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)

Follow-up data on 2700 subjects who had had maximum stress tests were assembled in life tables. A positive test, characterized by ST-segment depression of 1.5 mm, 0.08 sec from the J point, predicted an incidence of some new coronary event of 9.5% a year, as compared with 1.7% in those with a negative test. The incidence of infarction and death was also significantly higher than in the negative responders. Early onset of ischemia occurring at moderate exercise (4 metabolic equivalents-METS) resulted in an incidence of all coronary events of 15% a year, while ischemia first manifested at the seventh minute of exercise (approximately 8 METS) results in an incidence of only 4% per year. The magnitude of ST depression and the age of onset of ischemia failed to influence the incidence of coronary events. A myocardial infarction previous to the test increased the incidence of events in both positive and negative responders. The positives with a previous infarction had more than double the incidence of coronary events than the positive responders with no pre-existing infarction. Those with chronotropic incompetence had a high incidence of coronary events even though the ECG response to exercise was normal.
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PMID:Predictive implications of stress testing. Follow-up of 2700 subjects after maximum treadmill stress testing. 111 17

Adult rhesus monkeys were subjected to complete cerebral ischemia for one hour and subsequent recirculation for up to 24 h. Animals with signs of functional recovery (e.g. spontaneous EEG activity) exhibited a partial replenishment of cellular energy sources (ATP, phosphocreatine) and a progressive normalization of cerebral lactate levels. Glucose and pyruvate concentrations showed a transient increase over control values during the early stages of postischemic recirculation. Monkeys without functional recovery lacked a significant resynthesis of energy-rich compounds; adenine nucleotides continued to decrease and lactate concentrations were higher than in animals subjected to ischemia without recirculation. Cerebral polysome profiles remained unaltered during the ischemic period but in all animals a marked disaggregation of polyribosomes with a concomitant increase in ribosomal subunits occurred after the onset of recirculation. In monkeys with indications of functional recovery these changes were reversible but a normal polysome profile was only observed after 24 h of recirculation. The results obtained indicate a postischemic depression of protein synthesis due to an inhibition of peptide chain initiation. After recirculation of the brain for 3-6 h there was evidence for an induction of enzymes involved in polyamine synthesis (ornithine decarboxylase and S-adenosylmethionine decarboxylase). No changes in the activity of these enzymes were observed at the end of the ischemic period, indicating that during complete cerebral ischemia not only the synthesis but also the catabolism of proteins is inhibited.
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PMID:Resuscitation of the monkey brain after one hour complete ischemia. III. Indications of metabolic recovery. 115 69

The sensitivity of rest and stress myocardial perfusion studies using scintillation camera imaging of intravenously administered rubidium-81 (81Rb) in the detection of myocardial ischemia was compared to that of stress electrocardiography by relating results in 40 patients to the degree of stenosis delineated by coronary arteriography. Of 33 patients with greater than 75% stenosis of at least one of the three major coronary vessels (significant stenosis), rest and stress 81Rb imaging detected ventricular ischemia in 29 (88%) whereas simultaneous stress electrocardiography was positive (1 mm or greater horizontal ST-segment depression) in only 19 (58%) of the same patients. Five of the 29 patients who developed stress-induced scintigraphic evidence of ischemia did not develop angina or a positive electrocardiogram with stress. In 31 of the 33 patients with significant coronary stenosis, either the stress scintigram or the stress electrocardiogram was positive. In seven patients with less than 50% narrowing of a major coronary vessel on coronary arteriography, the stress scinitigrams were negative, whereas the stress electrocardiograms were positive in the two of these patients with the syndrome of angina with normal coronary arteriograms. It is concluded that high resolution images of the myocardium can be obtained with 81Rb using the scintillation camera with special shielding, and that rest and stress 81Rb scintigraphy appears to provide greater sensitivity and specificity when compared to stress electrocardiography in the nininvasive identification of significant coronary stenosis.
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PMID:Noninvasive detection of regional myocardial ischemia using rubidium-81 and the scintillation camera: comparison with stress electrocardiography in patients with arteriographically documented coronary stenosis. 115 74

The solid angle theorem was used to analyze the relationships between TQ and ST segment deflections recorded from precordial and epicardial locations and the time course, size, shape, and transmural location of the ischemic process in the ventricular myocardium. Mathematical predictions were compared with experimental data from the intact heart. Precordial electrograms obtained in anesthetized close-chest pigs were compared with epicardial electrograms recorded directly from the heart's surface. Various areas of ischemia were produced by occluding large and small coronary artery branches, and the resultant changes in ischemic shape were delineated with Thioflavin S injections and postmortem ultraviolet photography. Formally derived equations and cumulative experimental data were in close agreement, suggesting that in the ischemic ventricle (1) TQ depression always accompanies ST elevation, (2) TQ and ST segment changes in magnitude and polarity are complex functions of ischemic size, shape, and transmural location; (3) precordial electrocardiogram (ECG) ST segment elevation is directly related to ischemic size; and (4) epicardial ECG ST segment elevation is inversely related to ischemic size. It is thus concluded that precordial and epicardial ECG TQ and ST segment deflections are complex functions of ischemic geometry and that their accurate interpretation with respect to ischemic size and shape and in the presence of pharmacological interventions is often difficult and may be misleading.
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PMID:Precordial and epicardial surface potentials during Myocardial ischemia in the pig. A theoretical and experimental analysis of the TQ and ST segments. 118 39

Patients with prolapsing mitral leaflet syndrome (PML) frequently have chest pain of undetermined etiology. Twenty-three patients with PML underwent cardiac hemodynamic, angiographic, and metabolic studies. The latter were performed during control spontaneous heart rate and tachycardia by right atrial pacing. Myocardial supply-demand ratio (DPTI:SPTI) was estimated from the planimetric integration of the diastolic area (diastolic pressure time index = DPTI) and systolic area (systolic pressure time index = SPTI) of the central aortic pressure. Chest pain during pacing occurred in five patients. In two patients, it was associated with ST depression typical of ischemia on the electrocardiogram. Myocardial lactate abnormalities (lactate production or less than 10% extraction) occurred in seven patients during pacing tachycardia and was present in two patients during control state. DPTI:SPTI ratio during control state was 1.22 (+/- 0.07 SE) and decreased to 0.85 (+/- 0.05 SE) during pacing tachycardia. It is concluded that the myocardial lactate abnormalities in PML, which were present in approximately 30% of the patients in the present series, are most likely due to myocardial hypoxia. Whether or not the hypoxia is secondary to "small vessel disease" is not elucidated by this study.
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PMID:Myocardial metabolic studies in prolapsing mitral leaflet syndrome. 118 56

Interruption of coronary flow during cardiac surgical procedures provides a bloodless flaccid heart and allows precise and rapid correction of complex cardiac defects. However, myocardial damage occurs in direct proportion to the duration of the ischemia. As the induction of cardioplegia simulataneous with the initiation of cardiac ischemia helps to preserve cardiac energy reserves and thus myocardial integrity, the identification of a consistently reliable cardioplegic technique is desirable. Isolated perfused working rat hearts were made ischemic for one hour by aortic cross-clamping and were compared with hearts rendered cardioplegic at the onset of ischemia by the intracoronary administration of 5 ml of a hypothermic solution: 1) Krebs-Henseleit buffer, 2) Ringer's lactate, 3) tetrodotoxin, 4) potassium chloride, or 5) potassium citrate. Cardiac output, heart rate, aortic pressure and coronary flow were determined pre and post-ischemia. When compared to time-matched controls and hearts arrested with potassium or tetrodotoxin, the ischemia and ischemia-Ringer's lactate groups showed significant post cross-clamp depression of all measured parameters. Intracoronary Ringer's lactate, although often used as an adjunct to ischemic arrest, was not of significant value. In contrast, hearts arrested with tetrodotoxin, potassium chloride or potassium citrate showed no significant post-ischemic functional or histologic deficit. Perfusion with hypothermic Krebs-Henseleit buffer protected the myocardium better than did Ringer's lactate but less well than the tetrodotoxin or isotonic high potassium solutions. The induction of hypothermic metabolic arrest of the heart by briefly perfusing the coronary arteries via the aortic root with isotonic buffered solutions results in markedly improved myocardial tolerance to one hour of ischemia and avoids the problems of low cardiac output and ventricular irritability previously reported with hypertonic potassium citrate arrest.
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PMID:Amelioration of the effects of ischemic cardiac arrest by the intracoronary administration of cardioplegic solutions. 118 57

Carnitine palmityltransferase activity was measured in mitochondria isolated from control and ischemic dog heart. The ischemic activity demonstrated a decrease in both the Vmax and the Km of the enzyme for 1-carnitine when measured in the presence of 160 muM palmityl-CoA. The kinetic response of the mitochondrial carnitine palmityltransferase to ischemia was mimicked by assay of the enzyme from control mitochondria in a medium of low ionic strength. The effect of ionic strength on enzyme activity was directly correlated with binding of palmityl-CoA to the mitochondrial membranes. The decrease in carnitine palmityltransferase activity in ischemic mitochondria may reflect a decrease in palmityl-CoA binding to the enzyme active site. The depression in ischemic carnitine palmityltransferase activity may represent an early defect in mitochondrial metabolism.
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PMID:Carnitine palmityltransferase activity during myocardial ischemmia and at low ionic strengths. 122 48

The ampullar endolymphatic potential (AEP) was studied in the guinea pig during ischemia and asphyxia and following systemic application of ethacrynic acid. In addition the specialized and nonspecialized portions of the ampullar wall were analyzed for ATP and P-creatine at different conditions of metabolic interference. Under control conditions the AEP amounted to + 4.6 +/- 1.2 mV. In both types of hypoxia the decline of the AEP proceeded on a much slower time scale than that of the cochlear endolymphatic potential (CEP), and the maximum negativity reached was considerably less. Quantitative analysis of both types of ampullar wall tissue indicated a much slower decline in hypoxia of ATP levels than in the stria vascularis. Changes in P-creatine levels were considerably more rapid. The AEP became reduced and changed polarity also by intoxication with ethacrynic acid (EA), but higher dosages (above 70 mg/kg) were necessary than for effects upon the CEP and much longer time periods were required for attainment of maximum negativity. The maximum negativity of the AEP was significantly greater at a dosage of 100 mg/kg of EA than during ischemia. At the point of maximum depression of the AEP P-creatine levels in both types of ampullar tissue were unchanged, but ATP levels were significantly reduced in the specialized portions of ampullar wall.
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PMID:Effects of anoxia and ethacrynic acid upon ampullar endolymphatic potential and upon high energy phosphates in ampullar wall. 125 96

There is as yet no adequate animal mode for human myocardial ischemia. The commonly utilized technique of coronary arterial ligation in large animals may induce regional ischemia but introduces variables that make it difficult to compare studies in different laboratories. A model of global ischemia in an isolated perfused rat heart that offers a rapid, inexpensive means for producing graded, controlled, stable state and reproducible ischemia is described. The technique has been utilized with success to study the hemodynamic and metabolic effects of ischemia and to evaluate pharmacologic interventions designed to protect the ischemic myocardium. Propranolol has been shown to improve bioenergetics and reduce anaerobic glycolysis by a depression of the hemodynamic response of ischemic myocardium. Methylprednisolone appears to exert its primary effect by direct coronary vasodilation, increasing resting or control flow and providing an enhanced reserve when ischemia is imposed. Mannitol improves cardiac performance by reducing the increased myocardial cell water content induced by hypoxia or anoxia.
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PMID:Metabolic evaluation of agents designed to protect the ischemic myocardium and to reduce infarct size. 125 90

Inverted T waves due to coronary artery disease and previous myocardial infarction were observed to revert ot normal, upright position during ischemia in 38 patients. The normalization of inverted T waves was seen on the electroencephalograms of 19 patients during spontaneously occurring angina pectoris and of 11 patients when ischemia was provoked by treadmill exercise; for 8 patients, normalization occurred during the administration of isoproterenol hydrochloride and during the consequent episode of angina pectoris. The mechanism for normalization may be the algebraic sum of the extent of ST segment elevation and the amplitude of the T waves of acute ischemia plus the extent of preexisting ST segment depression and the degree of T wave inversion, to result in isoelectric ST segment and upright T wave. As with myocardial infarction, reciprocal changes may also be recorded. However, the reciprocal nature may be masked since either acute ST segment elevation of T wave inversion, or both, may not be recorded in the leads reflecting the ischemic area because of normalization.
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PMID:Normalization of abnormal T waves in ischemia. 126 47


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