Measurement of plasma volume in pregnancy.

1. Determination of the plasma volume in pregnant women is a useful research tool and may become an important clinical measurement. We used three methods to determine plasma volume using Evans Blue dye: (1) the 'usual' method, measuring serum absorbance at a wavelength of 610 nm, (2) a two-wavelength method, and (3) precipitation of non-albumin proteins by the addition of polyethyleneglycol before measuring serum absorbance at a wave-length of 620 nm. These were each compared with the standard 125I-human serum albumin method in 20 non-pregnant subjects. Subsequently, the polyethylene glycol method was considered the standard and the three Evans Blue dye methods were compared in 20 pregnant women. 2. In non-pregnant subjects mean plasma volumes did not differ significantly according to the method used. However, the limits of agreement with 125I-human serum albumin method were closest for the polyethyleneglycol method, for both clear and turbid sera. 3. In pregnant women, mean plasma volume values did not differ according to the Evans Blue dye method used, but the limits of agreement were significantly closer with the two-wavelength method than with the 'usual' method (P less than 0.05) largely owing to the effects of turbid sera. 4. These studies demonstrate that considerable error may occur when the Evans Blue dye concentration is determined in turbid sera by the 'usual' method. This can be overcome by the use of the two-wavelength method or the polyethyleneglycol method. The most accurate results will be obtained if the latter method is employed routinely to determine plasma volume in pregnant women.     

Stimulation of active renin release in normal and hypertensive pregnancy

1. Active plasma renin concentration but not total renin concentration is reduced in women with pregnancy-induced hypertension compared with normotensive pregnant women. This study was conducted to determine whether women with pregnancy-induced hypertension are able to stimulate release of active renin. 2. Active plasma renin concentration was measured as the generation of angiotensin I at physiological pH in the presence of excess renin substrate, and total renin concentration was determined in the same way after trypsin activation. Inactive plasma renin concentration was calculated as the difference between total renin and active plasma renin concentrations. 3. Resting active plasma renin concentration was significantly greater in third-trimester primigravidae compared with normotensive non-pregnant women and active plasma renin and total renin concentrations rose significantly without a fall in inactive plasma renin concentration in both groups after 2 h ambulation, suggesting increased release of active plasma renin and not conversion of circulating inactive to active renin. These responses were blunted in women taking oral contraceptives. 4. Although the active plasma renin concentration was significantly reduced in third-trimester primigravidae with pregnancy-induced hypertension, total renin concentration was not significantly different compared with normotensive women of similar gestation and in both groups 30 min 60 degrees head-up tilt increased active but not inactive plasma renin concentration. 5. These studies show that in normal pregnancy active plasma renin concentration can be stimulated to a similar extent as in non-pregnant women, despite a higher resting level. This appears to be due to increased secretion of active plasma renin rather than conversion of circulating inactive to active renin.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of posture on abnormalities of forearm venous tone in women with pregnancy-induced hypertension

1. Forearm venous tone was measured in the left lateral supine position and in response to passive leg elevation in a group of women with pregnancy-induced hypertension and compared with a group of normotensive pregnant women and a group of non-pregnant women. 2. The women with pregnancy-induced hypertension were venoconstricted in the supine position compared with the normal pregnant women (P less than 0.002). There was no difference in forearm venous tone between the women with pregnancy-induced hypertension and the non-pregnant women. 3. In response to passive leg elevation the women with pregnancy-induced hypertension venodilated (P less than 0.002) whereas there was no change in forearm venous tone in the normotensive pregnant women and the non-pregnant women. There was no change in blood pressure in any of the women after 35 min of leg elevation. 4. These results demonstrate that the abnormal venous vasoconstriction that occurs in women with pregnancy-induced hypertension in the supine position is corrected by passive leg elevation, a manoeuvre which leads to an increase in central blood volume.     

Endothelium-derived prostacyclin: effect of serum from women with normal and hypertensive pregnancy.

1. Pregnancy-induced hypertension (or pre-eclampsia) is characterized by vasoconstriction, platelet aggregation and altered capillary permeability, implying disordered endothelial function and/or structure. Serum from women with pregnancy-induced hypertension has been reported by others to be cytotoxic to endothelial cells in vitro. We hypothesized that such serum contains a factor that limits the ability of endothelial cells to produce and/or release prostacyclin. 2. Prostacyclin production by intact and damaged cultured human umbilical vein endothelial cells was measured after incubating these cells with serum from non-pregnant and normal pregnant women and women with pregnancy-induced hypertension. Confluent human umbilical vein endothelial cell monolayers (intact and damaged) were incubated with sera for 24 h at 37 degrees C followed by 1 h of incubation with added thrombin (stimulated production) or media (basal production). Supernatants were then collected for measurement of 6-keto-prostaglandin F1 alpha by radioimmunoassay. 3. Basal production of 6-keto-prostaglandin F1 alpha was greater in response to serum from non-pregnant women than to that from pregnant women. Within each group, sub-lethally damaged cells had a similar basal production of 6-keto-prostaglandin F1 alpha to that of intact cells. 4. Basal production of 6-keto-prostaglandin F1 alpha by intact or damaged cells incubated with sera from normal pregnant women and from women with pregnancy-induced hypertension was similar. 5. In all groups the addition of thrombin to intact endothelial cells increased 6-keto-prostaglandin F1 alpha production approximately 15-30-fold over basal levels, but only three- to five-fold in damaged endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)     

Abnormalities of peripheral venous tone in women with pregnancy-induced hypertension

Forearm venous tone was measured in two groups of pregnant women: one group with pregnancy-induced hypertension and the other group with normal blood pressure. The women with pregnancy-induced hypertension were venoconstricted in the forearm (P less than 0.01) compared with the pregnant women with normal blood pressure. However, there was no difference in venous tone between the women with pregnancy-induced hypertension and non-pregnant women. There was an inverse correlation between mean arterial blood pressure and forearm venous tone (r = -0.581, P less than 0.001) for all the pregnant women studied. Further evaluation of peripheral venous tone may provide valuable information about the pathophysiology and treatment of women with pregnancy-induced hypertension.     

A cross-sectional study of basal platelet intracellular free calcium concentration in normotensive and hypertensive primigravid pregnancies

1. The intracellular free calcium concentration ([Ca2+]i) in washed human platelets was measured using the fluorescent indicator, fura-2, in a cross-sectional study of 36 normotensive, primigravid volunteers, 12 in each trimester of pregnancy and a further 12 at 6 weeks post partum. The results were compared with those obtained from 30 normal female volunteers not using oral contraception. 2. The mean basal [Ca2+]i in the platelets of the pregnant women in the first two trimesters (115.6 +/- 6.7 and 120.1 +/- 5.7 nmol/l, respectively) was not shown to differ significantly from that of normal non-pregnant volunteers (112.3 +/- 2.9 nmol/l). However, during the third trimester a significant increase in [Ca2+]i was noted (134.0 +/- 4.9 nmol/l; P less than 0.05), with a return to normal values in the post-partum period (108.2 +/- 6.1 nmol/l). 3. [Ca2+]i was also measured in the platelets of a group of 12 primigravid pregnant women in the third trimester whose pregnancies were complicated by gestational hypertension (pregnancy-induced hypertension and pre-eclampsia). A significant rise in basal [Ca2+]i was noted in the platelets of primigravidae whose pregnancies were complicated by pre-eclampsia (163.6 +/- 8.8 nmol/l) as compared with normotensive, third-trimester primigravidae (P less than 0.02). However, no correlation could be demonstrated between [Ca2+]i and systemic blood pressure.     

Plasma volume contraction: a significant factor in both pregnancy-associated hypertension (pre-eclampsia) and chronic hypertension in pregnancy

The role of plasma volume in hypertension in pregnancy (pre-eclampsia) was investigated. Significant volume expansion from non-pregnant levels (16.5 +/- 1.60 ml/cm height) was present throughout pregnancy in 189 normal women, reaching 23.1 +/- 1.21 ml/cm at 33-36 weeks amenorrhoea. In another 40 initially normotensive pregnant women who developed hypertension, similar early volume expansion was followed by significant volume contraction in the third trimester, before evaluation of blood pressure in 29 (20.6 +/- 1.26 ml/cm), after it in 11 (18.6 +/- 1.27 ml/cm). Equivalent volume contraction was present in another 44 women studied only after hypertension developed in the third trimester. Oedema had no value as a clinical sign. In another 30 women with chronic hypertension, blood pressure was inversely related to plasma volume (r = 0.822) and to fetal growth (r = -0.710), which was directly related to plasma volume (r = 0.701). Plasma volume depletion plays a significant role in hypertension in pregnancy.     

妊娠期高血压病患者血液流变学与脐血流阻力指标的关系

目的：探讨妊娠期高血压病患者血液流变学与胎儿脐动脉血流阻力指标的相关性和对围产儿结局的影响。方法：用粘度仪检测正常妊娠孕妇及妊娠期高血压病孕妇全血比粘度高切（BVH）、全血比粘度低切（BVL）、全血还原比粘度（BRV）、血浆粘度（PV）;用离心机检测红细胞压积（HCT）;应用彩色多普勒超声检测胎儿脐动脉血流阻力指标,探讨妊娠期高血压病患者血液流变学各值与胎儿脐动脉血流阻力指标各值的相关性。结果：妊娠期高血压病患者血液流变学各值与胎儿脐动脉血流阻力指标各值呈正相关。子痫前期组围产儿结局不良发生率明显高于妊娠高血压组（P〈0.01）及正常妊娠组（P〈0.01）。结论：HCT、BVH、BVL、PV对妊娠期高血压病的发生、发展、严重程度及脐动脉血流阻力指标可能有重要影响。多项指标监测妊娠期高血压病患者血液流变学及胎儿脐动脉血流动力学,可提高预测妊娠期高血压病发生、发展及严重程度及其对围产儿预后影响的准确性。     

Glomerular filtration rate in pregnancy: a study in normal subjects and in patients with hypertension, preeclampsia and diabetes.

We have studied renal function during pregnancy using plasma clearance of iohexol to determine the glomerular filtration rate (GFR). In normal pregnancy, GFR was elevated by 40% throughout pregnancy and during the first week post partum, and fell to levels similar to those in non-pregnant women within 1 month. The development of GFR in diabetic pregnant women and in women with gestational hypertension was similar to that recorded in normal pregnancy. In subjects with preeclampsia the rise in GFR observed in normal pregnancy was absent, and no change in GFR was recorded after delivery. We conclude that the development of proteinuria and fluid retention typical of preeclampsia is paralleled by a deterioration of GFR.     

Serum digoxin-like substances in pregnancy-induced hypertension

1. Endogenous digoxin-like immunoreactivity (EDLI) was measured in the serum of 85 normotensive pregnant (NTP) women and 77 women with pregnancy-induced hypertension (PIH) by a radioimmunoassay (New England Nuclear). All women were in the third trimester. 2. EDLI, which was undetectable in serum from non-pregnant women, was present in NTP and PIH and was significantly higher in PIH. EDLI correlated with gestational age in NTP, but not in PIH. 3. Ouabain-sensitive Na+ transport was estimated in normal peripheral blood leucocytes after incubation with sera from 50 NTP and 42 PIH women. Significant inhibition of active Na+ transport occurred only with the serum of hypertensive patients without proteinuria. 4. EDLI did not correlate with the effect of the sera on active Na+ transport. The radioimmunoassay therefore provides a poor index of Na+ transport inhibitory activity in PIH.     

脐血流监测对妊娠期高血压疾病孕妇妊娠结局的意义探讨

目的探讨妊娠期高血压患者胎儿脐动脉血流阻力指标对围产儿结局的影响。方法用粘度仪检测正常妊娠孕妇及妊娠期高血压孕妇血浆粘度(PV);用离心机检测红细胞压积(HCT)等;统计分析其妊娠中期(20~27周)及妊娠晚期(28~36周),并测定收缩期最大血流速度和舒张期血流速度的比值(S/D)和脉搏指数(PI)、阻力指数(RI)。探讨血液流变学各值与胎儿脐动脉血流指标相关性。结果妊娠高血压组妊娠中、晚期S/D、PI及RI值与正常妊娠组比较均有统计学差异。随着病情进展,中度、重度妊娠高血压组RI、PI值逐渐升高。妊娠期高血压病患者血液HCT、PV等值与胎儿脐动脉血流阻力指标各值呈正相关。结论 HCT、PV对妊娠期高血压病的发生、发展、严重程度及脐动脉血流阻力指标可能有重要影响。多项指标监测妊娠期高血压病患者血液流变学及胎儿脐动脉血流动力学,可提高预测妊娠期高血压症发生、发展及严重程度及其对围产儿预后影响的准确性。     

Plasma prolactin concentrations and pregnancy-induced hypertension

Human prolactin (PRL) has been related to various pathologic disorders known to be associated with osmoregulation and hypertension. In this study, we compared changes in plasma PRL concentrations in normal pregnant patients to those in patients with severe pregnancy-induced hypertension (PIH). Comparison of plasma PRL concentrations collected antepartum, at delivery, and 48 hours postpartum failed to distinguish women with PIH from those without. Only women with PIH, however, showed a significant rise in systemic PRL concentrations between admission to the study and delivery. Antepartum abnormalities in plasma PRL concentrations associated with PIH may not have been detected because of diurnal variations in PRL secretion.     

Do heart rate and velocity variability derived from umbilical artery velocity waveforms change prior to clinical pregnancy-induced hypertension?

OBJECTIVE: To investigate the hypothesis that alterations in heart rate variability, peak systolic velocity variability and time-averaged velocity variability in the human umbilical artery may predict early signs of dysfunctional fetal-placental coupling in pregnancies that later develop pregnancy-induced hypertension. METHODS: Doppler flow velocity recordings from the umbilical artery were performed at 10-20 weeks of gestation in 12 nulliparous women who subsequently developed pregnancy-induced hypertension. From umbilical artery velocity waveforms of at least 12 s in duration we determined absolute values and beat-to-beat variability in fetal heart rate, peak systolic and time-averaged velocity and compared these findings with those in normal nulliparous pregnant women matched for gestational age. RESULTS: Absolute values for fetal heart rate, peak systolic and time-averaged velocity as well as beat-to-beat variability in fetal heart rate did not differ significantly between women later developing pregnancy-induced hypertension and normal controls. However, variability in peak systolic velocity and time-averaged velocity were decreased in women who subsequently developed pregnancy-induced hypertension. CONCLUSIONS: Whereas fetal heart rate variability was similar, umbilical artery flow velocity variability was reduced in women developing pregnancy-induced hypertension compared with controls. It is proposed from this study that variability of the umbilical artery flow velocity is associated with mechanical changes in the vascular bed of women who later develop pregnancy-induced hypertension.     

西安地区正常妊娠妇女孕早中晚期血常规检测指标参考区间的调查分析

目的建立西安地区妊娠女性孕早、中、晚期血液学相关参数的参考区间。方法选取空军军医大学第一附属医院2017年3月至2018年2月门诊妊娠女性1 197例,按照孕周分为孕早、中、晚期;选择同期体检健康的非孕育龄期女性300例作为健康人对照组;分别检测白细胞计数(WBC)、红细胞计数(RBC)、血红蛋白(Hb)、血细胞比容(Hct)、红细胞平均体积(MCV)、平均红细胞血红蛋白含量(MCH)、平均红细胞血红蛋白浓度(MCHC)、血小板(PLT)并进行统计分析,建立参考区间。结果妊娠女性在不同孕期RBC、Hb、HCT、MCV、MCH、MCHC的水平均低于健康人对照组,孕晚期下降达孕期最低水平(P0.05),不同孕期之间比较差异有统计学意义(P0.05)。妊娠女性WBC水平随孕周的增加逐渐升高,至孕晚期达最高水平,不同孕期之间WBC比较差异有统计学意义(P0.05)。妊娠女性PLT水平较健康人对照组降低,在孕晚期达最低水平(P0.05)。结论妊娠女性血液学相关参数不同于育龄期健康非孕女性,各临床实验室应建立女性妊娠各期血液学相关参数参考区间。     

Abnormal membrane cation transport in pregnancy-induced hypertension

An abnormality of sodium handling has been suggested as one of the mechanisms responsible for the development of pregnancy-induced hypertension. We analysed the plasma and urinary concentrations, and the intraerythrocyte activities of Na and K, and the RBC membrane Na+/K+-ATPase activity of 77 hypertensive and 133 normal pregnant women. Umbilical cord blood of infants from 21 hypertensive and 28 control women was studied. The Na+/K+-ATPase activity was determined by measuring the inorganic phosphate released by incubation in a reaction medium in the presence and absence of K ions or ouabain. The intra-erythrocyte sodium and potassium activities were measured by ion-selective electrode analysis of the haemolysates, after washing the RBCs in 110 mmol/l MgCl2. We found a significant increase in intracellular sodium and a reduction in Na+/K+-ATPase activity in the hypertensive women in comparison with the control subjects during pregnancy. No difference was observed in early puerperium. Cord blood from infants of pregnancy-induced hypertensive women showed an increase in intracellular Na+ activity and a decrease in the erythrocyte membrane Na+/K+-ATPase activity in comparison with cord blood samples from control subjects. The observed abnormalities in the plasma membrane sodium transport may play a major role in the pathophysiology of pregnancy-induced hypertension.     

妊娠高血压综合征预测阳性孕妇的社区护理干预

探讨妊娠高血压综合征预测阳性孕妇的社区护理干预效果。使用MP-妊娠高血压综合征监测仪结合妊娠高血压综合征诊断标准进行筛查预测;对妊娠高血压综合征预测阳性96例孕妇,使用妊娠高血压综合征监测仪进行监测,1次/2周,根据其结果进行社区护理干预,配合适当的药物治疗。经社区护理干预后96例妊娠高血压综合征预测阳性孕妇中只有5例发病,发病率5%,子痫为0例。提高孕妇参与监测、产检、学习、电话随访的自觉性,认为妊娠高血压综合征预测阳性孕妇进行社区护理干预,对预防、降低妊娠高血压综合征的发病率有明显的作用。     

叶酸代谢相关酶基因与妊娠期糖尿病、妊娠期高血压、羊水过少及早产的关系研究

目的探讨妊娠期糖尿病、妊娠期高血压、早产、羊水过少与叶酸代谢相关酶基因风险性及基因频率的关系。方法选择在该院接受叶酸代谢相关酶基因检测的孕妇19211例,分为羊水过少组1480例,妊娠期糖尿病组4506例,妊娠期高血压组513例,早产(先兆早产但不伴分娩)组648例,正常组12064例。分析所有研究对象叶酸代谢相关酶基因型分布特点,并利用χ²检验分析各基因型频率及叶酸利用风险性与妊娠期糖尿病、妊娠期高血压、早产、羊水过少的关系。结果在该院受检的孕妇5,10-亚甲基四氢叶酸还原酶(MTHFR)基因1298A>C位点AA、AC、CC基因型频率分别为62.75%、32.73%、4.52%,MTHFR基因677C>T位点CC、CT、TT基因型频率分别为44.22%、43.06%、12.72%,甲硫氨酸合成酶还原酶(MTRR)基因66A>G位点AA、AG、GG基因型频率分别为55.30%、37.82%、6.88%。羊水过少组孕妇检出叶酸利用能力高风险的比例增高,且MTHFR 677C>T基因型占比和等位基因频率与正常组比较,差异有统计学意义(P<0.05)。妊娠期高血压组孕妇检出叶酸利用能力中风险、高风险的比例均高于正常组,MTHFR 677C>T基因型占比和等位基因频率与正常组比较,差异有统计学意义(P<0.05)。妊娠期糖尿病组孕妇检出叶酸利用能力无风险的比例增高,MTHFR 677C>T基因型占比和等位基因频率与正常组比较,差异有统计学意义(P<0.05)。早产组孕妇检出叶酸利用能力高风险的比例增高,MTHFR 1298A>C和MTRR 66A>G基因型占比和等位基因频率与正常组比较,差异有统计学意义(P<0.05)。结论机体叶酸利用能力风险性越高,妊娠期发生高血压、早产、羊水过少等合并症的概率越大,并且妊娠期高血压对叶酸利用能力的变化更为敏感。MTHFR 677C>T与羊水过少、妊娠期高血压、妊娠期糖尿病的发生有关;早产的发生同时受MTHFR 1298A>C和MTRR 66A>G的影响。     

37例甲亢妊娠患者并发症的护理

目的探讨甲亢妊娠患者并发症的护理经验。方法回顾性总结和分析37例甲亢妊娠患者并发妊高征,心力衰竭,甲亢危象的护理经过。结果本组并发的6例妊高征、4例心力衰竭和2例甲亢危象患者经治疗和护理后,病情得到及时治疗,痊愈出院。结论在围生期加强并发症的监测治疗和护理,对提高甲亢妊娠患者的妊娠结局质量具有重要意义。     

Treatment of edema

Edema is the result of an imbalance in the filtration system between the capillary and interstitial spaces. The kidneys play a key role in regulating extracellular fluid volume by adjusting sodium and water excretion. Major causes of edema include venous obstruction, increased capillary permeability, and increased plasma volume secondary to sodium and water retention. A systematic approach is warranted to determine the underlying diagnosis. Treatment includes sodium restriction, diuretic use, and appropriate management of the underlying disorder. Leg elevation may be helpful in some patients. Loop diuretics often are used alone or in combination. In patients with New York Heart Association class III and IV congestive heart failure, spironolactone has been found to reduce morbidity and mortality rates. In patients with cirrhosis, ascites is treated with paracentesis and spironolactone. Dihydropyridine-induced edema can be treated with an angiotensin-converting enzyme inhibitor or angiotensin-receptor blocker. Lymphedema occurs when a protein-rich fluid accumulates in the interstitium. Compression garments and range-of-motion exercises may be helpful in patients with this condition.     

Cardiovascular responses to circulating catecholamines in normal pregnancy and in pregnancy-induced hypertension

Summary. Patients with pregnancy-induced hypertension (PIH) and healthy pregnant and non-pregnant women were compared with regard to cardiovascular responses to i.v. infusions of noradrenaline (NA) and adrenaline (ADR). This resulted in physiologically relevant concentrations in arterial plasma (maximally 10 nmol/litre for NA and 6 nmol/litre for ADR). Non-pregnant women responded to NA with concentration-dependent increases in blood-pressure, which were caused by peripheral vasoconstriction, as systemic vascular resistance (SVR) was increased by 21%. Cardiac output was reduced by 6%. ADR caused concentration-dependent decreases in SVR (to values 36% below basal) and calf vascular resistance (CVR), as well as increases in cardiac output. Healthy pregnant women responded to NA with similar increases in blood-pressure, but this was due to stroke volume-dependent increases in cardiac output (11%) and not due to vasoconstriction. ADR-induced vasodilatation was attenuated in this group. Cardiac responses to ADR were unaffected by pregnancy. PIH patients demonstrated an enhanced systolic blood-pressure response to NA (19% increase vs 7–8% in the other groups) due to the combined effects of vasoconstriction (11% increase in SVR) and an essentially unchanged cardiac output. ADR-induced decreases in CVR and diastolic blood-pressure were similar to those found in the non-pregnant group. Increases in heart rate were less pronounced, but cardiac output increased as normal. These results indicate that normal pregnancy is associated with attenuated vascular responses to circulating catecholamines. PIH patients do not seem to have undergone this normal adaptation of the vascular system to pregnancy.