摘要:

Systolic and diastolic blood pressures are the exclusive mechanical factors considered as predictors of cardiovascular risk for members of populations of normotensive and hypertensive subjects. However, if hypertension is considered as a mechanical factor acting on the arterial wall with deleterious consequences, the totality of the blood pressure curve should be considered in order to investigate the risk. The purpose of this review is to show that in addition to systolic and diastolic blood pressures, other hemodynamic indexes with particular relevance for cardiac complications and that originate from pulsatile pressure should be taken into account, namely brachial pulse pressure, pulse pressure amplification, early wave reflections, and pulse wave velocity.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Patients with obstructive sleep apnea experience repetitive apneic events during sleep, with consequent hypoxia and hypercapnia. Hypoxia and hypercapnia, acting via the chemoreflexes, elicit increases in sympathetic nerve activity. The sympathetic responses to hypoxia and hypercapnia are potentiated during apnea, when the sympathetic inhibitory influence of the thoracic afferent nerves is eliminated. As a consequence of the sympathetic vasoconstrictor response to apneic events, patients with obstructive sleep apnea manifest marked increases in blood pressure during sleep, especially evident at the end of the apnea.The increases in sympathetic activity and blood pressure during sleep in these patients appear to carry over into the daytime such that patients with sleep apnea have an increased prevalence of hypertension and high levels of sympathetic nerve activity. Although the mechanism underlying the persistent elevation in sympathetic activity during the daytime is not known, it is likely that the increased sympathetic drive is implicated in the higher daytime blood pressures in these patients.Whereas patients with sleep apnea have an increased prevalence of hypertension, in those patients with sleep apnea who do have hypertension, the sympathetic response to apneic events may be potentiated. This may be secondary to impaired baroreflex sensitivity, since the baroreflexes exert an inhibitory influence on the chemoreflex responses to hypoxia.Treatment with continuous positive airway pressure results in an acute reduction in blood pressure and sympathetic activity during sleep. Prolonged effective treatment of sleep apnea may also reduce daytime blood pressure levels.This review examines the physiology of the chemoreflex responses to hypoxia, hypercapnia and apnea, as well as the physiologic responses to sleep in normal humans. These physiologic responses are compared with the pathophysiologic sympathetic and hemodynamic responses that characterize obstructive sleep apnea. Increases in sympathetic activity and blood pressure in patients with obstructive sleep apnea may play a role in linking sleep apnea to hypertension and cardiac and vascular events.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo assess spontaneous baroreceptor-heart rate reflex sensitivity during sleep in patients with obstructive sleep apnea syndrome, a condition associated with increased cardiovascular morbidity and mortality and characterized by marked sympathetic activation, which is believed to originate from hypoxic chemoreceptor stimulation, although little is known of other possible mechanisms such as baroreflex impairment.Design and methodsIn 11 patients with severe obstructive sleep apnea syndrome (mean ± SD age 46.8 ± 8.1 years, apnea/hypopnea index 67.9 ± 19.1 h), who were normotensive or borderline hypertensive during wakefulness by clinic blood pressure measurements, finger blood pressure was monitored beat-by-beat non-invasively (Finapres) at night during polysomnography. Periods of wakefulness and sleep were identified based on electroencephalographic recordings. Baroreflex sensitivity was assessed by the sequence technique, as the slope of the regression line between spontaneous increases or reductions in systolic blood pressure (SBP) and the related lengthening or shortening in the RR interval, occurring over spontaneous sequences of four or more consecutive beats. The number of these sequences was also computed, as an additional index of baroreflex engagement by the spontaneous blood pressure fluctuations. The controls were age-related normotensive or borderline hypertensive subjects without sleep apnea who had been investigated in previous studies; in these subjects blood pressure was recorded intra-arterially over 24 h in ambulatory conditions and spontaneous baroreflex sensitivity was assessed by the sequence technique.ResultsIn our patients the lowest nocturnal arterial oxygen saturation was 78.6 ± 12.1% (mean ± SD). During sleep, the number of pooled +RR/+SBP and −RR/−SBP sequences per hour was 20.3 ± 2.7 per h in patients with sleep apnea and 27.1 ± 2.1/h in controls (means ± SEM). The average baroreflex sensitivity during sleep periods was 7.04 ± 0.8 ms/mmHg in sleep apnea patients and 10.05 ± 2.1 ms/mmHg in controls. Both the pooled number of sequences and baroreflex sensitivity values of the sleep apnea patients were significantly (P <0.01) less than the corresponding night values of control subjects. In the sleep apnea patients, at variance from controls, baroreflex sensitivity did not show any increase during sleep compared with its values during wakefulness (6.9 ± 1.0 ms/mmHg).ConclusionsOur data provide evidence that spontaneous baroceptor reflex sensitivity is depressed in severe obstructive sleep apnea syndrome. This suggests that in such patients baroreflex dysfunction and not only chemoreceptor stimulation by hypoxia may be involved in the sympathetic activation which occurs during sleep. Such dysfunction may contribute to the higher rate of cardiovascular morbidity and mortality reported in these patients.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectivesTo determine the association between birth weight and systolic blood pressure (SBP) in male adolescents at the age of 18 years.DesignA prospective study by means of a register linkage between the Swedish Medical Birth Register and the national register for conscript testing before military service.MethodsFrom the birth registry we collected data on birth weight, gestational age, maternal age and parity for 149 378 individuals. At conscript testing, subjects were given a physical examination, and weight, height, and mean blood pressure were recorded after 5–10 min rest.ResultsMean ± SD birth weight was 3543 ± 551 g after a mean of 39.7 ± 2.0 gestational weeks. Mean ± SD blood pressure at the conscript testing was 128.8 ± 10.9/65.2 ± 10.6 mmHg. SBP, but not diastolic blood pressure, differed significantly (test for trend,P< 0.001) between birth weight strata (deciles), with a higher SBP in strata with lower birth weight. A difference in birth weight of 1000 g decreased SBP by 0.8 mmHg. This was most pronounced in subjects with a rapid growth development (n = 1057), coming from the lowest decile of birth weight and reaching to the highest decile of body mass index, in a very consistent manner. The odds ratio for being in the top decile of SBP was 1.55 (95% confidence interval 1.32–1.81) for this growth ‘catch-up’ group compared with the rest of the cohort.ConclusionsBirth weight was inversely associated with SBP in a large cohort of young men in their late teens. This supports the notion of a programming effect of fetal growth retardationin uteroon haemodynamic regulation in early adult life.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveThe adhesion of monocytes to endothelium, an early event in atherosclerosis is mediated by cell adhesion molecules. Signal-transduction pathways for these binding molecules include the translocation of the transcription factor NF-κB; moreover, intracellularly generated oxygen-derived free radicals play a major role in this process. In this study we evaluated the extent to which lacidipine, a calcium antagonist with antioxidant properties, affects the expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin on human umbilical vein endothelial cells, induced by different pro-oxidant signals such as oxidized low density lipoprotein (LDL) and tumor necrosis factor-α (TNF-α).MethodsWe incubated 5 mmol/l Cu2+-oxidized LDL and TNF-α (2 ng/ml) with human umbilical vein endothelial cells for 48 and 6 h, respectively. ICAM-1, VCAM-1 and E-selectin were measured by flow cytometry. NF-κB was evaluated by electrophoretic mobility shift assay.ResultsThe incubation of 5 μmol/l Cu2+-oxidized LDL not only caused a dose-dependent increase in ICAM-1, VCAM-1 and E-selectin (P <0.001), but also synergically increased their TNF-α–induced expression (P <0.001). The addition of lacidipine to human umbilical vein endothelial cells significantly reduced the expression of ICAM-1, VCAM-1 and E-selectin induced by TNF-α alone or with oxidized LDL (P <0.001). The reduction in adhesion molecule expression caused by lacidipine was paralleled by a significant fall in NF-κB translocation.ConclusionsThe results suggest that lacidipine may have prevented NF-κB-mediated adhesion molecule expression by exerting its effects on oxygen-derived free radicals. The results support previous observations that lacidipine may have therapeutic effects in atherosclerosis.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

BackgroundTissue-type plasminogen activator (t-PA) is the key mediator of intravascular fibrinolysis. We showed recently that local administrations both of methacholine (MCH) and of desmopressin (1-desamino-8-D-arginine vasopressin, DDAVP) induced a massive local release of t-PA in the human forearm vasculature.ObjectiveTo determine whether the human vascular endothelium could respond to repeated stimulation with the same agonist, and, if so, to further evaluate the releasable endothelial pool of t-PA.MethodSeven young, healthy men participated. MCH and DDAVP were administered as local infusions into the brachial artery. In protocol 1 (n = 3) 2 μg/min MCH was infused for 2 (30 min with a free interval of 20 min. In protocol 2 (n = 4) 70 ng/min DDAVP was infused for 2 (20 min with an interval of 75 min. Dosages and time intervals were based on the different release profiles of the two drugs observed in previous studies. Brachial arterial and venous blood samples were obtained at baseline and throughout infusions. Net release of t-PA was calculated as the product of the arteriovenous concentration gradient and forearm plasma flow.ResultsForearm blood flow was increased 3–4-fold by MCH and 2–3-fold by DDAVP infusions. During the first and second infusions of MCH, the average amounts of t-PA released were 1600 and 1000 ng/l forearm tissue, respectively. In contrast, DDAVP induced similar t-PA responses during both infusions; the average total releases of t-PA were 2300 and 2400 ng/l tissue, respectively.ConclusionThe results show that the vascular endothelium is responsive to repeated stimulation both with MCH and with DDAVP. The diminished t-PA response to the second MCH infusion can not be explained in terms of depletion of intracellular pools, in view of the large amount of t-PA released by a single infusion of DDAVP. The dynamic pool of t-PA available for release is very large, but further studies are required in order to quantify the releasable endothelial stores.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo evaluate the vascular response of the human hypertensive kidney to endothelial stimulation with acetylcholine (ACh) and to assess whether this effect can be inhibited by the non-specific muscarinic receptor antagonist atropine.Patients and methodsThree stepwise increasing doses of ACh (0.3, 1.0 and 3.0 μg/kg per min) in combination either with placebo or with 100 or 300 ng/kg per min atropine were infused into the right renal artery of 20 hypertensive patients. Renal blood flow was determined using the133Xe wash-out technique.ResultsInfusion of ACh induced a dose-dependent increase in renal blood flow (P= 0.02). Both doses of atropine attenuated the ACh-induced renal vasodilatation (P< 0.05).ConclusionsAdministration of ACh to the human hypertensive kidney induces a dose-dependent increase in renal blood flow. This effect is, at least partially, mediated by muscarinic receptors.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveTo evaluate the functional responses of mesenteric small resistance arteries of spontaneously hypertensive rats (SHR) and Wistar–Kyoto (WKY) rat controls to endothelin-1 (ET-1), in the presence and absence of an ETAreceptor antagonist drug as well as to an ETBreceptor agonist.MethodsTwenty rats aged 12 weeks were studied. They were 10 SHR and 10 WKY rats. Mesenteric small resistance arteries (relaxed diameter 100–180 μm) were dissected and mounted on a micromyograph (Mulvany's technique). A dose-response curve for response to ET-1 was plotted for cumulative concentrations (from 10‴11to 10−8mol/l) in the presence and absence of 10−6mol/l FR 139 317 (a selective antagonist of ETAreceptors). In addition, the effects of 10−7mol/l N-succinyl-[Glu9, Ala11,15]-endothelin 1 fragment 8–21 (IRL 1620, a selective agonist of ETBreceptors) were evaluated.ResultsThe response of ET-1 was greater in WKY rats than it was in SHR. Almost all the vasoconstrictor effect of ET-1 could be prevented by addition of FR 139 317, whereas the agonist of ETBreceptors had no effect (no change in active force).ConclusionsThe contractile effects of ET-1 on mesenteric small resistance arteries of SHR and WKY rats are mediated mostly by ETAreceptors, whereas ETBreceptors play a minor role, if any. It is possible, however, that a vasoconstrictor effect of ETBreceptors on the smooth muscle could be masked by the concomitant stimulation of endothelial ETBvasodilator receptors.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveCigarette smoking acutely induces a marked increase of blood pressure and heart rate. This is accompanied by a marked reduction of radial artery distensibility. Whether this reflects an alteration of arterial mechanics of large elastic arteries as well is not established, however.Design and methodsIn this study we addressed the acute effects of smoking on the stiffness of a peripheral medium-sized muscular artery and a large elastic vessel. We studied seven healthy normotensive smokers (age 28 ± 7 years, mean ± SEM), in the absence of smoking for at least 24 h. Radial artery (NIUS 02) and carotid artery diameter (WTS) were concomitantly acquired beat-to-beat in the 5 min before, during and after smoking of a cigarette containing 1.2 mg of nicotine. Blood pressure and heart rate were concomitantly recorded by a Finapres device. Radial and carotid artery distensibility were calculated according to the Langewouters and Reneman formulae, respectively. Data were collected for consecutive 30 s periods. Statistical comparisons were performed between the three different phases and, within each phase, between 30 s periods. In five subjects the protocol was repeated after 1 week using a stran rather than a cigarette to obtain data under sham smoking.ResultsSmoking increased systolic blood pressure by 14%, diastolic blood pressure by 10% and heart rate by 27%. Radial artery diameter was reduced during smoking (−3.7%) and more so after smoking (−14.8%), while carotid artery diameter did not change significantly either during or after smoking. Radial artery distensibility was also significantly reduced only after smoking (−41.3%,P< 0.01), while carotid artery distensibility was significantly reduced both during (−33.3%) and after smoking (−27.2%) (P< 0.01 versus before). No changes in blood pressure, heart rate and arterial wall mechanics were induced by sham smoking.ConclusionsAcute cigarette smoking reduces distensibility not only in medium-sized but also in large elastic arteries, therefore causing a systemic artery stiffening. The mechanisms of these effects remain to be determined. However, it is likely that adrenergic mechanisms are responsible for the arterial distensibility alterations.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

ObjectiveIn essential hypertension, the mechanical properties of the radial artery have been shown to be largely unaltered, whereas more controversial and less reliable data have been obtained for the common carotid artery. We therefore examined the distensibility/pressure relationships of the predominantly elastic common carotid artery and of the predominantly muscle-type femoral artery in 12-week-old normotensive Wistar–Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).MethodsEleven 12-week-old SHR and 10 age-matched WKY rats were anesthetized with sodium pentobarbitone. Blood pressure and pulse rate were measured by catheters inserted in the common carotid and in the femoral arteries, while contralateral arterial diameter was continuously recorded via an echo-tracking device. Arterial compliance was derived according to the Langewouters formula, and its values were normalized for the diameter, to obtain distensibility/pressure curves and to calculate the distensibility index. The Peterson elastic modulus was also calculated in order to obtain a pressure-independent estimate of arterial mechanical properties.ResultsFemoral artery distensibility/pressure curves and distensibility index were similar in the two groups of rats, the latter being 1.13 ± 0.13 mm/mmHg10−3in SHR and 1.28 ± 0.15 mm/mmHg10−3in WKY rats (means ± SEM; NS). In contrast, in SHR, common carotid artery mechanical properties were clearly impaired, as shown by a marked reduction in distensibility index (2.55 ± 0.16 mm/mmHg10−3in SHR versus 3.4 ± 0.3 mm/mmHg10−3in WKY rats;P< 0.05), and by a significant increase in the Peterson elastic modulus.ConclusionsIn the SHR model, high blood pressure alters the mechanics of large arteries even in the relatively early stage of the disease; however, the alterations are not homogeneous inasmuch elastic-type vessels are affected to a much greater extent than muscle-type vessels.

ISSN:0263-6352    

出版商:OVID    

年代:1997

数据来源: OVID