Aggression and personality: association with amino acids and monoamine metabolites.

Associations in 52 normal individuals were examined between plasma and cerebrospinal fluid (CSF) concentrations of tryptophan (Trp) and tyrosine, and concentrations of monoamine metabolites in the CSF, and scores on an aggression questionnaire, the Kinsey Institute Reaction List II, and the Eysenck Personality Questionnaire. There was a significantly positive correlation between CSF 5-hydroxyindoleacetic acid (5-HIAA) levels and extroverted aggression scores, and a significantly negative correlation between CSF 5-HIAA levels and introverted aggression scores. Males showed higher plasma Trp concentrations than females, and significantly positive correlations between plasma Trp concentrations and scores on extroverted aggression and the Eysenck E scale. Males, furthermore, showed a significantly negative correlation between CSF Trp levels and scores on the Eysenck P scale, and a significantly positive correlation between concentrations of 3-methoxy-4-hydroxy-phenylglycol in CSF and scores on moral aggression. These results suggest that central serotonin influences aggression in normal individuals through effects on personality.

Effect on collagen metabolism of thrombolytic therapy with tissue-plasminogen activator. A randomized, placebo-controlled study.

This paper assesses alterations in collagen metabolism following thrombolytic therapy of acute myocardial infarction with tissue-plasminogen activator. Sequential serum measurements of the amino-terminal propeptide of type III procollagen (S-PIIINP) and the carboxyterminal propeptide of type I collagen (S-PICP) in patients suspected of acute myocardial infarction randomized to tissue-plasminogen activator or placebo were used. S-PIIINP increased at 3 h in patients with acute myocardial infarction treated with tissue-plasminogen activator (P < 0.05). S-PIIINP was higher in patients treated with tissue-plasminogen activator compared with placebo-treated patients at 3 and 6 h (P < 0.05). S-PICP decreased independently of therapy and diagnosis. Tissue-plasminogen activator, therefore, induces breakdown of collagen, some of which is located in the wall of atheromatous arteries. Vascular patency following thrombolytic therapy may partly be mediated by breakdown of thrombogenic collagen in the vessel wall. The findings may suggest a role for S-PIIINP as a non-invasive indicator of the risk of reocclusion.

Localization of thermogenesis induced by single infusion of ephedrine in dog.

The localization of the thermogenic effect of ephedrine (1 mg.kg-1 infused intravenously over 10 min.) was studied in 6 fasted dogs anaesthetized with etorfin-acepromazin-N2O. Three experiments were performed in each animal to determine the effect of ephedrine on a) splanchnic oxygen uptake, b) lower leg oxygen uptake and c) the work of the heart. In all experiments whole body oxygen uptake was monitored. Following ephedrine administration the following significant changes were seen as whole body oxygen uptake increased 16%, and splanchnic and lower leg oxygen uptakes increased respectively from 38.4 to 42.3 and from 7.3 to 12.1% of the whole body control oxygen uptake. The pressure-volume work of the heart more than doubled. Significant changes were also seen in mean arterial blood pressure, pulse rate, cardiac output, splanchnic blood flow, and haematocrit and haemoglobin concentration. Plasma glycerol and free fatty acid concentrations increased after ephedrine, and the effects were not elicited by circulating catecholamines.

Atrial natriuretic factor during exercise in male endurance athletes: effect of training.

Nine male endurance runners were evaluated with bicycle exercise testing before a training break of 3 weeks duration, and 0, 2 and 4 weeks after resumption of training to assess the effects of training on resting and exercise plasma atrial natriuretic factor (ANF) measured at 50% and 100% of predetermined maximal workload. Maximal oxygen uptake and lean body mass (LBM) were calculated at each time point. Maximal oxygen uptake decreased during training break, but rose 4 weeks after resumption of training (P less than 0.01). LBM was unchanged after inactivity, but rose after resumption of training (P less than 0.01). Plasma ANF at rest did not change throughout the experiment. ANF levels rose after training break at maximal workload (P less than 0.05), and decreased 4 weeks after resumption of training, but only at submaximal workload (P less than 0.05). No correlations between systolic blood pressure, mean blood pressure or heart rate and ANF could be demonstrated. These results indicate that the haemodynamic changes associated with endurance training are reflected in plasma ANF levels during exercise, but not at rest. The full adaptation of ANF release to training probably requires more time than the 4 weeks reported for the haemodynamic adjustments.

[Drug abuse in body builders. A questionnaire study]. / Medicinmisbrug blandt bodybuildere. En spørgeskemaundersøgelse.

A questionnaire about the use of anabolic steroids (AS) was distributed in weight-training and sports centre's and was completed by 157 persons. In the group of 138 men, 85 had employed AS but only 60% had employed preparations registered in Denmark. In the group who consumed AS in connection with intensive training periods, average weights and heights were found lower at the commencement of the training and greater increase in weight in connection with training. In the group who consumed AS, participation in competitive sports was greater and higher protein supplements and more supplementary medicine were observed. The average maximal 24 hour dosage of AS was ten times greater than that recommended therapeutically and this dosage was consumed during approximately 1/3 of the year. Side-effects were such that 25% of the men consulted their doctors. Less than half of the consumers of AS had sought information about the effects and side-effects and only 40% had consulted their own general practitioners which suggests a considerable illegal market. An important aspect of the prophylactic activity appears to be information about the injurious effects of AS consumption which appears to be widespread in Denmark together with intensive muscular training.

Influence of magnesium substitution therapy on blood lipid composition in patients with ischemic heart disease. A double-blind, placebo controlled study.

In a double-blind, placebo-controlled study, 47 patients with ischemic heart disease and acute myocardial infarction were allocated to 3 months' treatment with peroral magnesium (15 mmol/d) or placebo. Before, during, and after treatment, blood samples were taken to determine serum concentrations of cholesterol; triglyceride; high-density, low-density, and very-low-density lipoprotein; apolipoprotein A1 and B; and magnesium. We found a 13% increase in molar ratio of apolipoprotein A1:apolipoprotein B after magnesium treatment, as compared with a 2% increase in the placebo group (for mean differences between changes of the magnesium and the placebo groups). This increase was caused by a decrease in apolipoprotein B concentrations, which were reduced by 15% from 1.44 to 1.23 mmol/L in the magnesium group as compared with a slight increase in the placebo group. Triglyceride, and thereby very-low-density lipoprotein concentrations decreased by 27% after magnesium treatment (from 2.41 to 1.76 mmol/L, and from 1.1 to 0.79 mmol/L, respectively) as compared with much smaller decrements in the placebo group. Likewise, we found tendencies toward an increase in high-density lipoprotein cholesterol and in high-density lipoprotein cholesterol ratio/(low-density lipoprotein cholesterol:very-low-density lipoprotein cholesterol) after magnesium treatment. The observed findings support the hypothesis that magnesium deficiency might be involved in the pathogenesis of ischemic heart disease by altering the blood lipid composition in a way that disposes to atherosclerosis.

Hemodynamic effects of intravenously administered magnesium on patients with ischemic heart disease.

Central hemodynamic parameters were registered by right-side heart catheterization before and after intravenous administration of 12 mmol magnesium chloride (MgCl) in 15 patients with chronic ischemic heart disease and heart failure, New York Heart Association classes II and III. Serum magnesium concentrations increased from 0.76 +/- 0.03 (mean +/- SD) to 1.54 +/- 0.05 mmol/l, which resulted in a reduction in mean arterial as well as pulmonary artery pressure by 10% (p less than 0.0001) and 7% (p less than 0.05), respectively. This reduction was caused by a marked decrease in systemic as well as pulmonary vascular resistance (from 1323 +/- 205 to 1132 +/- 158 dyn.s/cm5, p less than 0.001 and from 156 +/- 73 to 133 +/- 72 dyn.s/cm5 (p less than 0.05). Heart rate, cardiac index, stroke volume index, and stroke work index increased slightly, although these differences did not reach statistical significance. Right and left ventricular filling pressures were not influenced, which indicates that the dilatory effect of magnesium, at the dosages used in the present study, is pronounced only at the arterial side of the vascular bed. The observed hemodynamic effects of the magnesium infusions may be beneficial in the setting of an acute myocardial infarction by reducing left ventricular afterload, which, together with the antiarrhythmic effect of magnesium may contribute to the positive effect of magnesium infusions on mortality in patients with acute myocardial infarction.

Magnesium deficiency in patients with ischemic heart disease with and without acute myocardial infarction uncovered by an intravenous loading test.

An intravenous magnesium-loading test with 30 mmol/L of magnesium was used to evaluate the magnesium status in 38 patients with ischemic heart disease (IHD) admitted to the coronary care unit with suspected acute myocardial infarction (AMI), in ten healthy volunteers (control group), and in nine patients with chronic IHD in a stable phase of their disease (chronic IHD group). Sixteen of the patients admitted with acute disease proved to have AMI (AMI group) and 22 did not (non-AMI group). Patients with IHD both with and without AMI retained significantly more magnesium (9.3 and 10.7 mmol/L [22.6 and 26 mg/dL], respectively) than did the control group (1.4 mmol/L [3.4 mg/dL]). This 34% magnesium retention points to a state of magnesium deficiency in patients with IHD. However, since the patients with and without AMI did not differ, the observations do not indicate that AMI is associated with a more severe magnesium deficiency than that found in other IHD patients without AMI. When the patients with IHD were subgrouped according to long-term diuretic treatment, the patients (n = 19) receiving long-term diuretic treatment had a 39% retention of magnesium (11.6 mmol/L [28.2 mg/dL]) compared with a 29% retention (8.7 mmol/L [21.1 mg/dL]) observed in 19 patients who were not receiving long-term diuretic treatment. This observation was not influenced by the presence or absence of AMI. An even higher level of magnesium retention (17.1 mmol/L [41.6 mg/dL] equals 57% retention) was found when investigating patients with chronic ischemic heart disease in a stable phase of their disease. This indicates that patients with IHD may be severely magnesium deficient; that long-term diuretic treatment contributes to this deficiency, but that diuretic treatment per se is not the only cause of this condition.