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 biochemical mechanism of acute contractile failure in the hypoxic rat heart was investigated using phosphorus nuclear magnetic resonance to measure intracellular acidosis and the concentrations of phosphocreatine, adenosine triphosphate (ATP), and inorganic phosphate while cardiac mechanical function was simultaneously monitored. The cytosolic free [ADP] was calculated from the creatine kinase equilibrium expression. Mechanical activity, phosphocreatine and ATP concentrations, and intracellular pH all decreased after the onset of hypoxic perfusion. Neither a reduction in ATP concentration nor limitation in its rate of production contributed to the early contractile failure. Calculations suggest only a modest (approximately 10%) difference in cytosolic free energies of ATP hydrolysis. Neither the time course nor the extent of depression of mechanical function correlated well with intracellular acidosis. In conjunction with other observations, these results were consistent with the view that the myocardial inotropic state may be directly responsive to the ambient PO2. The overall rate of ATP turnover was assessed from measurements of oxygen utilisation and lactate production in both normoxic and hypoxic hearts. Surprisingly, despite more than an 80% reduction in mechanical activity during hypoxia, no significant decrease in the rate of ATP utilisation was noted during hypoxia. This suggests that unidentified non-contractile processes may hydrolyse ATP at relatively higher rates during hypoxia.
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PMID:Biochemical mechanisms of acute contractile failure in the hypoxic rat heart. 370 37

Forty-three consecutive patients with acute inferior transmural myocardial infarction but no history or electrocardiographic evidence of prior myocardial infarction were evaluated prospectively to assess the clinical and prognostic importance of persistent precordial (V1-V4) ST segment depression. Patients were evaluated within 24 hr of admission by history, physical examination, cardiac enzyme levels, right heart catheterization, and radionuclide angiography; all were followed for 1 year. Ten of the 43 patients (group I) had persistent anterior precordial ST segment depression, defined as 1 mm or greater in one or more precordial leads (V1-V4) 24 hr after admission to the coronary care unit, and 33 patients (group II) did not. Clinical variables that differed between groups I and II, respectively, included mean age (67 +/- 9 [+/- 1 SD] vs 59 +/- 8 years; p less than .01), incidence of Killip class II to IV (100% vs 33%; p less than .001), and average peak creatine kinase concentration (2878 +/- 1139 vs 1511 +/- 1034 IU/liter; p less than .001). Hemodynamic differences between groups I and II included a higher pulmonary arterial wedge pressure (19 +/- 4 vs 11 +/- 5 mm Hg; p less than .001) and a lower cardiac index (2.0 +/- 0.5 vs 2.6 +/- 0.7 liters/min/m2; p less than .05). An evaluation of left ventricular ejection fraction and wall motion index by radionuclide angiography showed that group I had a lower ejection fraction (44 +/- 11% vs 53 +/- 10%; p less than .05) and higher wall motion index (1.7 +/- 0.4 vs 1.4 +/- 0.3; p less than .05) compared with group II.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and prognostic importance of persistent precordial (V1-V4) electrocardiographic ST segment depression in patients with inferior transmural myocardial infarction. 370 78

This study examined the effects of ethanol and hereditary cardiomyopathy on sodium and water excretion by golden Syrian hamsters of both sexes. Ethanol (4 g/kg) or the isotonic saline vehicle were injected IP into 60-70-day-old hamsters of normal and cardiomyopathic (BIO 14.6) strains. Urine and blood were collected after 90 or 350 min in different groups. Cardiomyopathic hamsters more quickly lost their righting responses, eliminated ethanol more slowly, and had lower urine volume and sodium excretion than normal hamsters after ethanol injections. Plasma creatine kinase levels were normal in all animals tested, indicating no active skeletal or cardiac lesioning in the cardiomyopathic hamsters at the time of the experiment. Some factors which could contribute to the increased CNS and renal sensitivity to ethanol in cardiomyopathic hamsters include impaired ethanol metabolism, enhanced myocardial depression, and reduced atrial content of natriuretic peptides. The results do not owe to decompensated heart failure. Thus, the genetic mutation which causes skeletal and cardiac myopathy in these hamsters may also affect the metabolism and sensitivity to ethanol.
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PMID:Ethanol in cardiomyopathic hamsters: Na and water excretion and righting response. 371 87

The effects of 15 min periods of coronary occlusion on global and regional myocardial function, plasma creatine kinase (CK) and isoenzyme MB CK activity and subsequent myocardial necrosis were studied in 15 conscious dogs and 9 conscious baboons. Overall left ventricular (LV) function was assessed with measurements of LV systolic and diastolic pressures, rate of change of LV pressure, LV dP/dt. Regional LV function was assessed with measurements of regional segment length and velocity of shortening and/or regional LV wall thickening. An implanted hydraulic occluder on either the left anterior descending or circumflex coronary artery was inflated for 15 min. This induced complete loss of segment length shortening and systolic wall thickening (ultrasonic transit time technique). With release of the occlusion and reperfusion, recovery of regional mechanical function was delayed, but did occur after 6 hrs. Serial plasma enzyme activity revealed a significant increase in total CK as well as MB CK. At autopsy, neither gross pathological evidence (TTC-technique) nor histological evidence of myocyte necrosis was observed. Thus, in the conscious dog as well as in the conscious baboon, short episodes of intense myocardial ischemia do not result in a permanent deficit of myocardial function or necrosis. However, during the early phase of reperfusion, significant depression of regional mechanical function is observed associated with significant appearance of total CK and MB CK in the blood.
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PMID:Effects of brief periods of myocardial ischemia on regional myocardial function and creatine kinase release in conscious dogs and baboons. 375 86

Prompt management of patients suffering acute myocardial infarction requires accurate early diagnosis based on the electrocardiogram. To assess the predictive value of ST segment elevation and ST segment depression (both greater than or equal to 0.1 mV) for the diagnosis of evolving myocardial infarction, we studied 100 consecutive patients admitted to the coronary care unit of The New York Hospital with at least 30 minutes of chest pain. Of 31 patients with ST segment elevation, 26 patients (84%) evolved myocardial infarction (positive test results for serum creatine phosphokinase-MB isoenzyme fraction), while only 13 (48%) of 27 patients with ST segment depression had myocardial infarctions. Among patients with ST segment elevations with a history of prior myocardial infarction, only five (50%) of ten evolved myocardial infarction, compared with 21 of 21 with no prior infarction. False-positive diagnoses of acute injury were due to ST elevation in the area of prior Q wave infarction. Prior myocardial infarction did not alter the lower predictive value of ST segment depression for evolving infarction. We conclude that patients presenting with chest pain and ST segment elevation have approximately twice the likelihood of myocardial infarction than patients with ST segment depression; incorporation of historic information regarding prior myocardial infarction can improve the predictive value of ST segment elevations to 100% but does not improve prediction with ST segment depressions.
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PMID:Relationship of prior myocardial infarction to false-positive electrocardiographic diagnosis of acute injury in patients with chest pain. 381 42

Precordial ST-segment depression is typically observed in anterior non-Q-wave acute myocardial infarction (AMI), and is generally not regarded as an indication for acute thrombolytic therapy. Of 544 patients with creatine kinase (CK)-MB-confirmed non-Q-wave AMI randomized to the prospective multicenter Diltiazem Reinfarction Study, 50 patients (9.2%) had isolated precordial ST-segment depression of 1 mm or more in 2 or more contiguous precordial electrocardiographic leads (V1-V4). Serial electrocardiograms recorded at study entry (mean 50.5 hours after onset of chest pain), on study day 2, study day 3 and at predischarge showed that in 23 of 50 patients (40%) electrocardiographic evidence of posterior AMI evolved, defined as an R wave of 0.04 second or more in lead V1 and an R:S greater than or equal to 1 in lead V2. In 18 of these 23 patients (78%), posterior AMI had evolved by study day 3, and none had an abnormal reelevation of CK-MB (every 12-hour sampling) for up to 14 days of hospitalization. Compared with the remaining 27 patients who had electrocardiographic features of anterior non-Q-wave AMI only, the 23 with initial precordial ST segment depression in whom posterior AMI developed had significantly higher mean peak CK values (1,051 +/- 172 vs 663 +/- 89 IU, p less than 0.009) and greater mean precordial ST-segment depression in lead V1 (0.28 vs + 0.19 mm, p = 0.01), in lead V2 (1.3 vs 0.26 mm, p = 0.003) and in lead V3 (2.0 vs 0.93 mm, p = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrocardiographic evolution of posterior acute myocardial infarction: importance of early precordial ST-segment depression. 382 38

A group of 123 consecutive patients with acute transmural inferior myocardial infarction were compared according to the presence or absence of precordial ST segment depression on admission to hospital. There was a significant increase in mean age, peak creatine kinase levels, and the incidence of left ventricular failure and high grade atrioventricular block in the group with precordial ST segment depression. There was also an increase in in-hospital mortality in this group but this difference was not significant. Despite these differences in in-hospital progress, during a follow-up period of over two years there was no difference in long term mortality, recurrence of angina, or subsequent cardiac-related admissions between the two groups.
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PMID:Long term follow-up of inferior myocardial infarction. Prognostic significance of precordial ST segment depression. 386 34

It is now appreciated that mitochondrial creatine kinase (CKm) may play an important role in heart high-energy phosphate metabolism and that this isozyme is solubilized in vitro by dilute solutions of Pi. Since an increase in cellular Pi is known to occur with even brief periods of myocardial ischemia, we investigated the relationship between CKm activity and myocardial performance in rabbit hearts subjected to total global ischemia. CKm activity is expressed as a ratio to mitochondrial malate dehydrogenase (MDHm), a stable marker enzyme. A significant decline in this ratio was observed after only 10 min of ischemia, a time prior to changes in total homogenate creatine kinase activity. After 60 min of ischemia, the CKm/MDHm ratio was depressed by more than 70%. Since there was no restoration of activity following 30 min of reperfusion, we correlated changes in enzyme activity to contractile dysfunction following variable periods of total ischemia. The data showed a close correlation between the decline in the CKm/MDHm ratio and the reduction in performance, measured as left ventricular developed pressure. No correlation was observed between State 3 respiratory rates and performance. Using KCl arrest at 27 degrees C or hyperthermic ischemia at 40 degrees C, the CKm/MDHm ratio consistently correlated to the degree of postischemic functional depression, independent of the duration of ischemia. Isoenzyme electrophoresis failed to detect soluble CKm activity in the postischemic supernatant. Therefore, CKm activity appears to be altered rapidly and irreversibly by ischemia. The implications of these observations on the integration of myocardial high-energy phosphate metabolism are discussed.
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PMID:Creatine kinase of heart mitochondria. The progressive loss of enzyme activity during in vivo ischemia and its correlation to depressed myocardial function. 396 47

Anaesthesia was induced in 24 horses with xylazine and ketamine and maintained with halothane (12 cases) or enflurane (12 cases) in oxygen. Pulse rate, arterial blood pressure, arterial blood gas values, respiratory rate and tidal volume were measured at regular intervals during anaesthesia. Serial venous blood samples were taken for assay of glucose, urea, haemoglobin, packed cell volume, gamma glutamyl transpeptidase, aspartate aminotransferase, alanine aminotransferase and creatine kinase. Operating conditions and the horses' behaviour in the recovery period were also recorded. In the case of the group of horses receiving enflurane, difficulty was experienced maintaining anaesthesia deep enough for surgery. This group also displayed greater respiratory depression. There were no significant differences between arterial blood pressure values, or any of the haematological or biochemical parameters recorded in each group. Recovery from anaesthesia was significantly faster in horses receiving enflurane but less smooth. It was concluded that, although enflurane appeared to be safe in the horse, the respiratory depression and the unpleasant recovery did not make it a desirable alternative to halothane.
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PMID:Clinical anaesthesia in the horse: comparison of enflurane and halothane. 397 74

Electroconvulsive therapy (ECT) is an effective, safe, and controversial treatment of severe depression. In order to further evaluate its safety, the effect of ECT on serial electrocardiograms and serum cardiac enzyme values was studied prospectively in 29 patients. Neither persistent electrocardiographic changes nor elevations in creatine phosphokinase or serum glutamic oxalaminase transaminase levels were observed following 85 treatments. Twenty-four percent of our patients had stable, preexisting cardiovascular disease, which included conduction system disease, recent myocardial infarction, and depressed ventricular function. Electroconvulsive therapy was well tolerated by all of these patients. The proposed mechanisms for transient or persistent electrocardiographic changes and cardiovascular complications of ECT are reviewed.
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PMID:The effects of electroconvulsive therapy on serial electrocardiograms and serum cardiac enzyme values. A prospective study of depressed hospitalized inpatients. 398 80


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