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We investigated the changes in the cardiovascular system [resting blood pressure (BP) and heart rate (HR), measured by means of a 24-h ambulatory BP and a holter-electrocardiogram (ECG)], glycemic parameters, and lipid metabolism of subjects suffering from metabolic syndrome during a 3-week sojourn at 1,700 m in the Austrian Alps. A total of 22 male subjects with metabolic syndrome were selected. Baseline investigations were performed at Innsbruck (500 m above sea level). During the 3-week altitude stay the participants simulated a holiday with moderate sports activities. Examinations were performed on days 1, 4, 9, and 19. After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days and 6-7 weeks, respectively. The 24-h ambulatory BP and holter ECG revealed a decrease in average HR, BP, and rate pressure product (RPP: systolic blood pressure x HR) after 3 weeks of altitude exposure. In some patients, an increase in premature ventricular beats was observed at the end compared to the beginning of the exposure to moderate altitude. The ECG revealed no ischemic ST-segment changes. Maximal physical capacity as measured by symptom-limited maximal cycle ergometry tests remained unchanged during the study. Six weeks after the altitude exposure the blood pressure increased again and returned to pretest levels. The Homeostasis Model Assessment index, which is a measure of insulin resistance, decreased significantly and glucose concentrations obtained after an oral glucose tolerance test were significantly lower after the stay at altitude compared to the basal values. We conclude that after a 3-week exposure to moderate altitude, patients with metabolic syndrome (1) tolerated their sojourn without any physical problems, (2) exhibited short-term favorable effects on the cardiovascular system, and (3) had significant improvements in glycemic parameters that were paralleled by a significant increase in high-density-lipoprotein-cholesterol.

The activity of the sympathetic nervous system during the course of severe closed head injury has been evaluated in 15 patients by measuring plasma levels of epinephrine and norepinephrine. With the onset of the transition stage from midbrain syndrome to the apallic syndrome the plasma levels mainly of norepinephrine started to increase and remained high during the further course of the disease. During the remission from the apallic syndrome the elevated norepinephrine levels started to decline. The data indicate that a longlasting overactivity of the sympathetic nervous system is a characteristic feature in the course of severe head injury. As a rational therapy to protect the peripheral tissues against the consequences of a longlasting sympathetic overactivity we suggest the use of beta-adrenergic blocking agents and adrenergic neuron blocking drugs.

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Radcliffe Infirmary, Oxford OX2 6HE I An existing radioenzymatic assay for plasma catecholamines using catechol-o-methyl transferase and 13HI-S-adenosyl-methionine has been modified resulting in a more sensitive assay for the measurement of plasma adrenaline and noradrenaline. 2 The lower limit of sensitivity for this method is 25 pg for adrenaline and 30 pg for noradrenaline/ml of plasma. 3 Resting supine (60 min) plasma adrenaline concentration was (mean ± s.d.) 124 + 76 pg/ml (n= 11) in males and 130 ± 71 pg/ml (n = 7) in females; plasma noradrenaline concentrations were respectively 444 + 129 pg/ml and 550 ± 87 pg/ml. 4 The changes in plasma catecholamine concentrations in response to 40°head-up tilt have been determined in a group of healthy normal subjects and have been shown to be related to changes in blood pressure and heart rate.

Adrenaline and noradrenaline concentrations in arterial and simultaneously collected "arterialised" capillary plasma (vasodilated ear-lobe) obtained from unmedicated resting subjects (n = 9) were measured radio-enzymatically and found to be indistinguishable (adrenaline: 112 +/- 42 ng/l versus 109 +/- 52 ng/l; noradrenaline: 378 +/- 174 ng/l versus 410 +/- 219 ng/l; mean +/- SD; paired t-test: P greater than 0.10). The fitted regression lines did not differ significantly from the line of identity (slope = 1). The correlation coefficient was 0.969 for adrenaline and 0.945 for noradrenaline. Adrenaline and noradrenaline concentrations in plasma from freely flowing capillary blood (non-hyperaemic fingertip) were very similar to those in arterial plasma (adrenaline: 101 +/- 89 ng/l versus 90 +/- 72 ng/l;noradrenaline: 399 +/- 240 ng/l versus 395 +/- 240 ng/l; n = 13 each; paired t-test: P greater than 0.10). The correlation coefficient was 0.981 and 0.917 for adrenaline and noradrenaline, respectively. Adrenaline concentrations in capillary plasma (vasodilated earlobe), however, were significantly higher than those in venous (forearm) plasma (100 +/- 51 ng/l versus 61 +/- 23 ng/l; n = 15; P less than 0.01; capillary-venous difference = 35 +/- 18%) while noradrenaline concentrations did not differ significantly. We conclude that capillary plasma resembles arterial plasma in its catecholamine content and we show that arterial catecholamine levels may be determined in capillary, especially "arterialised" specimens, eliminating the need for arterial blood sampling.

No satisfactory explanations have been offered for the smoker's paradox, the greater short-term survival of smokers after a myocardial infarction nor for the large variations in the coronary risk rate for smoking ranging between 1 and 5.9. These discrepancies as well as the smoker's paradox may be caused by different baseline characteristics of smokers and nonsmokers, whereas the usually quoted coronary risk of 2 is derived from studies based on the assumption of equal baseline characteristics. As neither this assumption nor the possibility of unequal starting conditions have been tested, we examined the main cardiovascular risk factors in smoking and nonsmoking boys as near as possible to baseline, at the age of fourteen. This age appeared to be best suited, because boys starting to smoke early are most likely to become regular and heavy smokers. Of 336 boys, 39 had smoked 8.3+/-6.0 cigarettes/day for 15.5+/-11.2 months. Compared to nonsmokers, boys who started to smoke early had lower LDL cholesterol and alpha2-antiplasmin, greater handgrip strength, vital capacity and forced expiratory volume, better perfomance on bicycle ergometry and higher testosterone. The differences in total cholesterol, LDL cholesterol, vital capacity, handgrip strength, testosterone and alpha2-antiplasmin persisted after adjustment for age, body mass, and testosterone. In addition, the differences in perfomance on bicycle ergometry and forced expiratory volume persisted after adjustment for age. These favourable baseline characteristics of those starting to smoke early can explain the smoker's paradox. In addition, they suggest that the individual coronary risk in smokers is considerably higher than 2, because the assumption of equal baseline characteristics of smokers and nonsmokers cannot be upheld.