摘要:

Angioplasty of renal artery stenosis has been used extensively in the last two decades for treating renovascular hypertension, and, more recently, for preserving the jeopardized renal function. A large body of evidence has accumulated indicating that this approach is by far the most convenient for patients with fibromuscular stenosis, in whom the technical success of the procedure is followed by a high cure rate (50%) or at least by some improvement of blood pressure (40%). In contrast, in patients with atheromatous stenosis, the rate of cure is very low (8–10% at best) and the rate of improvement is between 40 and 50% irrespective of whether the stenosis is treated with angioplasty or with stent implantation. Thus, before undergoing procedures which are not devoid of potentially serious side-effects, these patients should be thoroughly investigated to select those in whom the benefit actually outweighs the risks. Studies investigating the effects of angioplasty on renal function are less numerous than those addressing the effects on blood pressure, and, in most cases, suffer the limitation of using the levels of serum creatinine as the sole marker of the changes in glomerular filtration rate induced by the procedure. These investigations have shown that some amelioration can be achieved in one-third of patients, with another third having unmodified levels of creatinine at follow-up. Radioisotopic techniques, which allow a more precise and separate evaluation of the function of the two kidneys, appear to be a promising alternative for the investigation of the effects of angioplasty; indeed, preliminary studies which took advantage of these methodologies have shown that the function of the stenotic kidney can possibly be rescued by slowly reversing the multiple mechanisms by which chronic ischaemia damages the kidney.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectivesIn a large general French population of 100 000 subjects, the relationship of resting heart rate with age, gender, demographic parameters, physical activity and classical risk factors was evaluated.Population and methodsA population composed of all the subjects who had a free health check-up at the IPC Centre between 1992 and 1995 (62 353 men and 35 371 women) was analysed. Heart rate was considered either as a continuous parameter or as a qualitative parameter. The study population was divided into four heart rate classes: < 65, 65-74, 75-84 and ≥ 85 beats/min.ResultsWomen had significantly higher heart rate values than men, and this gender difference was constant in the different age groups. In both genders, heart rate was positively associated with blood pressure, triglycerides, glycaemia and physical inactivity, and negatively with body height. Heart rate was also correlated with total cholesterol but only in men. The only factor having opposite effects on heart rate in men and women was tobacco smoking (positive in men and negative in women). Among untreated hypertensive men, 21.3% had a heart rate ≥ 85 beats/min compared with only 4.0% among normotensive men. In women, these percentages were 23.6 and 7.6%, respectively. Subjects with untreated mild hypertension or uncontrolled treated hypertension also showed increased rates of tachycardia compared to normotensives.ConclusionsThe present analysis, performed in a large French population, shows that high heart rate is associated with several other risk factors, especially hypertension, suggesting that tachycardic subjects have a high risk profile.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo determine the extent to which the correlation of systolic blood pressure, diastolic blood pressure, body mass, fasting total cholesterol and fasting triglycerides in young adulthood reflects common genetic or environmental influences.DesignCardiovascular risk factors were measured in a community sample of 129 monozygotic and 67 dizygotic twin pairs, ages 18–30 years.MethodsMultivariate twin structural equation modelling allows estimation of the extent to which the covariation of two or more variables is attributable to common genetic and environmental factors and was used to analyse the correlation among systolic blood pressure, diastolic blood pressure, body mass index, fasting total cholesterol and triglycerides.ResultsThe covariation of risk factors was partially attributable to a single common genetic factor, while the covariation of systolic blood pressure, body mass index and triglycerides was also, in part, attributable to a common non-shared environmental factor.ConclusionsGenetic and, to a lesser extent, non-shared environmental factors contribute to the covariation of cardiovascular risk factors in young adult twins. Nonetheless, it should be noted that these common influences account for a relatively small percentage of the variance in each risk factor compared to genetic and environmental factors that are risk factor-specific.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

BackgroundIncreases in vascular resistance (or the reciprocal, vascular conductance) in response to constrictor drugs are amplified (or attenuated) in the hindquarter vascular bed of hypertensive rats and rabbits. However, such changes have not been observed for the total peripheral circulation.ObjectiveTo assess whether the vascular amplifier applies to the total peripheral circulation in conscious hypertensive rabbits.MethodsRabbits were implanted with a flow probe for measuring cardiac output, a left atrial catheter for infusing dilator (adenosine) and constrictor (methoxamine) drugs, and ear artery and vein catheters for measuring mean arterial pressure (MAP) and for giving ganglion blockade. Data from full dose-total peripheral resistance (TPR) or total peripheral conductance (TPC) response curves to adenosine and methoxamine were combined into a logistic function extending from near full dilatation to near maximum constriction.ResultsChanges in MAP induced by methoxamine and adenosine were markedly greater in the ‘wrap’ rabbits (those with renal cellophane wrapping) compared with the sham animals. In the ‘wrap’ rabbits, the slopes and ranges of the adenosine-TPR response curve and the methoxamine-TPC response curve were 200% and 60%, respectively, of sham values. These data show that TPR changes are amplified, and TPC changes attenuated, to dilator and constrictor stimuli. The relationship between dose-average vascular radius (&OV0401;; based on Poiseuille's law) over the full range of vascular tone showed that &OV0401; was narrower in hypertension, but, in contrast to TPR, the degree of narrowing was almost the same between maximum dilatation and constriction.ConclusionThe total peripheral circulation in experimental hypertension is a TPR amplifier, or TPC attenuator, in the rabbit, consistent with well-established data in the major vascular beds.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectivesWe hypothesized that the loss of cerebral blood flow (CBF) auto-regulation under hypertensive conditions could promote cerebrovascular over-perfusion and haemorrhage formation. The possibility that CBF auto-regulation becomes defective prior to haemorrhagic stroke development was assessed in Wistar–Kyoto stroke-prone spontaneously hypertensive rats (SHRsp) and related to the myogenic responsiveness of the cerebrovasculature to pressure.MethodsLaser Doppler techniques were used to measure relative CBF in relation to mean arterial pressure (MAP 130-260 mmHg) within the perfusion domains of the middle (MCA) and posterior (PCA) cerebral arteries. The ability of isolated MCAs and PCAs to constrict to a 120 mmHg pressure step (pressure-dependent constriction) was measured using a pressure myograph.ResultsTwo weeks prior to stroke, 10-week-old pre-stroke SHRsp exhibited near-constant CBF regulation to a 200 mmHg MAP. Thirteen-week-old pre-stroke SHRsp and age-matched post-stroke SHRsp lost their ability to auto- regulate CBF in the MCA and PCA perfusion domains. CBF increased at a high rate and in a linear manner with MAP. A distinct upper limit to CBF auto-regulation was absent. Pressure-dependent constriction was attenuated prior to stroke, and lost after stroke in isolated MCAs, but not the PCAs, of SHRsp.ConclusionsThe loss of CBF auto-regulation prior to stroke in SHRsp could enhance cerebral perfusion and facilitate the initiation of haemorrhage. Such dysfunction after stroke could produce secondary haemorrhages. Defects in pressure-dependent constriction cannot fully account for the pattern of CBF auto-regulation loss observed in post-stroke SHRsp.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveThe present study investigated whether the nitric oxide (NO) system is involved in cyclosporin A (CsA)-induced changes in cardiovascular and renal function in man.Subjects and methodsTen healthy volunteers were investigated twice - with and without intake of a single dose of CsA (8 mg/kg). NG-monomethyl-L-arginine (L-NMMA; 3 mg/kg) was injected 4 h after study start on each day.ResultsThere was no change in glomerular filtration rate (GFR) on the day without CsA. CsA alone did not change GFR, but after L-NMMA injection, GFR decreased significantly from 101 ± 4 to 91 ± 4 ml/min. L-NMMA increased renal vascular resistance with no difference between the two study days. CsA increased significantly the diastolic blood pressure (BP) by 8 ± 2% and the heart rate (HR) by 30 ± 4%, without changes in cardiac output. L-NMMA further increased BP by around 8%, and decreased HR by 11% and cardiac output by 20% on both study days. L-NMMA decreased urinary flow rate by around 25% and renal sodium clearance from 1.1 to approximately 0.6 ml/min on both study days. CsA decreased plasma renin significantly and increased the urinary excretion rate of prostaglandin E2(PgE2), 6-keto-prostaglandin F1α(6-keto-PgF1α) and thromboxane B2(TxB2) when compsbared to the control day. The urinary excretion rate of NOxand cGMP declined gradually on the control day. In contrast, there was a minor, non-significant increase in NOxand cGMP excretion after CsA, followed by a decrease (29 ± 2 and 16 ± 4%, respectively) after L-NMMA in parallel with the decrease in GFR.ConclusionThe present findings suggest that NO does not play a major role during acute CsA-induced changes in cardiovascular function and renal haemodynamics in man. Renal NO synthesis, however, may attenuate the acute CsA-induced decrease in GFR.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectivesTo investigate the roles of cardiac output and systemic and regional resistances in corticotropin (ACTH)- induced hypertension in the rat.MethodsThis study consisted of three series of experiments with eight groups of male Sprague-Dawley rats (n= 132). Series 1 comprised groups 1–4, where group 1 = sham (0.9% NaCl, subcutaneous (sc) injection); group 2 = ACTH (0.5 mg/kg per day, sc); group 3 = atenolol + sham; group 4 = atenolol + ACTH treatments. Series 2 comprised groups 5 and 6, where group 5 = minoxidil + sham and group 6 = minoxidil + ACTH treatments. Series 3 comprised groups 7 and 8, where group 7 = ramipril + sham and group 8 = ramipril + ACTH treatments. Systolic blood pressure, water and food intakes, urine volume, and body weight were measured every second day. After 10 days of treatment, mean arterial blood pressure was measured by intra-arterial cannulation, and cardiac output (CO), and renal, mesenteric and hindquarter blood flows (RBF, MBF and HBF) determined using transonic small animal flowmeters.ResultsACTH treatment increased blood pressure (P< 0.001) with a rise in CO (P< 0.01) and renal vascular resistance (RVR,P< 0.05), but did not affect total peripheral resistance (TPR). Atenolol blocked the rise in CO without affecting the rise in blood pressure produced by ACTH treatment. Minoxidil lowered TPR, but did not prevent the rise in blood pressure or renal vascular resistance. Ramipril blunted the rise in RVR and blood pressure without significantly affectingTPR.ConclusionNeither preventing rise in CO nor lowering TPR altered the ACTH-induced rise in blood pressure in the rat. However, both the hypertension and rise in RVR were prevented by ramipril. These data suggest that increase in RVR may play a role in the pathogenesis of ACTH-induced hypertension in the rat.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveOverall obesity is associated with elevated serum triiodothyronine concentrations and insulin resistance. Oral triiodothyronine is known to induce hypertension in laboratory rats, while triiodothyronine also increases the expression of genes encoding for enzymes involved in the synthesis and secretion of insulin by pancreatic beta cells. We investigated the hypothesis that central obesity and insulin resistance are linked with an increased blood pressure and insulin production through elevated free serum triiodothyronine concentrations.DesignA cross-sectional study of 47 healthy euthryroid subjects (17 men, 30 women; 34 ± 15 years, mean ± SD).MethodsThe waist: hip ratio was used as measure of central obesity, and insulin-stimulated glucose disposal during a hyperinsulinaemic euglycaemic clamp was used as measure of insulin sensitivity. Insulin production was calculated from the insulin clearance during the clamp and fasting insulin concentrations.ResultsFree serum triiodothryronine concentrations correlated, independent of age and gender, positively with systolic and diastolic blood pressure, insulin production and fasting insulin. There was only a borderline significant correlation of free serum triiodothyronine with the waist-to-hip ratio, and no correlation with insulin sensitivity as assessed during the clamp. The correlations of free serum triiodothyronine with blood pressure, insulin production and fasting insulin were independent of the waist: hip ratio and insulin sensitivity.ConclusionOur hypothesis of free serum triiodothyronine as an intermediate factor in the insulin resistance syndrome is refuted by these data, but we identified free serum triiodothyronine concentrations as a new determinant of blood pressure, insulin production, and fasting insulin in healthy euthyroid subjects.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo assess inter-observer agreement in the interpretation of renal angiograms.DesignComparison of the assessment of renal angiograms by three experienced radiologists, who evaluated the number of renal arteries and the presence, location, aspect and severity of a renal artery stenosis.SettingGeneral hospital and university hospital serving urban and rural populations.PatientsPatients with difficult-to-treat hypertension referred for diagnostic work-up; 312 angiograms with the intra-arterial digital subtraction technique were obtained from 289 consecutive patients.Main outcome measuresInter-observer agreement was tested for the following parameters: number of arteries per kidney, presence of stenosis, location of stenosis (truncal, ostial), aspect of stenosis (concentric, eccentric, post-stenotic dilatation), severity of stenosis (reduction of lumen diameter in categories of 30%, 40%, etc. to 100%), and overall quality of the angiographic images. Kappa (κ) values and weighted κ between the three pairs of radiologists were used as estimates of inter-observer agreement.ResultsAgreement about the number of renal arteries was reasonable (κ = 0.50–0.72), as was agreement about the presence of stenosis (κ = 0.68–0.86). Agreement about stenosis location and aspect was poor (κ = 0.26–0.47 and κ = 0.15–0.26, respectively). There was general agreement about the severity of stenosis (weighted κ = 0.65–0.70), but it was not possible to distinguish between 50 and 60% stenosis or between 60 and 70% stenosis (κ < 0.40). No correlation was found between agreement on severity of stenosis and the quality of the images.ConclusionsIt is not realistic to make statements about what degree of renal artery stenosis is clinically significant, as long as the intra-arterial angiogram with digital subtraction remains the gold standard. It is likewise risky to rely too strongly on stenosis morphology as visualized by renal angiography in choosing between balloon angioplasty and stent deployment.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID