摘要:

ObjectiveThis study aimed to identify those factors in the non-pregnant state that distinguished women who developed pre-eclampsia from those who had normotensive pregnancies.Design and settingThis was a retrospective analysis of anthropometry, blood pressure, biochemical and haematological variables in 62 women with pre-eclampsia and 84 normotensive pregnant women who took part in studies of the pathophysiology of pre-eclampsia. Pregnant volunteers were seen, after admission to hospital or in the outpatient clinic, and followed-up at 6 weeks and 6 months post-partum in the outpatient clinic or their home.ParticipantsProteinuric pre-eclampsia was defined as blood pressure > 140/90 mmHg with proteinuria of at least 300 mg/24 h after 20 weeks gestation, in women with no history of hypertension and whose blood pressure returned to normal levels by 6 months post-partum. Normotensive pregnancy was defined as blood pressure ≥ 130/90 mmHg without proteinuria.Main outcome measuresThe primary outcome measures were blood pressure, body mass index (BMI), triglycerides, total cholesterol, low density lipoprotein (LDL) and high density lipoprotein cholesterol and markers of severity of pre-eclampsia.ResultsRegardless of parity, women with pre-eclampsia had elevated BMI before, during and after pregnancy compared with women who had normotensive pregnancies. Triglycerides were significantly elevated in women who had pre-eclampsia both before and after delivery, while total and LDL cholesterol were elevated significantly at both visits after delivery. Systolic and diastolic blood pressure, which by definition were elevated antepartum in women with pre-eclampsia, remained higher at post-partum visits compared with women who had normotensive pregnancies. Women with pre-eclampsia reported a greatly increased frequency of both maternal hypertension and pre-eclampsia. Markers of severity of pre-eclampsia, which normalized by 6 months post-partum, included plasma creatinine, uric acid, albumin, endothelin 1 and urinary protein, 2,3, dinor-6-keto-PGF1α, blood platelet and neutrophil counts.ConclusionThe relative elevation of blood pressure, BMI and lipids in the non-pregnant state are features of the metabolic syndrome and may be important sensitizing factors contributing to the pathogenesis of pre-eclampsia. A familial predisposition to pre-eclampsia may operate partly through these mechanisms.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo determine the relationship between endothelin-1 (ET-1), human atrial natriuretic peptide (hANP), plasma-renin activity (PRA) and 24-h urinary excretion of aldosterone (U-Ald) in pregnancy-induced hypertension (PIH).Design and methodsPlasma hANP (pg/ml), ET-1 (pg/ml), PRA (ng/ml per h) and U-Ald (Mg/24 h) were measured and 24 h ambulatory mean arterial pressure (MAP) was monitored in 178 normotensive subjects (NT) and 79 gravidas with PIH at the 8th, 18th, 23rd, 28th, 32nd and 36th weeks.ResultsThe PIH group had higher MAP than the NT group from the 23rd week (91.64 ± 8.76 versus 83.48 ± 4.36 mmHg,P< 0.01) until the end of the pregnancy. ET-1 levels (pg/ml) in both groups were identical at the beginning of pregnancy and different in the 23rd week [(NT versus PIH) (35.11 ± 17.42 and 40.2 ± 19.51, respectively,P< 0.05)] and the 36th week (37.36 ± 18.07 and 42.7 ± 16.43,P< 0.05). hANP levels (pg/ml) in the NT group decreased insignificantly from the 8th till the 32nd week, then increased to 101.94 ± 17.4 in the 36th (P< 0.001 versus any other week). In the PIH group, hANP increased from 104.8 ± 26.8 pg/ml at the 8th week to 161.3 ± 28.6 pg/ml at the 36th week (P< 0.0001). hANP correlated with MAP in the NT group (r= 0.252,P< 0.0005) but not the PIH group. U-Ald in the NT group increased from 23.52 ± 6.83 μg/24 h at the 8th week to 54.07 ± 19.62 μg/24 h at the 36th week (P< 0.0001) and in the PIH group it increased from 27.90 ± 11.6 to 53.66 ± 20.4 μg/24 h (P< 0.0001). In the PIH group, PRA was lower compared with the NT group from the 8th (2.99 ± 1.26 versus 4.10 ± 1.82 ng/ml per h,P< 0.05) until the 36th week (3.34 ± 2.16 versus 4.46 ± 2.13 ng/ml perh). In the forced multiple regression analysis model with hANP as a dependent variable, a value ofP< 0.003 was found with PRA, U-Ald and MAP, which indicates an interaction between the two vasoactive and homeostatic systems: the renin-angiotensin-aldosterone system and hANP.ConclusionsIn PIH, elevated hANP might be important as a counterbalance to the presence of the active vasopressors and sodium retention. By inhibiting renin release, enhancing the transcapillary fluid migration and with its action as vasodilator, it acts as a corrective factor of the imbalance between the contracted circulating fluid volume and the vasoconstricted vascular bed.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveThe purpose of this study was to test the robustness of the measurement of left ventricle mass (LVM), using Devereux's formula, in the presence of a rapid change in left ventricular volume induced by nitroglycerin.DesignForty-eight healthy volunteers with excellent echocardiographic recordings were included. The intrapatient variability of LVM measurement was assessed by two consecutive echocardiograms. The intraobserver reproducibility was assessed by the rereading of 19 echocardiograms by the same observer. The effects of nitroglycerin were compared with those of a placebo in a double-blind random manner on, the left ventricular internal dimension in diastole (LVIDd), the interventricular septum thickness, the posterior wall thickness and the LVM.ResultsIt was shown that both the intrapatient and the intraobserver reproducibility were high. Nitroglycerin induced a significant decrease in LVIDd compared with placebo (−20.21 ± 0.24 versus 0.01 ± 0.21 cm, respectively,P< 0.01) and a non-signifificant increase in wall thickness. These variations were negatively correlated with each other (r= −0.58,P< 0.01). Despite the change of ventricular dimensions, the variation of LVM induced by nitroglycerin was not significantly different from that induced by placebo (2.0 ± 16.0 versus 4.7 ± 17.0 g, respectively, not significant) and close to the intrapatient variability.ConclusionThis experiment failed to demonstrate any influence of a rapid variation of ventricle size on the calculation of LVM with the Penn convention and strongly supports the robustness of the methodin vivo.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveThe activation of protein tyrosine kinases (PTKs) has been postulated to be involved in cell differentiation and proliferation. To elucidate the involvement of tyrosine kinase genes in normal and pathological conditions, we analysed the expression patterns of receptor-type PTKs in the normal and hypertensive hypertrophied heart in rats.Materials and methodsHypertrophied and normal rat hearts were obtained from hypertensive rats; deoxycorticosterone acetate (DOCA)-salt and 2 kidney-1 clip (2K-1C), and their sham-operated rats, respectively. A reverse transcription-polymerase chain reaction (RT-PCR) was performed using degenerated primers which were designed from highly conserved regions in the catalytic domains of receptor-type PTKs. The PCR products were ligated into a sequence vector, and subcloned by transforming bacteria. To compare the expression level of these PTK mRNAs in the normal and hypertrophied heart, we performed semi-competetive RT-PCR and immunohistochemical and Western blot analyses.ResultsNucleotide sequencing of approximately 80 clones of PTKs revealed 10 receptor-type, five nonreceptor-type and two unknown types in the rat heart. Tie-2/Tek, Ryk, insulin-like growth factor-I receptor were abundantly expressed in the rat heart as members of receptor-type PTKs. Immunohistochemistry and RT-PCR demonstrated the presence of platelet-derived growth factor (PDGF)-α receptor, PDGF-β receptor and fibroblast growth factor-3 receptor in both normal and hypertrophied hearts. We also confirmed the presence of Flt-1, KDR/Flk-1, and their ligand vascular endothelial growth factor, c-Met and its ligand hepatocyte growth factor (HGF), and Tie-1, Tie-2/Tek by immunohistochemistry and RT-PCR. The co-expression of cardiac HGF and c-Met in hypertrophied hearts, especially in 2K-1C rats, was induced more intensively than that in DOCA-salt rats.ConclusionThese findings suggest that HGF/c-Met interactions may play an important role in cardiac hypertrophy and remodeling, probably as a result of the activation of the local renin-angiotensin system.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo evaluate in a selected population of subjects with a recent diagnosis of hypertension whether a blunted nocturnal fall in blood pressure is associated with more advanced cardiac and vascular damage.MethodsOne hundred and eleven recently diagnosed and never-treated patients with mild essential hypertension underwent 24-h ambulatory blood pressure monitoring (ABPM), echocardiography and carotid ultrasonography.ConclusionThese results suggest that a blunted reduction in night-time blood pressure does not play a major role in the development of cardiovascular changes during the early phase of essential hypertension.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID

摘要:

ObjectiveTo determine the effect of short-term angiotensin converting enzyme inhibition (enalapril) or angiotensin II AT1receptor blockade (losartan) on medullary hemodynamics in the spontaneously hypertensive rat (SHR).DesignLaser-Doppler flowmetry allowed for the characterization of medullary blood flow (MBF) over a wide range of renal arterial pressure (RAP), and was used for comparison among treatment groups. Renal interstitial hydrostatic pressure (RIHP) was also determined over a wide range of RAP.MethodEnalapril or losartan was given to male 12–13-week-old SHR for 3 days (25 mg/kg per day in drinking water). Rats were anesthetized with Inactin, renal function was measured at resting levels of RAP and then RAP was varied over a range of 50-150 mmHg in 25 mmHg steps. MBF and RIHP were determined at each pressure.ResultsResting mean arterial pressure (MAP) (mmHg ± SE) for enalapril- and for losartan-treated SHR [114 ± 3(n= 18) and 124 ± 3(n= 20), respectively] were both significantly lower than for untreated SHR [159 ± 5 (n= 20)]. Renal function at resting levels of MAP was not significantly different among groups. Enalapril and losartan both increased MBF by 30% at levels of RAP of 125 mmHg and over. Enalapril did not alter the relation between RAP and RIHP, but losartan shifted the RAP versus RIHP curve by approximately 40 mmHg to lower levels of RAP. Acute administration of the B2 kinin receptor antagonist HOE 140 [20 μg/kg intravenous (i.v.) bolus, then 10 μg/kg per h i.v.] did not significantly alter MAP in any group. HOE 140 did not significantly alter MBF or RIHP in the untreated or losartan-treated SHR. MBF in enalapril-treated rats receiving HOE 140 was not significantly different from that of the enalapril-only group; however, the relation between RAP and RIHP was shifted to lower levels of RAP by approximately 45 mmHg.ConclusionsBoth enalapril and losartan increase MBF in SHR, suggesting that the medullary circulation of SHR is influenced by endogenous levels of angiotensin II. The failure of enalapril to increase RIHP in parallel with MBF appears to be due to an enhanced effect of kinins.

ISSN:0263-6352    

出版商:OVID    

年代:1999

数据来源: OVID