[Autonomic and peripheral neuropathies in diabetic patients: correlation with clinical aspects and duration of diabetes and with ocular complications].
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Biomedical subjects
Publications and source records attributed to A Scheen.
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A double-blind placebo-controlled trial was conducted, involving 97 obese diabetic and glucose intolerant patients receiving either 60 mg fluoxetine daily (47 patients) or a placebo (50 patients); a similar calorie-restricted diet was prescribed to all patients. Weight loss was significantly higher in the fluoxetine-treated patients, whose diabetic status improved. Drop-out rate was not significantly different for both groups of patients.
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The effects of beta-adrenergic blockade on the exercise-induced hyperlactatemia (Lap) have been studied in 31 adult male subjects [age: 25 +/- 1 years; body weight: 69 +/- 1 kg; VO2max: 54 +/- 1 ml O2.kg-1.min-1 (mean values +/- SEM)] randomly divided in 3 groups. All exercises were performed on a 10% inclined treadmill. In group 1 (n = 11), the subjects were walking during 20 minutes at 5 km.h-1 (55.6 +/- 1.4% VO2max). In group 2 (n = 10), they were running during 9 minutes at 8 km.h-1 (79.4 + 1.5% VO2max). The subjects of the third group (n = 10) were submitted to a 4 minutes run at 9.5 km.h-1 92 +/- 1.6% VO2max). These exercises were performed 1 hour after ingestion of a placebo or a single dose of 40 mg propranolol, in a double-blind randomized order. Blood samples were drawn at regular time intervals from an antecubital vein. Exercise tachycardia was reduced by about 20% (P less than 0.001) by propranolol in each group. Lap was significantly reduced by 15% by propranolol (P less than 0.005) at the lowest exercise intensity (55.6% VO2max), remained unchanged at 79.4% VO2max and was significantly enhanced by 16% during the recovery period following the run at 92% VO2max. These results clearly showed that the effects of acute beta-adrenergic blockade on Lap depend on exercise intensity.
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Eleven normal subjects underwent epinephrine perfusions (1.9; 6.1; 11.8 ng/min) during a short (20 min) and mild (50% VO2 max) exercise. VO2 was not modified by epinephrine perfusion, while heart rate ventrilation and plasmatic lactate were increased proportionally to epinephrine doses.
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The slow increase in heart rate which is observed in normal man submitted to heavy muscular exercise is due for a part to an activation of orthosympathetic cardiac activity which is blocked by beta antagonists. It is also explained by direct action of hyperthermia on the heart.
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VO2 max, maximum oxygen uptake, has been measured in 4 normal young men, before and after beta-adrenergic blockade (0.5 to 5 mg Pindolol by mouth). Pindolol induces bradycardia and reduces VO2 max. A statistically significant positive correlation appears between posology of Pindolol and bradycardia, this posology and reduction of VO2 max, and finally between bradycardia and reduction of VO2 max. These correlations indicate that the reduction of VO2 max is best explained by a circulatory limitation of oxygen supply to active muscles.
In normal man, food ingested two hours before the beginning of physical exercise increases the lactacidemia (+ 27%).
In normal subjects, beta-adrenergic blockage by propranolol or pindolol reduces exercise hyperventilation (40 to 60% VO2 max).