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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 68 (1990), S. 320-323 
    ISSN: 1432-1440
    Keywords: Blood pressure ; Hypertension ; Sleep ; Waking up ; Antihypertensive therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The coincidence of the circadian peak of cardiovascular events with the morning blood pressure rise suggests causal connections. Rapidly acting antihypertensives taken before getting up may attenuate the increase early enough, if the onset does not occur before awakening. In 111 normotensives and in 109 subjects with untreated essential hypertension ambulatory blood pressure monitoring was performed to study whether the onset of the blood pressure rise occurs before or after waking up. The individual 24 h blood pressure profiles obtained by intermittent readings at intervals of 15 minutes were synchronized by the time of waking up. The resulting blood pressure curves showed no substantial blood pressure rise during sleep, but steep increases after awakening: Within the first hour after waking up blood pressure increased from 107.3+11.4/62.3±9.6 mm Hg (mean+sd) to 121.4±16.0/75.3+12.6 mm Hg in normotension and from 124.7+16.0/72.7+12.2 mm Hg to 140.3+17.2/84.5+13.3 mm Hg in hypertension. The velocity of this increase was dependent on the lag between waking up and getting up. There was no phase difference between early morning blood pressure and heart rate rises. Thus to attenuate the morning blood pressure increase, rapidly acting drugs after awakening may be considered instead of long acting antihypertensives administered prior to sleep.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 70 (1992), S. 142-147 
    ISSN: 1432-1440
    Keywords: Erythropoietin ; Acute renal failure ; Thrombotic thrombocytopenic purpura
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In this study, erythropoietin serum levels were serially determined in eight patients with acute renal failure to get a lead on the etiology of anemia in acute renal failure and to address the relationship between erythropoietin synthesis and renal excretory performance. Erythropoietin serum levels rapidly decreased after onset of acute renal failure to values of 12.8 ± 10.3 mU/ml compared to 16.8 ± 9.4 mU/ml in healthy controls. After restoration of renal function, erythropoietin levels climbed slowly in six patients (15.2 ±5.3 mU/ml), and in relation to prolonged anemia in these patients, a relative deficiency of erythropoietin could be observed. In one patient with thrombotic thrombocytopenic purpura causing acute renal failure, the decline of erythropoietin secretion was not observed, and in a phase of the disease when plasma exchange therapy was interrupted, markedly increased erythropoietin levels, up to 182 mU/ml, were detected despite the renal failure. Focusing on erythropoietin secretion in thrombotic thrombocytopenic purpura, we followed hormone synthesis in two other patients with the same disease, one of whom had mild renal insufficiency and one had normal renal function. High erythropoietin levels of up to 205 mU/ml were found in these patients, similar to the peak levels found in the patient with complete renal failure. Plasmapheresis treatment reduced erythropoietin production in all three patients with thrombotic thrombocytopenic purpura. In summary, our study indicates that in most cases of acute renal failure, erythropoietin synthesis is compromised and may contribute to the development of anemia in renal failure and aggravate the persistence of anemia after restoration of renal function. Comparing erythropoietin production in patients with acute renal failure and in those with thrombotic thrombocytopenic purpura with varying renal involvement we conclude that erythropoietin secretion is not closely linked to renal excetory performance, and that hemolysis or other stimuli in thrombotic thrombocytopenic purpura can override the decline of erythropoietin production implied by renal failure.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    International archives of occupational and environmental health 61 (1989), S. 463-466 
    ISSN: 1432-1246
    Keywords: Shift work ; Night shift ; Blood pressure ; 24-h blood pressure monitoring ; Circadian rhythm
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The dependence of blood pressure upon internal rhythms and the short-term effects of shift rota on the blood pressure were investigated in shift workers. Blood pressure was measured every 30 min using automatic recorders for 24 h in 17 physically working men in a chemical factory during their morning and night shifts. Mean 24-h blood pressures were identical in the morning and night shifts. There were no differences of the mean blood pressure between the respective sleeping phases or between the working periods. The amplitudes of circadian blood pressure variations were equal. There was a phase difference of 8 h corresponding to the lag between the working periods. At this 8-h lag the hourly means of the 24-h blood pressure were closely correlated (r = 0.69). Comparisons of 24-h blood pressure profiles during the first and last days of a night shift week showed that the effects of night work on the blood pressure were already fully developed within the first 24h (r = 0.86). Thus the diurnal variations of the blood pressure are determined by the working and sleeping periods and largely independent of endogenous rhythm. There is no short-term alteration of the mean 24-h blood pressure after shift rota.
    Type of Medium: Electronic Resource
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