Blood pressure and heart rate of 15 male shift workers were measured every 15 minutes for 24 hours during three work shifts: morning, 4:00 AM to noon; afternoon, noon to 8:00 PM; and night, 8:00 PM to 4:00 AM. For each shift, 24-hour systolic and diastolic blood pressure showed a large "trough" (the low pressure span) and a continuous range of elevated pressure (the high pressure span). Fourier series were used to model the 24-hour blood pressure profiles. A careful examination of the residuals (measured minus predicted pressures) showed that four harmonics were necessary to describe the data accurately. The model enabled localization in each blood pressure profile of the high and low pressure spans that did not coincide with the subject's work and rest periods. The time and slope of blood pressure entering and leaving these spans could also be individually determined. Mean blood pressure during the high pressure span was the same for the three shifts, but mean blood pressure during the low pressure span was lower when the subject worked in the afternoon. During that shift, the systolic blood pressure slopes entering and leaving the low pressure span were steeper than during the two other shifts. The high pressure span was longest during the night shift and shortest during the afternoon shift.Therefore, a change in the working time profoundly perturbed the 24-hour blood pressure profile. We conclude that internal regulation mechanisms, subjects' activities, and the circadian rhythm are the three main factors that govern a 24-hour blood pressure level; a complete change in the time of activities modifies the combined effects of these three factors. (Circulation 1989;80:341-347) S everal noninvasive semiautomatic or automatic devices are presently available that enable blood pressure and heart rate to be measured in ambulatory conditions over 24-hour periods at a frequency arbitrarily set in advance.
Cardiac output, blood pressure, and the characteristics of diastolic pressure decay were studied in 12 normal subjects and 23 sustained hypertensive patients of the same age. In normal subjects and in hypertensives, analysis of the diastolic decay showed that i) the form of the decay approximated a simple monoexponential curve during the last two-thirds of the diastolic segment, and ii) the time constant (t) of the curve was positively correlated with the total peripheral resistance (TPR), with an intercept of nearly zero. The validity of the relationship t = K x TPR was demonstrated both in groups of patients and also in individuals. Using a simple model for the vascular system, the K value was identified as the large arteries compliance and could thus be calculated in each individual. The values of arterial compliance was 1.26 +/- 0.04 ml.mmHg-1.m-2 in normal subjects and was significantly reduced in hypertensive patients (0.88 +/- 0.02 ml.mmHg=1.m-2,. P less than 0.001).
Because the use of spectral powers of blood pressure (BP) and R-R interval (RR) in the low (LF) and high frequencies (HF) to quantify sympathetic and parasympathetic activities is still under debate, we questioned whether nonlinear methods may give better results. The BP signal was recorded for 30 min before and after intravenous injection of hexamethonium (20 mg/kg), atropine (0.5 mg/kg), atenolol (1 mg/kg), and prazosin (1 mg/kg) in conscious, normotensive Wistar-Kyoto rats. Three nonlinear indexes [percentage of recurrence, percentage of determinism, and length index ( L max)] extracted from the recurrence plot method were used to analyze the BP signal. Sympathetic but not parasympathetic blockade reduced BP level and its LF component. RR increased and decreased after β- and α-blockades, respectively. Hexamethonium increased HF, and atropine reduced LF, of RR. Sympathetic blockade and, in particular, α-sympathetic blockade increased nonlinear indexes of BP. In contrast, parasympathetic blockade by atropine increased nonlinear indexes of RR. These results suggest that, compared with spectral indexes, nonlinear indexes may be more specific markers of sympathetic and parasympathetic tones.
In a rabbit model of Escherichia coli endocarditis, we studied the penetration into infected vegetations and the antibacterial effect of ceftriaxone. Ceftriaxone was given at different dosages, alone or with an interfering agent, diclofenac, a nonsteroidal anti-inflammatory drug, to determine the predictive value of the antibiotic levels in serum or infected vegetations on the antibacterial efficacy. Diclofenac increased the serum terminal half-life of ceftriaxone and increased its extravascular diffusion in tissue cage fluid, as well as in infected vegetations, allowing us to obtain various antibiotic concentrations in the infected site. Two hours after the fourth injection, around the time of peak level in serum, we observed a linear relationship between (i) serum and local antibiotic levels in vegetations, (ii) In severe infections, a bactericidal effect at the site of infection is essential for effective cure, as demonstrated by Scheld and Sande in experimental pneumococcal meningitis in rabbits (23) and by Decazes et al. in Escherichia coli meningitis (8). In the latter study, ceftriaxone levels in cerebrospinal fluid had to be at least 10 to 20 times higher than its MBC to obtain efficacy. The in vivo bactericidal effect depends on in vitro antibiotic activity and on the pharmacokinetic properties of the antibiotic molecule, which include the degree of diffusion at the infected site and consequently the local antibiotic concentration. In a previous study comparing the efficacy of cefotiam, cefmenoxime, and ceftriaxone in experimental E. coli endocarditis, we have shown that the antibiotic local level/MBC ratio roughly correlated with the antibacterial effect and could represent an adequate basis to explain the differences observed among these three drugs in vivo (19). We have also demonstrated that ceftriaxone was the most efficient of these three cephalosporins, even when given at relatively long dosing intervals, i.e., 24 h. Apart from the demonstration of this threshold of activity, the precise relationship between the range of concentrations and the antibacterial effect has not yet been determined.The purpose of this work was to assess the predictive value of serum antibiotic levels for the antibiotic concentrations in vegetations and for the local antibacterial effect. At the same time, we attempted to establish a correlation between the ceftriaxone levels in infected vegetations and * Corresponding author. the antibacterial effect. Because it is impossible to study these principles in humans, we used the experimental model of E. coli endocarditis that we have previously described (7). Although this type of infection is uncommon in humans, the model is reliable and the infection is easily reproducible. As it provides a rigourous test of in vivo antibiotic efficacy on a severe infection due to a gram-negative bacillus, the model appeared to be appropriate for studying the properties of ceftriaxone, a long-acting broad-spectrum cephalosporin. We administered different doses of ceftriaxone alone or com...
SUMMARY Hemodynamic parameters were studied before and after rapid dextran infusion in 34 men including 17 patients with sustained essential hypertension and 17 normotensive controls. In both groups of patients, dextran infusion induced a significant increase (p < 0.001) in central venous pressure (CVP), cardiac output (CO), and stroke rolume. The percent change in stroke volume was significantly higher in hypertensives (p < 0.001) than in controls. Three indices of volume expansion were calculated: 1) the ratio between the change in CO and the change in volume, which was significantly higher in hypertensives (p < 0.025), 2) the ratio between the change in CO and the change in CVP, which was similar in both groups, and 3) the ratio between the change in volume and the change in CVP, which was significantly reduced in hypertensives (p < 0.001). In the overall population, the latter ratio was negatively correlated with the change in CO (or in 4 The explanation for this volume-flow correlation is considered to be very simple: increased blood volume causes elevated venous pressure, and consequently increases venous return and CO.8 This is supported by the observation that increased venous pressure coincides with increased volume and flow in several of the experimental models studied.1~l " However, such a simple relationship between fluid volumes and CO has not been observed in man. Usually, normal or increased values of CO are associated with normal or decreased values of intravascular volume.7 In a previous study, 8 we showed that, in basal conditions, a strong positive relationship between blood volume and CO is found in human essential hypertensives but not in normotensives. This observation raised several problems. First, the result was obtained from the investigation of a wide range of subjects, by means of a new type of statistical evaluation, the smoothing technique.8 Such a methodology requires an experimental validation. Second, the cause of the close relationship between volume and flow in hypertensives was not explained. Changed performance of the heart might be involved. Reduced effective compliance of the total vascular bed has recently been shown in essential hypertension* 1 10 and could also modulate the volume-flow relationship.In the present investigation, volume expansion by rapid dextran infusion has been performed in hypertensive patients in comparison with normotensive controls. With this methodology, the relationship between CO and blood volume has been studied in basal conditions and after volume changes. An 615
Brachial artery diameter and compliance were measured in 23 normotensive control subjects and 49 hypertensive patients. The results were compared in isobaric conditions by a modeling analysis extrapolating from the measured data a short segment of the pressure-diameter and pressure-compliance curves in the artery. A logarithmic diameter-pressure function was used as well as measurements of brachial artery blood pressure and lumen diameter (by pulsed Doppler), and of brachial-to-radial pulse wave velocity (by mechanography). The measured values of diameter and compliance in the hypertensive patients were 109% and 63%, respectively, of the control group values. By extrapolating the data via the model at the same pressure level in all subjects (the average level of mean blood pressure of the two groups), the isobaric values of diameter and compliance in the hypertensive patients were 107% and 81%, respectively, of the control group values. Overall, measured isobaric diameters and measured compliance correlated with systolic, diastolic, and mean blood pressure values (/><0.001), whereas isobaric compliance correlated only with systolic (/?<0.05) and pulse (p<0.01) pressure values. Thus, the increased diameter and reduced compliance of the brachial artery observed in hypertensive humans cannot be attributed solely to the stretching effect of elevated blood pressure, but also to intrinsic alteration of the arterial walls. These could represent either adaptative structural or functional changes secondary to the chronic increase in arterial pressure, or primary abnormalities of the vessel wall. (Hypertension 1991; 18:657-664) E ffects of hypertension on large arteries has become an important field of investigation in hypertensive disease and has received considerable attention recently. 1 -4 Indeed, the large artery changes associated with hypertension may suggest a trend toward early atherosclerotic lesions. 5Reduction in arterial compliance is a well-known alteration observed in large arteries of hypertensive subjects. It may, in the long term, affect cardiovascular function, particularly by increasing systolic blood pressure and creating an extra load on the heart. 6 Increase in lumen diameter is another large artery change that occurs in sustained hypertension.7 However, little is known of the physiopathological mechanisms of this increase in large artery diameter and decrease in compliance, particularly its precise relation with elevated blood pressure.7 It seems likely Received April 9, 1991; accepted in revised form July 9, 1991.that pressure elevation per se may be a common factor responsible for increased arterial diameter and decreased arterial compliance. 7 Increasing blood pressure stretches and dilates arteries and reduces their distensibility. 8 The latter effect is explained by the fact that, for the same arterial segment, compliance is a nonlinear function of blood pressure. 9 Therefore, unless the blood pressure is controlled at the same level, it is impossible to know whether the increase in arterial d...
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