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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of aspartate (Asp) and 2-oxoglutarate (2-OG) on metabolism and function of isolated rat heart during hypoxia and reoxygenation were studied. Hearts were subjected to oxygenated perfusion with Krebs-Henseleit buffer supplied with 11 mM glucose (20 min) and anoxic perfusion with the buffer saturated with N2 (20 min), followed by reoxygenation (30 min). The substrate concentrations in the perfusate were 3.5 mM each. The additives had no effect on the energy metabolism and function of the oxygenated heart despite a two-fold rise in myocardial Asp and 2-OG. Substrate supplementation during anoxic perfusion resulted in reduced lactate dehydrogenase release and less depression of cardiac function. Prevention of Asp, glutamate, and 2-OG degradation in hypoxic myocardium was accompanied by relief of glycolytic flux and better preservation of ATP, phosphocreatine (PCr), and total creatine (Cr). Reoxygenation without the additives after supplemented anoxic perfusion failed to improve recovery of high-energy phosphates and cardiac function compared to control. However, during reoxygenation with the additives the treated hearts showed less cell membrane damage and enhanced recovery of contractile and pump function. These effects were associated with higher myocardial contents of ATP, PCr, and adenine nucleotides and a smaller Cr loss during reoxygenation. A more effective restoration of oxidative metabolism was related to promoted glucose oxidation due to replenishment of the malate-aspartate shuttle reactants. The results substantiate the use of substrates of cytosolic aspartate aminotransferase for myocardial protection against hypoxia/reoxygenation stress.
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PMID:Substrate accessibility to cytosolic aspartate aminotransferase improves posthypoxic recovery of isolated rat heart. 758 71

Long-term treatment with sodium pivalate, a compound conjugated to carnitine and excreted in the urine, results in carnitine deficiency and cardiac dysfunction. Since L-propionylcarnitine (LPC) is generally of benefit to cardiac function, it was of interest to determine whether it is effective in preventing the reductions in both heart carnitine content and function from occurring in carnitine deficiency. Secondary carnitine deficiency was induced in male Sprague-Dawley rats by supplementing the drinking water with 20 mM sodium pivalate for 26 weeks. Control animals received an equimolar concentration of sodium bicarbonate. At 13 weeks into treatment, a subgroup of control and sodium pivalate animals were given 80 mg/kg of LPC in their drinking water. Following treatment, isolated working hearts were perfused with buffer containing 11 mM glucose and 0.4 mM palmitate. Hearts from sodium pivalate treated animals demonstrated a severe reduction in tissue carnitine. When mechanical function was measured in these hearts, heart rate, rate-pressure product, and aortic flow were significantly depressed. Treatment with LPC, however, prevented the depletion in cardiac carnitine content and improved these cardiac parameters. Our results demonstrate that LPC treatment is beneficial in preventing the depression in cardiac function from occurring in this model of secondary carnitine deficiency.
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PMID:L-propionylcarnitine effects on cardiac carnitine content and function in secondary carnitine deficiency. 767 Nov 93

Empirical tests of the diathesis-stress component of A. T. Beck's (1976; A. T. Beck, A. J. Rush, B. F. Shaw, & G. Emery, 1979) cognitive theory of depression have generally not yielded positive results. The resulting focus on conceptual and methodological concerns has diverted attention from the more fundamental issue of how validly vulnerability is measured. The present investigation uses the Dysfunctional Attitude Scale (DAS; A. N. Weissman, 1979; A. N. Weissman & Beck, 1978), the most commonly used measure of vulnerability in this area, but adopts a more in-depth approach by examining DAS factors in addition to the typical total score. This study involved a sample of undergraduates who had never before taken a college-level examination. The dimension of the DAS measured by the Perfectionistic Achievement factor had the strongest relationship to increased depressive symptoms in response to poorer-than-expected performance on the examination. Implications for future research in this area are discussed.
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PMID:Dimensions of dysfunctional attitudes as vulnerabilities to depressive symptoms. 767 66

We have previously shown that administration of Escherichia coli to a rat induces cardiac dysfunction, but also prevents the myocardium from being further damaged by total ischemia. We have also previously shown that induction of sepsis in a rat that has consumed alcohol as 36% of its caloric intake for 8-10 weeks, results in a potentiation of the cardiac depression resulting from sepsis. In this study, we determined if administration of Gram-negative bacteria to a chronically alcoholic rat would still protect the heart from ischemia-reperfusion injury. We tested the protective effect of sepsis using an in vitro, isovolumically contracting heart preparation. Global ischemia was maintained for 35 min, followed by 25-min reperfusion. In the present experiments, sepsis produced a 40% decrease in cardiac performance, but was also protective of hearts made ischemic the next day. Hearts from septic and alcoholic septic rats recovered 100% of preischemic ventricular function after 35-min ischemia, whereas hearts from the control and alcohol groups recovered only 80% of preischemic left ventricular performance. Whereas preischemic function was significantly decreased in the septic groups compared with the two nonseptic groups, postischemic function was no longer significantly different in the four groups. Thus, sepsis resulted in development of protection of the hearts from ischemia-reperfusion injury, even in hearts that were severely compromised by the combination of chronic alcoholism and Gram-negative sepsis.
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PMID:Sepsis protects the heart of alcoholic rats from ischemia-reperfusion injury. 769 39

We tested the hypothesis that the variable functional properties of rat versus guinea pig hearts are due to differences in intracellular Ca2+ handling. Hearts isolated from rats and guinea pigs were perfused with physiological saline, and isovolumic left ventricular (LV) pressure as well as coronary perfusion pressure were recorded simultaneously with Ca2+ transients from aequorin-loaded cells. Guinea pig hearts developed 47% less LV pressure than rat hearts, and the time to peak pressure was prolonged by 71% at similar heart rates. Diastolic and systolic levels of myoplasmic Ca2+ were approximately the same in both species at normal external Ca2+ concentration (1 mM); however, at low Ca2+ concentration (0.5 mM), guinea pig hearts maintained a higher level of myoplasmic Ca2+ than rat hearts, and the relative depression of LV systolic pressure was less. Guinea pig hearts also exhibited higher resistance to the negative inotropic effect of caffeine and did not respond to increments in perfusion pressure with increases in LV-developed pressure and systolic Ca2+ levels as did rat hearts. These contrasting findings with regard to intracellular Ca2+ handling may be attributed to a different organization of the ionic transport system with higher dependence of rat cardiomyocytes on normal function of the sarcoplasmic reticulum.
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PMID:Intracellular calcium and mechanical function in isolated perfused hearts from rats and guinea pigs. 789 33

Patients in the National Institute of Mental Health Treatment of Depression Collaborative Research Program (TDCRP) were administered at intake with the Dysfunctional Attitude Scale (DAS; A. N. Weissman & A. T. Beck, 1978). Factor analyses of the DAS in the TDCRP data as well as in several independent samples reveal two primary factors: an interpersonal factor, Need for Approval, and a self-critical factor, Perfectionism. This study explored the hypotheses that these factors, assessed prior to treatment, would have differential interactions with the two forms of psychotherapy evaluated in the TDCRP as well as differential relationships to various outcome measures (depression, clinical functioning, and social adjustment). DAS Perfectionism had consistently significant negative relationships with all the outcome measures in all four treatment conditions. Contrary to expectations, however, there were no significant interactions between the two DAS factors and the four types of brief treatment (cognitive-behavioral therapy, interpersonal therapy, imipramine, and placebo).
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PMID:Impact of perfectionism and need for approval on the brief treatment of depression: the National Institute of Mental Health Treatment of Depression Collaborative Research Program revisited. 789 77

In this study, we separated the effects of low oxygen supply and low coronary flow in isolated perfused rat hearts to focus on the genesis of free radicals-induced reperfusion injury. Hearts were exposed to either hypoxemia/reoxygenation or ischemia/reperfusion in various sequences, with hypoxemia and ischemia matched for duration (20 min), temperature (37 degrees C), and oxygen supply (10% of baseline). Hypoxemia/reoxygenation (n = 7) resulted in lower (developed pressure) x (heart rate) (p < 0.001) and higher end-diastolic pressure (p < 0.001) than ischemia/reperfusion (n = 9). The presence of 40 IU/ml superoxide dismutase and 104 IU/ml catalase nearly blunted the rise of the end-diastolic pressure (p = 0.02 vs. baseline), but could only partially prevent the depression of myocardial contractility (p < 0.001 vs. baseline, n = 7). Similar patterns were observed when hearts were made ischemic after hypoxemia, eliminating the intermediate reoxygenation step. We conclude that the major determinant of the reperfusion injury is associated with low oxygen supply rather than low coronary flow. Part of the injury is mediated by oxygen-derived free radicals, but a substantial portion of it is associated with energetic processes.
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PMID:Oxidative injury in reoxygenated and reperfused hearts. 800 21

Verapamil can produce depression of left ventricular function, delayed atrioventricular conduction, and hypotension, which can be potentiated by hyperkalemia. We sought to investigate a direct cardiac interaction between verapamil and hyperkalemia. Studies utilized isolated guinea pig hearts (Langendorff) paced at 250 beats/min. Hearts were randomly assigned to perfusion (Krebs-Henseleit buffer) with potassium concentrations ([K]+) of 1.5, 3, 6 and 9 mmol/l. Infusion of verapamil at rates of 0.2 to 60 micrograms/min (approximately 3 x 10(-8) to 10(-5) mol/l) produced concentration-dependent reduction of isovolumic left ventricular developed pressure. As [K]+ increased, concentration response curves showed parallel shifts to the left. The ED50 for reduction of left ventricular developed pressure significantly decreased: 8.2 +/- 3.7, 2.9 +/- 1.4, 1.2 +/- 0.7, 0.6 +/- 0.2 micrograms/min (mean +/- SD), respectively. Nifedipine and diltiazem were also studied in hearts perfused with 3 and 9 nmol/l [K]+. Infusion of nifedipine 0.003-1 microgram/min (approximately 10(-9) to 3 x 10(-7) mol/l) produced concentration-dependent reduction of left ventricular developed pressure but the ED50 was not affected by [K]+: 0.06 +/- 0.03 and 0.05 +/- 0.04 microgram/min, respectively. Nifedipine vehicle was without effect at the infusion rates tested. Infusion of diltiazem 2-200 micrograms/min (approximately 3 x 10(-7) to 3 x 10(-5) mol/l) also produced concentration-dependent reduction of left ventricular developed pressure. The ED50 for diltiazem-induced reduction of left ventricular developed pressure was significantly reduced by elevated [K]+: 20.1 +/- 6.7 and 3.5 +/- 0.9 micrograms/min with 3 and 9 mmol/l [K]+, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of hyperkalemia on myocardial depression by verapamil in isolated hearts. 826 19

The aim of this study was to examine the effect of initial hyperkalemic reperfusion (HKR), with and without added adenosine, on coronary flow, myocardial function, and endothelium-dependent and endothelium-independent coronary vascular function. Cardioplegic arrest was induced in 40 isolated guinea pig hearts by infusing oxygenated cardioplegic (high in potassium ion) Krebs solution for 5 minutes. Hearts were then stored at room temperature for 3.5 hours. On reperfusion, hearts were divided into four groups of 10 hearts each: control, reperfusion with regular Krebs solution (4.6 mmol/L potassium chloride); base hyperkalemic reperfusion, initial reperfusion with 37 degrees C oxygenated, cardioplegic Krebs solution for 5 minutes; hyperkalemic reperfusion with addition of 1 mmol/L adenosine during HKR; and hyperkalemic reperfusion with addition of 5 mmol/L adenosine. Coronary reserve (adenosine bolus 2 mmol/L) and responses to acetylcholine (1 mumol/L) and nitroprusside (100 mumol/L) were examined before and after ischemia and reperfusion. Flow did not return to preischemic values in any group after reperfusion. Adenosine treatment during initial reperfusion increased coronary flow (percentage of baseline +/- standard error of the mean) from 57% +/- 4% in control and 45% +/- 3% in hearts with hyperkalemic reperfusion to 79% +/- 3% and 83% +/- 5% in hearts with hyperkalemic reperfusion also treated with, respectively, 1 mmol/L adenosine and 5 mmol/L adenosine (p < 0.05). At 30 and 60 minutes of reperfusion, however, flow remained elevated only in the group treated with 5 mmol/L adenosine. Coronary reserve and responses to acetylcholine and nitroprusside were equivalently depressed in all groups after reperfusion. Recovery of left ventricular systolic and diastolic function was improved in all groups after hyperkalemic reperfusion (54% +/- 4% of preischemic value) compared with control (39% +/- 3%), and recovery was further enhanced in the group treated with 5 mmol/L adenosine (60% +/- 4%). In this ex vivo model, hyperkalemic reperfusion improved myocardial function after cardioplegic arrest and the addition of 5 mmol/L adenosine improved coronary flow. Adenosine may counteract the potassium chloride-induced vasoconstriction that occurs during hyperkalemic reperfusion and may thus improve coronary flow and myocardial function. Postischemic depression of endothelium-dependent or endothelium-independent vascular functions, however, was not alleviated by hyperkalemic reperfusion with or without adenosine.
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PMID:Improvement in functional recovery of the isolated guinea pig heart after hyperkalemic reperfusion with adenosine. 855 91

Adenosine is an endogenous cardioprotective substance. The present study examines whether exogenous adenosine attenuates cardiac injury induced by oxidative stress. Rat hearts (Langendorff model) were perfused with H2O2 (180 microM) for 10 min, then recovered for 60 min (n = 10). In other groups adenosine 55 microM, 11 0 microM, or 220 microM (n = 10 in each) was given in addition to H2O2 throughout perfusion. Control perfusion with Krebs Henseleit only (n = 7), adenosine 110 microM throughout perfusion (n = 7), and adenosine 110 microM as an intervention (n = 7) was performed. The hearts were paced at 320 beats/min. Left ventricular systolic (LVSP) and end-diastolic (LVEDP) pressures were measured together with coronary flow (CF), and left ventricular developed pressure (LVDP = LVSP - LVEDP) was calculated. H2O2 decreased LVSP from 105 +/- 8 to 60 +/- 5 mmHg (mean +/- SEM) after 10 min infusion (p < 0.008). Adenosine did not attenuate the decrease of LVSP. LVEDP increased from 0 to 59 +/- 10 mmHg (p < 0.004) and 62 +/- 11 mmHg 5 and 15 min after end of infusion of H2O2, respectively. Neither 55 microM nor 220 microM adenosine inhibited the H2O2-induced increase of LVEDP. Adenosine 110 microM attenuated the increase after 15 (15 +/- 4 mmHg, p < 0.004) and 25 min observation (26 +/- 7 mmHg, p < 0.012). Adenosine did not attenuate the reduction of LVDP. CF initially increased during infusion of H2O2, thereafter decreased. Hearts given adenosine had higher basal CF, and CF did not increase after H2O2. Control perfusion with adenosine, given throughout perfusion or as an intervention, increased CF and tended to increase LVSP. In summary, adenosine did not inhibit H2O2-induced depression of contractility or reduction of CF. One concentration of adenosine (110 microM) attenuated H2O2-induced impairment of relaxation. Exogenous adenosine does not have an important influence on functional injury caused by exogenous oxidants.
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PMID:The effect of exogenous adenosine on functional injury caused by hydrogen peroxide in the isolated rat heart. 874 90


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