Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet-activating factor (PAF; 1-alkyl-2-acetyl-glycero-phosphocholine) is a biologically active phospholipid which is synthesized by a variety of blood cells and organ systems. PAF exerts many effects on the cardiovascular system including hypotension, depression of myocardial contractility and coronary constriction. The present study has examined the capacity of the guinea-pig heart to regulate the levels of exogenous PAF in two different models: isolated perfused heart and isolated ventricular myocytes. In the first model, isolated hearts were perfused with labeled PAF (10(-10) M) in a recirculating manner at flow rates of 15 ml/min (normal flow perfusion; NFP) and 2 ml/min (low flow perfusion, LFP). Exogenously provided PAF appeared in the tissue in a time-dependent manner. The rate of extraction of PAF was higher during LFP than during NFP. PAF was metabolized by the heart to two major products, lyso-PAF and 1-alkyl-2-acyl-sn-glycero-3-phosphocholine (1-alkyl-2-acyl-GPC). Lyso-PAF was found primarily in the perfusion buffer while both lyso-PAF and 1-alkyl-2-acyl-GPC were detected in the tissue. No qualitative difference in the metabolic products derived from PAF catabolism was observed between hearts undergoing NFP and LFP. Acetyl hydrolase activity was detected in the perfusion fluid at both flow rates, probably accounting for the formation of lyso-PAF in the perfusate. However, perfusion fluid from LFP contained a higher acetyl hydrolase activity, per micrograms of protein as compared to fluid from NFP. Isolated ventricular myocytes incubated with labeled PAF (3 x 10(-9) M) also converted it to 1-alkyl-2-acyl-GPC. Kinetic experiments suggested that PAF was initially deacetylated to form lyso-PAF and that this intermediate was then rapidly reacylated with a fatty acyl moiety at the sn-2 position. HPLC analysis of the fatty acids inserted at the sn-2 position of 1-alkyl-2-acyl-GPC revealed that the myocytes reacylated lyso-PAF predominantly with arachidonic acid. These data indicate that the guinea-pig heart may regulate PAF levels by at least two mechanisms: (1) it may release acetyl hydrolase into the vascular compartment, particularly under low flow conditions; and (2) the ventricular myocyte has the capacity to take up PAF and catabolize it to inactive products.
J Mol Cell Cardiol 1992 Oct
PMID:Metabolism of platelet-activating factor in the guinea-pig heart. 147 12

We studied 266 consecutive patients with acute myocardial infarction to assess the significance of electrocardiographic "mirror images". Ninety-four (group A) had anterior wall and 132 (group B) had inferior wall infarction. Thirty-one group A patients had stenosis of the right coronary artery greater than 85% in diameter (subgroup A1), and 63 either had a normal right coronary artery or less than 85% stenosis (subgroup A2). Of group B patients 62 had greater than 85% stenosis of the left anterior descending (subgroup B1) and 70 had a left anterior descending or less than 85% stenosis (subgroup B2). ST-segment depression was significantly greater in depth and duration in subgroup A1 than A2 (p = 0.02) and in subgroup B1 than B2 (p = 0.02, p = 0.01, respectively). Left ventricular ejection fraction was lower in subgroup A1 than A2 (p less than 0.001) and in B1 than B2 (p less than 0.001). There was a strongly positive correlation between depth and duration of ST-segment depression and the Gensini index (r = 0.78, 0.84) for anterior and inferior infarction, respectively. In conclusion, increased depth and duration of ST-segment depression opposite the infarct are indicative of ischemia, and are related to the extent of coronary artery disease, the degree of stenosis of the vessels supplying the opposite wall and of left ventricular dysfunction.
Int J Cardiol 1992 Aug
PMID:Correlation of reciprocal ST-segment depression after acute myocardial infarction with coronary angiographic findings. 151 54

1,1,1-Trichloroethane is a widely used solvent that is annually linked to several cases of sudden death following accidental exposure or abuse. Sudden death is believed to be due to ventricular fibrillation or myocardial depression. The purpose of this study was to investigate the mechanism of myocardial depression by assessing the influence of 1,1,1-trichloroethane on intracellular Ca transients in single neonatal rat ventricular myocytes using spectrofluorometric analysis of fura-2-Ca binding. Cells were exposed to 1,1,1-trichloroethane in Hanks' balanced salt solution aliquoted as a 0.2% DMSO solution by a single pass suffusion in an environmentally controlled chamber. 1,1,1-Trichloroethane (0.25 mM-8 mM) reduced the height of electrically (1 Hz, 60 V, 10 ms) induced Ca transients concentration dependently and reversibly to a maximum of about 50% with no effect on diastolic Ca concentration. Video motion analysis revealed an inhibition of contractility in the same concentration range. 1,1,1-Trichloroethane inhibited cytosolic Ca increase in response to KCl-induced (90 mM) depolarizations and further decreased the limited Ca transients in ryanodine (1 microM) pretreated myocytes. Increased external Ca (5 mM) antagonized the effect of 0.5 mM 1,1,1-trichloroethane on the Ca transients. 1,1,1-Trichloroethane reduced the caffeine (10 mM) releasable Ca pool in myocytes. These results show that 1,1,1-trichloroethane inhibits Ca mobilization during excitation-contraction coupling in ventricular myocytes. An inhibitory action on the influx of extracellular Ca as well as on sarcoplasmic reticulum Ca release and sequestration is likely to be responsible for this action.
J Mol Cell Cardiol 1992 Jun
PMID:Calcium transients in isolated cardiac myocytes are altered by 1,1,1-trichloroethane. 151 78

Myocardial ischemia is associated with accumulation of lyso-phospholipids, including lyso-platelet activating factor, the degradation product and precursor of platelet activating factor. These compounds produce cellular and microvascular damage and, in the myocardium, depression of contractility and arrhythmia. The potent platelet activating factor antagonist, WEB 2086, or placebo, was infused (IV) 10 min before constriction of the proximal left anterior descending coronary artery in open-chest dogs. Two protocols were followed: the dose of WEB 2086 was 0.5 mg/kg in those subjected to 20 min ischemia with 10 min reperfusion (n = 40) and 5 mg/kg preceding 60 min ischemia alone (n = 24). There was no significant difference in the number of ventricular premature complexes between WEB 2086 and placebo treated dogs during either period of ischemia. On reperfusion in those surviving 20 min of ischemia, 5 of the 18 WEB 2086 and 9 of the 18 placebo treated dogs developed ventricular fibrillation (NS). After 60 min of myocardial ischemia, there was no statistical difference in histological changes (nuclear swelling, aggregation of chromatin, myofibrillar separation) between groups. Hence, no substantial effect of relatively large doses of WEB 2086 on ischemia-induced histological change or arrhythmia was found in this preparation.
J Mol Cell Cardiol 1992 Jun
PMID:The effects of a PAF antagonist on ischemic myocardial damage and arrhythmia in the dog. 151 80

This study was conducted to determine the zinc status and assess relationship between serum zinc and in vivo cell mediated immunity (CMI) in patients with rheumatic heart disease (RHD). The study comprised 22 patients with active rheumatic heart disease (ARHD), 15 patients with chronic rheumatic heart disease without activity (CRHD) (selection based on Jone's Criteria--Revised), and 15 age and sex matched healthy control. Zinc estimation was done by atomic absorption spectrophotometer. To assess CMI in vivo, phytohaemagglutinin skin test and skin window test were done. Serum zinc and in vivo CMI in patients with ARHD and CRHD compared with controls. Mean serum zinc was significantly decreased in patients with ARHD and CRHD, more pronounced in the former (P less than 0.001); and mean 24 h urinary zinc was significantly increased in patients with ARHD (P less than 0.001) as compared to controls. A significant depression in CMI in vivo was observed in patients with ARHD and CRHD (P less than 0.001). A significant positive correlation was seen among serum zinc and markers of in vivo CMI (P less than 0.001). In conclusion, depletion of zinc, observed in RHD, probably causes immune alterations and suggest role of zinc in immunopathogenesis of RHD. Zinc supplementation may alter the course of rheumatic fever and RHD.
Acta Cardiol 1992
PMID:A correlative study of serum zinc and in vivo cell mediated immune status in rheumatic heart disease. 152 10

Of 150 consecutive patients with sustained monomorphic ventricular tachycardia (VT) (n = 116) or ventricular fibrillation (VF) (n = 34) late after acute myocardial infarction, 17 had reproduction of their sustained monomorphic VT during exercise testing. Data from these patients (group I) were compared with data from patients without exercise-induced VT (group II). No statistical difference was found between groups I and II with relation to age, sex, number of vessels with greater than 70% stenosis, left ventricular ejection fraction, number of previous myocardial infarctions, inducibility during programmed stimulation and total mortality during follow-up. In group I, only 1 patient (6%) developed ST depression during exercise compared with 47 patients (35%) in group II (p less than 0.01). After a 34-month mean follow-up, 6 patients in group I (35%) and 18 patients in group II (13%) died suddenly (p = 0.02). It is concluded that sustained monomorphic VT is reproduced during exercise in only 11% of patients with spontaneous late sustained monomorphic VT or VF. Electrocardiographic findings do not support ischemia as a triggering mechanism of exercise-induced sustained monomorphic VT. Patients with exercise-induced sustained monomorphic VT have a high incidence of sudden death.
Am J Cardiol 1992 Oct 01
PMID:Incidence, pathophysiology and prognosis of exercise-induced sustained ventricular tachycardia associated with healed myocardial infarction. 152 40

The accuracy of ST/heart rate (ST HR) index was evaluated in patients presenting for exercise electrocardiography with suspected coronary disease. In all, 420 patients (235 men and 185 women) with normal electrocardiograms at rest underwent exercise testing, followed within 3 months by coronary angiography. The sensitivity and specificity for standard ST criteria (greater than or equal to 1 mm horizontal or downsloping depression) were 48% (78 of 162) and 81% (208 of 258), respectively. An ST HR-index threshold of 1.86 microV/beta/min had the exact same specificity with a sensitivity of 44% (71 of 162; p = not significant). Consideration of greater than or equal to 1.5 mm upsloping depression had no significant impact on the aforementioned results. Using multivariate logistic regression analysis, age, sex, symptoms, cigarette smoking, diabetes mellitus, qualitative ST slope, rate-pressure product, METs achieved and exercise angina were evaluated with and without ST HR index and ST depression. According to this analysis, age, sex, symptoms and ST slope were good predictors of presence or absence of disease. Neither ST HR index nor ST depression had significance in the multivariate analysis. However, when a separate analysis was performed in men and women, the 2 quantitative ST variables showed significance in men, but not in women. Comparisons of discriminative accuracy using receiver-operating characteristic curves demonstrated differences between men and women, but no difference between ST HR index and ST depression. Therefore, concerning questions of coronary disease diagnosis, consideration of ST HR index was not better than standard ST criteria, and added nothing to multivariate analysis of other available variables.
Am J Cardiol 1992 Mar 01
PMID:Accuracy of ST/heart rate index in the diagnosis of coronary artery disease. 153 8

Long-term variation in the frequency of myocardial ischemia during daily activity in patients with coronary artery disease who do not experience symptomatic changes has not been documented. Because at one point in time, the magnitude of such ischemia is strongly related to the ischemic threshold measured during exercise testing, this study was undertaken to determine whether patients with stable coronary artery disease show long-term variations in the frequency and duration of myocardial ischemia and to establish whether such variability is related to parallel changes in the ischemic threshold during exercise testing. Forty consecutive patients (mean age 61 +/- 8 years) who showed a stable clinical course over greater than or equal to 12 months were studied with a repeat exercise treadmill test and ambulatory electrocardiographic (ECG) monitoring after withdrawal of antianginal medications. The ischemic threshold was determined as the exercise time at 1 mm of ST segment depression. The mean interval to both follow-up evaluations was 15 +/- 3 months. Among the 23 patients with myocardial ischemia on ambulatory ECG monitoring at initial evaluation, the number and duration of ischemic episodes at follow-up were increased in 5 patients (mean increase 3.6 +/- 2 episodes and 123 +/- 98 min), unchanged in 1 patient and decreased in 17 patients (mean decrease 2.6 +/- 2 episodes and 98 +/- 72 min). Of the 17 patients without ischemic episodes at initial evaluation, 3 had evidence of ischemia on follow-up ambulatory ECG monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1992 Mar 01
PMID:Long-term variation in myocardial ischemia during daily life in patients with stable coronary artery disease: its relation to changes in the ischemic threshold. 153

There is scant information regarding the effect of exercise training begun soon after hospital discharge for myocardial infarction (MI) with respect to subsequent improvement in exercise tolerance, enhancement of regional myocardial perfusion, or left ventricular function. Accordingly, 19 post-MI patients (mean age 53 +/- 7 years) underwent treadmill exercise quantitative thallium-201 (Tl-201) scintigraphy and rest radionuclide angiography (RNA) prior to and after 12 weeks of thrice-weekly exercise training which was targeted to 70-85% of maximum exercise heart rate achieved. Training was begun at 25 +/- 3 days after hospital discharge. Eight Tl-201 scan segments were each scored from 1-6 points based upon uptake and washout criteria with 6 being the most severe defect (greater than 50% reduction in Tl-201 events with no delayed redistribution). When matched to the pretraining peak workload on exercise testing, 12 weeks of training significantly lessened heart rate (120 +/- 4 to 97 +/- 4, p less than 0.001), peak systolic blood pressure (142 +/- 6 to 129 +/- 5 mmHg, p less than 0.01), and significantly reduced double product [17.2 +/- 10.8 to 12.7 +/- 9 (x10(3), p less than 0.001]. Training was associated with a reduction of exercise-induced ST depression or angina (42 to 16%) which was not statistically significant. The mean resting by RNA ejection fraction was 50 +/- 3% prior to training and 51 +/- 3% after training. There was no significant change in overall Tl-201 defect score or the number of defect regions per patient scan comparing pre- and post-training scintigrams.(ABSTRACT TRUNCATED AT 250 WORDS)
Clin Cardiol 1992 Jan
PMID:Influence of exercise training soon after myocardial infarction on regional myocardial perfusion and resting left ventricular function. 154 Oct 70

Silent ischemia after myocardial infarction has definite prognostic significance but should be interpreted within the context of other prognostic indicators. The rationale for therapeutic intervention is based on the prognostic implications of silent ischemia and the potentially deleterious effect of repeated episodes of ischemia on the integrity of the left ventricle. We measured parameters of ischemia in 20 patients who showed asymptomatic ischemic ST-T changes on exercise testing in the early phase after myocardial infarction. After diltiazem administration, a reduction of exercise-induced ST-T depression from 2.3 +/- 0.8 to 0.7 +/- 0.6 mm (p less than 0.01) occurred, and regional wall-motion score at exercise, determined by radionuclide angiography, improved significantly (p less than 0.02). These and other observations warrant further studies in which the duration, severity and frequency of the ischemic episodes should be quantified and correlated with prognosis after myocardial infarction.
Am J Cardiol 1992 Mar 06
PMID:Silent myocardial ischemia after acute myocardial infarction. 154 37


<< Previous 1 2 3 4 5 6 7 8 9 10