheral chemoreceptor and nonperipheral chemoreceptor mechanisms. In each of six goats, single breaths of CO failed to elicit any immediate ventilatory response. However, slow buildup of carboxyhemoglobinemia in the same animals always elicited ventilatory stimulation (from a mean of 7.43 to 16.02 liter/min, P less than 0.001) beginning 5-6 min after onset of 1% CO in O2 inhalation when COHb saturation reached 50-60%. In eight studies of six animals HCO3- concentration fell (from 21.3 to 15.8 meq/liter; P less than 0.001) and lactate concentration rose (from 2.5 to 4.2 meq/liter; P less than 0.05) in the cisternal cerebrospinal fluid during the CO-induced hyperpnea. Additional studies ruled out ventilatory stimulation from left heart failure or enhanced chemo-sensitivity to carbon dioxide. Although the delayed hyperpnea was associated with a hyperdynamic cardiovascular response to CO, blockade of these circulatory effects with propranolol (2 mg/kg) failed to abolish the delayed hyperpnea; however, the propranolol did unmask an element of ventilatory depression which preceded the hyperpnea. Conclusions were: (a) hyperventilation in response to CO inhalation is not mediated by the carotid bodies; (b) the delayed hyperpnea in response to CO inhalation is primarily due to brain-cerebrospinal fluid acidosis; (c) mobilization of body CO2 stores due to the circulatory response to CO may obscure an initial depression of ventilation by CO.
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PMID:Mechanism of the ventilatory response to carbon monoxide. 94 62

1. Nine subjects with severe coronary artery disease were studied during graded "sprint" and "steady-state" exercise before and after intravenous administration of the beta-receptor antagonist alprenolol. During "sprint" workload was increased every minute until maximum work capacity (Wmax) was reached. "Steady-state" exercise was performed at work rates of 0.250, 0.50, and 0.75 of each subject's sprint Wmax. Variables measured included ST-segment depression, changes in heart rate, blood pressure, respiratory gas exchange, and arterial blood composition. Cardiac output (indirect Fick) was measured during "steady-state" exercise. 2. Alprenolol did not alter Wmax during "sprint" but reduced the incidence of angina in both types of exercise. After the drug work capacity was limited by symptoms and signs suggestive of mild left ventricular failure. 3. The relationship between workload (normalized in terms of Wmax) and ST-segment depression was curvilinear. Under control conditions a given rate of work during "steady-state" exercise was assocaited with more marked ST-segment depression than during "sprint". Alprenolol displaced the work-ST-depression curve to the right in each type of exercise; now a given rate of work produced similar ST-depressing during "steady-state" and "sprint" exercise. 4. Alprenolol attentuated the exercise tachycardia during both types of exercise. Cardiac output was lower in "steady-state" exercise after the drug than under control conditions. Metabolic effects included significant reduction in body oxygen consumption after alpreprenolol at 0.25 Wmax and diminished arterial lactate at 0.75 Wmax. The beneficial effects of the drug thus appeared to involve not only cardiac but peripheral effects on beta receptors. 5. Before alprenolol cardiac output was relatively fixed at all workloads, but after the drug there was a work-related rise in output in five out of nine subjects. Comparison with data in normal subjects suggested that in anginal subjects cardiac output at low "steady-state" workloads was inappropriately high.
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PMID:Effect of beta-adrenergic blockade with alprenolol on ST-segment depression and circulatory dynamics during exercise in patients with effort angina. 96 82

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

The following prospective study was undertaken to observe the clinical course, early prognosis and coronary anatomy of patients with subendocardial infarction. Subendocardial infarction was defined as typical chest apin (greater than 15 minutes), serum enzyme elevation and persistent (greater than 48 hours) new T wave inversion and/or S-T segment depression in the absence of new pathologic Q waves. Fifty consecutive patients were defined, followed in a prospective manner and subjected to early coronary arteriography. A prior history of unstable angina was found in 33 patients (66 per cent); 22 patients (44 per cent) had significant dysrhythmias during the acute hospital phase, and seven patients (14 per cent) had evidence of mild left ventricular failure. Coronary arteriography demonstrated significant lesions (greater than 75 per cent narrowing in at least one vessel) in all 50 patients, with 30 patients (60 per cent) having either double- or triple-vessel disease. Follow-up (mean 10.6 months) revealed that 15 patients (30 per cent) had stable angina, 23 patients (46 per cent) unstable angina and only 12 patients (24 per cent) remained free of angina. Of 28 patients in a medically treated group, acute transmural infarctions developed in six (21 per cent) and one died (3 per cent). We conclude that subendocardial infarction is symptomatically an unstable entity, is associated with severe coronary artery disease and, in a medically treated group, is followed by a significant incidence of early transmural myocardial infarction (21 per cent). Therefore, these patients require in-hospital monitoring, careful follow-up and consideration for early coronary arteriography.
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PMID:The clinical course, early prognosis and coronary anatomy of subendocardial infarction. 102 Jul 51

In summary, rapid atrial pacing prior to surgery may be able to assess LVF and the degree of coronary insufficiency by measuring lactate production. Functional contraction abnormalities of the left ventricle are described by the anginal depression of the LVF, whereas a preanginal depression should be a sign of organic, fibrotic impairment of myocardial function. In cases of the former, after successful bypass surgery, a normal LVF may be observed. Moreover, myocardial metabolism is normalised. In the latter group, despite clinical improvement, functional abnormalities can persist.
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PMID:[Dynamics and metabolism in coronary heart disease before and after revascularization intervention]. 108

Study on 108 patients of acute myocardial infarction has shown the incidence of reciprocal ST depression in ECG in 58.3% patients. Those showing reciprocal changes had higher (65.0% Vs 15.5%) incidence of complication such as dysrhythmias, conduction disorders. hypotension, left ventricular failure or CCF which was more conspicuous in inferior myocardial infarction. There was higher incidence of complications (74.4% vs 18.7%) whenever ST depression was 2 mm or more (P < 0.001) and there was steep rise in complications whenever the ST depression persisted for 2 days and beyond.
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PMID:Prognostic significance of reciprocal changes in acute myocardial infarction. 130 28

To determine the effects of myocardial infarction-induced left ventricular failure on the mechanical characteristics of the remaining viable myocytes, coronary arterial occlusion was performed in rats, and cell function was examined 1 wk later. Moreover, to establish the mechanisms by which treatment with angiotensin-converting enzyme inhibitors ameliorates cardiac dynamics, captopril was administered immediately after surgery, and the contractile behavior of the unaffected cells was similarly analyzed 7 days later. The severe impairment in left-side pump function was found to be associated with a decrease in the velocities of myocyte shortening and relengthening and peak shortening despite a prolongation of contraction duration. In addition, a uniform property was recognized in myocytes from infarcted and noninfarcted hearts. Longer cells manifested greater velocity of shortening, whereas wider cells of identical length exhibited depressed shortening velocity. After infarction, the depression in cell contractility coupled with lateral expansion of myocytes exceeded the influence on cell mechanical behavior linked to myocyte lengthening leading to an overall decrease in contractility of the hypertrophied cells. Captopril therapy preserved, in part, the ability of myocytes to shorten and relengthen, which was accompanied by a decrease in the lateral and longitudinal expansions of these cells.
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PMID:Mechanical performance of spared myocytes after myocardial infarction in rats: effects of captopril treatment. 141 11

Overnight studies were performed in 10 patients with severe chronic left heart failure (New York Heart Association grades III and IV) without pulmonary disease and in eight controls. Transcutaneous oxygen (Po2) and carbon dioxide tensions (Pco2) and oxygen saturation were measured and the electro-cardiogram was recorded. During sleep mean oxygen saturation fell to 92.7% (minimum 86.1%) from 95.1% when awake. During the night oxygen saturation was below 95% for 62% of the time, below 90% for 6% of the time, and below 85% for 1% of the time. In four patients there were oxygen desaturation dips (a fall of greater than 4% in oxygen saturation from a stable baseline that lasted greater than 30 s) with concurrent increases in Pco2. Two patients had bradycardia during the dips: in one there was non-sustained ventricular tachycardia during the dips and in the other there was ST depression (greater than 0.1 mV at 80 ms after the J point) during a dip. In the controls the fall in mean oxygen saturation from 95.4% when they were awake to 94.4% when they were asleep was less than the fall in patients with heart failure and there were no desaturation dips or arrhythmias. Thus patients with severe heart failure had episodes of oxygen desaturation during sleep, some of which were associated with arrhythmia. Such episodes may be related to the increased risk of sudden death in chronic heart failure.
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PMID:Overnight studies in severe chronic left heart failure: arrhythmias and oxygen desaturation. 190 36


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