UMLS:C0011570 - FACTA Search

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)

Samples of myocardium from four areas of ischemic and infarcted canine ventricle were examined over a 20-day period for content of the three adenine nucleotides as well as inosine, hypoxanthine, adenosine, and inosine monophosphate. The adenosine triphosphate (ATP) content of central and peripheral areas within the infarct fell to 11% and 8% of control, respectively, 1 day after coronary occlusion. The total adenine nucleotide (TAN) content in these areas fell to 17% of control and showed no significant recovery during the period of study. In the functional myocardium immediately surrounding the infarct the ATP content was depressed to 58% control after 1 day, and the TAN content was also depressed. In the healthy myocardium near the apex, the ATP content was significantly depressed only at the 3-day sample period. Adenine nucleotide derivatives were detected only at 30 min in the central ischemic area. The absence of the nucleoside and nucleobase compounds formed during adenine nucleotide degradation is attributed to their high membrane diffusibility. Loss of these compounds is considered a contributing factor in the prolonged depression of adenine nucleotide content in both ischemic and non-ischemic regions.
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PMID:Effect of ischemia and infarction on regional content of adenine nucleotides and derivatives in canine left ventricle. 101 95

The effects on myocardial function, metabolism and ultrastructure of 60 minutes of reperfusion, instituted after 30, 60 and 90 minutes of occlusion of the left anterior descending coronary artery, were studied in 48 dogs. Twelve sham-operated dogs served as controls. Coronary occlusion for 60 or 90 minutes caused significant depression in the first derivative of left ventricular pressure (dP/dt) (P less than 0.05) that could not be reversed by reperfusion. Upon reperfusion, creatine phosphate stores in myocardium made ischemic for 30 and 60 minutes, but not for 90 minutes, returned toward control levels, but stores of adenosine triphosphate (ATP) and total nucleotides and the ATP/adenosine diphosphate ratio of myocardium subjected to 60 and 90 minutes of ischemia were further decreased. After 60 and 90 minutes of ischemia, swelling of the sarcoplasmic reticulum and mitochondrial damage (swelling, decreased matrix density and partial loss of cristae) were seen. Myofibrils were relaxed in all these groups. Reperfusion produced gross contraction of myofibrils and aggravated these changes in mitochondria and sarcoplasmic reticulum. In the hearts subjected to 90 minutes of ischemia these changes were gross. The levels of creatine phosphokinase, glutamic oxaloacetic transaminase and lactic dehydrogenase in the coronary sinus blood increased dramatically (P less than 0.05) upon reperfusion after 60 or 90 minutes of occlusion, indicating severe impairment of cell membranes. This secondary rise in serum enzyme activity during reperfusion should be taken into consideration when estimating the size of a myocardial infarct from enzyme changes alone. It appears that 60 and 90 minutes of ischemia cause severe myocardial damage that is not reversed by reperfusion maintained for 1 hour although longer periods of reperfusion may be beneficial.
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PMID:Alterations in energy metabolism and ultrastructure upon reperfusion of the ischemic myocardium after coronary occlusion. 108 Mar 52

The influence of acute myocardial depression on ventricular stiffness and on its elastic and viscous components was studied in 19 dogs. After the animals were placed on cardiopulmonary bypass, stiffness was measured by sinusoidally injecting volume changes of 0.5 ml (deltaV) at 22 Hz into paced, isovolumically (deltaP) of the sinusoidal pressure response. Stiffness was linearly related to pressure (P) throughout the cardiac cycle, so that deltaP/delta V = alpha P + beta, where alpha and beta are constants. Myocardial depression was induced in one of three different ways: by coronary artery ligation, by administration of propranolol (Inderal), or by administration of pentobarbital. All three interventions caused significant increases in the slope, alpha, of the stiffness-pressure relationship, while the intercept, beta, remained unchanged. Release of the coronary occlusion or administration of acetylstrophantidin partially reversed depression and the change in alpha; Approximation of the mechanical nature of the left ventricle in terms of a linear second-order mechanical system permitted the division of stiffness into its elastic and viscous components. Like total stiffness, both the elastic and the viscous components were linearly related to ventricular pressure. Elastic stiffness was not changed, but the slope of the line relating viscous stiffness to pressure was significantly increased during ischemic depression, indicating that a change in viscosity was primarily responsible for the increase in total ventricular stiffness.
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PMID:Influence of acute myocardial depression on left ventricular stiffness and its elastic and viscous components. 115 Aug 70

The effects of the positive-inotropic drug Canrenoat-Kalium (CRK) on the extent and severity of myocardial ischemic injury and on hemodynamic parameters were studied in 17 dogs following coronary occlusion. Acute myocardial infarction causes depression of left-ventricular function. There eas a significant decrease in dp/dtmax, stroke volume and cardiac output; average values for mean arterial pressure were reduced, but not significantly. There was a significant increase in left-ventricular enddiastolic pressure. Heart rate was unchanged. In the healing phase of myocardial infarction a significant elevation of left-ventricular enddiastolic pressure and a significant decrease of arterial pressure persisted, but the other parameters had returned toward normal. Intravenous administration of CRK (20 mg/kg) one hour after coronary occlusion causes a significant increase in left-ventricular dp/dtmax, cardiac output and stroke volume, but no significant change in arterial pressure, heart rate and left-ventricular enddiastolic pressure. Four days after myocardial infarction administration of CRK causes also a significant incrrease in left-ventricular dp/dtmax and -n 4 out of 5 animals an increase in stroke volume. Heart rate, arterial pressure and left-ventricular enddiastolic pressure are unchanged. There is a continuous deterioration of all hemodynamic parameters in the control group 1 hour and 96 hours after experimental myocardial infarction. This spontaneous deterioration has to be taken into consideration estimating the effect of CRK in experimental conditions. 120 epicardial electrocardiographic recordings were used to assess the extent and severity of myocardial ischemic injury. The average ST-segment elevation and the number of sites with abnormal ST-segments were significantly reduced 20 min after CRK administration. The study suggests a beneficial therapeutic role for CRK treatment of left-ventricular failure in the acute and healing phase after myocardial infarction.
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PMID:[Influence of canrenoate potassium (aldactone pro injections) on hemodynamics and myocardial ischemia in experimental myocardial infarct]. 116 92

The performance characteristics of both ischemic and "adjacent" and "remote" nonischemic myocardium were studied in open chest dogs by three mercury-in-Silastic length gauges sutured to the anterior surface of the left ventricle before and after occlusion of the distal left anterior descending coronary artery. The adjacent gauge was separated from the ischemic segment by one large nonoccluded diagonal branch of the left anterior descending artery. Remote myocardium was separated from the ischemic area by two such branches. At the time of occlusion epicardial S-T segment elevation appeared in the ischemic region but not in the adjacent or remote regions. Immediately after occlusion, typical changes of ischemic dysfunction appeared. Late systolic lengthening, depression of systolic shortening and increased diastolic compliance occurred consistently and simultaneously in ischemic and adjacent regions and inconsistently in the remote region. Five minutes after occlusion, fiber shortening was depressed to 21, 58 and 67 percent of control values in ischemic, adjacent and remote regions, respectively. Heart rate did not change, and mean arterial pressure decreased slightly. These changes persisted over time. In 11 of these dogs, end-diastolic pressure was maintained constant 20 minutes after occlusion. Systolic shortening was depressed to 40 and 74 percent of control values in the ischemic and adjacent regions, respectively. In six dogs, end-diastolic pressure was varied form 5 to 20 mm Hg by rapid volume loading during the control state and 30 minutes after occlusion. Systolic shortening in ischemic, adjacent and remote regions was depressed to 20, 40 and 65 percent of control values, respectively. The severity of all functional alterations after coronary occlusion was directly related to proximity to the ischemic region. These results indicate that depression of left ventricular function after coronary occlusion may be partially related to previously unrecognized depression of function in apparently "nonischemic" myocardium.
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PMID:Functional abnormalities in nonoccluded regions of myocardium after experimental coronary occlusion. 125 69

Because the Na+ pump is considered to modulate the contractile force development by the cardiac muscle and depressed cardiac pump function is the hallmark of congestive heart failure, we characterized the sarcolemmal Na(+)-K(+)-ATPase activity in failing rat hearts after myocardial infarction. For this purpose, the left ventricular coronary artery was ligated, and hearts were examined 4, 8, and 16 wk later; sham-operated animals served as controls. Hemodynamic assessment revealed the presence of abnormal cardiac function at 4, 8, and 16 wk. Although accumulation of ascites in the abdominal cavity was present in experimental animals at 4 wk, other clinical signs of congestive heart failure in experimental rats including lung congestion and cardiac dilatation were evident 8 and 16 wk after induction of myocardial infarction. The depression in Na(+)-K(+)-ATPase activity in purified sarcolemmal membrane from the uninfarcted experimental left ventricle at 8 wk was associated with depressed Vmax without any changes in the affinities for Mg-ATP, Na+, and K+ or the pH optimum for the enzyme. The Kd values of both the high- and low-affinity binding sites for [3H]ouabain, which is believed to interact with Na(+)-K(+)-ATPase, were increased; however, no change in the density of either class of ouabain binding site was evident. The depression of Na(+)-K(+)-ATPase activity in failing hearts at 16 wk of myocardial infarction was not different from that observed at 8 wk but the enzyme activity was not altered at 4 wk of coronary occlusion. These data support the view that depression of Na(+)-K(+)-ATPase activity may serve as an adaptive mechanism during the development of congestive heart failure.
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PMID:Sarcolemmal Na(+)-K(+)-ATPase activity in congestive heart failure due to myocardial infarction. 131 80

Non q wave myocardial infarction has been attributed to occlusion of a vessel with no ECG representation, early reperfusion of the occluded artery or occlusion of a vessel with generous collateral flow. The coronary arteriography of 84 patients with non Q wave myocardial infarction performed at 16 + 17 (SD) days after infarction was analyzed. Main left lesion was found in 6 (17%), single vessel disease in 30 (36%), two vessel disease in 18 (24%) and 3 vessel disease in 16 (19%). The "culprit" vessel had a critical residual lesion in 38 patients (45%): 22 affected the left anterior descending artery, 10 the circumflex, and 5 the right coronary artery. No residual lesion was found in 10 patients (12%). An occluded artery was found in 32 patients (38%): circumflex in 20, right coronary artery in 9 and left anterior descending in 3 (p < 0.01). Significant collateral flow to the occluded vessel was present in 41% of cases. The ST segment was analyzed in 82 patients. Depression of ST was found in 29 (35%), elevation in 22 (27%), negative T waves in 17 (21%) and minimal alterations in 17%. There was no correlation between ST levels and coronary occlusion of the culprit artery. Depression of ST was more commonly (p < 0.01) associated with severe coronary artery disease (main left or 3 vessel disease), which may be related to the poorer prognosis in these cases.
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PMID:[Angiographic findings in non-Q wave infarction and their relation to ST-T changes]. 134 94

The effects of ischemic preconditioning on epicardial T-Q and S-T segment mapping, local activation, and coronary blood flow were analyzed in nine barbiturate-anesthetized pigs during four coronary occlusion (5 min)-reperfusion (20 min) sequences. In seven sham pigs, one occlusion was performed after a control period of 75 min. The first reperfusion induced a marked coronary hyperemia [11 +/- 4 ml/min (baseline) to 33 +/- 16 ml/min, P < 0.005] and a rapid recovery (30 to 150 s) of epicardial activation delays, T-Q segment depression, and S-T segment elevation in the ischemia area. This recovery was transiently associated with enlargement of intersite T-Q potential variability (alpha: 2.5 +/- 0.6 to 3.4 +/- 0.7 mV, P < 0.05), T-Q segment overshoot to +1.4 +/- 0.9 mV, and S-T segment reelevation. A brief T-Q segment depression (-2.3 +/- 0.9 mV) occurred during early reperfusion in 60 of 91 electrodes overlying the normal myocardium. Compared with the first, the fourth occlusion induced lower S-T segment elevation (3.4 +/- 2.0 to 1.7 +/- 1.9 mV, P < 0.05), and the fourth reperfusion elicited a faster reversal of T-Q segment dispersion (53 +/- 21 to 43 +/- 16 s, P < 0.05), S-T segment elevation (149 +/- 101 to 81 +/- 45 s, P < 0.05), and coronary hyperemia (8 +/- 2 to 5 +/- 1 min, P < 0.05). This trend of changes was not observed during a fourth occlusion in sham pigs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:T-Q, S-T segment mapping and hyperemia in reperfused pig heart with ischemic preconditioning. 148 98

To evaluate, in the absence of lung inflation, the cardiovascular effects of single and repetitive pleural pressure increments induced by thoracic vest inflations and timed to occur during specific portions of the cardiac cycle, seven chronically instrumented dogs were studied. Reflexes and left ventricular (LV) performance were varied by autonomic blockade, circumflex coronary occlusion (with and without beta-blockade), or cardiac arrest. Single late systolic, but not early systolic, vest inflations significantly increased LV stroke volume both before (+12.4%) and after myocardial depression by coronary occlusion+beta-blockade (+18.5%) when performed after a period of apnea to control preload and rate. During vest inflations, LV and aortic pressures increased to a greater degree than esophageal pressure (by 51 vs. 39 mmHg, P = 0.0001). Lung inflations (26 trials in 3 dogs) during early or late systole failed to increase stroke volume, despite peak esophageal pressures of 11-26 mmHg. With autonomic reflexes intact, repetitive vest inflations coupled to early systole, late systole, or diastole induced a large (40%) but unspecific systemic flow increase. In contrast, during autonomic blockade, flow increased slightly (7.5%, P < 0.05) with late systolic compared with diastolic inflations but not relative to baseline. During coronary occlusion (with or without beta-blockade), no cycle-specific differences were seen, whereas matched vest inflations during cardiac arrest generated 20-30% of normal systemic flow. Thus only single late systolic thoracic vest inflations associated with large increments in pleural pressure increased LV emptying, presumably by decreasing LV afterload and/or focal cardiac compression. However, during myocardial ischemia and depression, coupling of vest inflation to specific parts of the cardiac cycle revealed no hemodynamic improvement, suggesting that benefits of this circulatory assist method, if any, are minor and may be restricted to conditions of cardiac arrest.
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PMID:ECG-synchronized thoracic vest inflation during autonomic blockade, myocardial ischemia, or cardiac arrest. 149 Sep 33

Influence of fructose++-1,6-diphosphate, succinate, malate and cytochrome C on free lipid peroxidation (FLP), infarct sizes and metabolic acidosis was studied in experiments on rats. The good correlation between inhibition of FLP and cardioprotector activity was established for activators of glycolytic energy production only. Krebs' cycle metabolites limited the zone of myocardial necrosis after coronary occlusion without any significant depression of FLP. Succinate and malate were practically inactive under acute metabolic acidosis of isolated rat heart.
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PMID:[Relationship of antioxidant and anti-ischemic effects of various energy-yielding compounds]. 166 19

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