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Objective: By means of laser Doppler flowmetry to describe the changes in resting microvascular perfusion and post-occlusive reactive hyperaemia in skin of the forearm and finger pulp throughout the menstrual cycle., Design: Prospective descriptive study., Setting: University Hospital of Tromso, Norway., Sample: Fifteen nonsmoking healthy women were studied in the follicular (days 2 to 7) and the luteal (days 19 to 24) phase of the menstrual cycle., Results: Resting perfusion in forearm and finger pulp as well as post-occlusive reactive hyperaemia in finger pulp were unchanged from the follicular to the luteal phase. The peak perfusion value of the reactive hyperaemic response after 1 min of arterial occlusion was significantly reduced from the follicular to the luteal phase (P<0.01) in forearm skin. The repayment for the blood flow debt, which is the hyperaemic response in percentage of the ischaemic build-up, was also reduced (P<0.01). After 3 min of arterial occlusion, significant reductions in peak post-occlusive flow (P<0.01), recovery time, which is the total duration of the hyperaemic response (P<0.01), and the repayment (P<0.01) were observed. A significant correlation was found between the ratio serum oestradiol/progesterone and repayment after 3 min of arterial occlusion in forearm skin (r=0.71,P<0.001)., Conclusions: Vascular reactivity is altered during the menstrual cycle. In the luteal phase, significant reductions in peak perfusion, repayment and recovery time were seen. The mechanisms behind these findings are unclear, but probably involve changes in both serum oestradiol and progesterone levels.

Objective: To investigate the plasma vasoactive peptide (VIP) levels in pregnancies complicated by pre-eclampsia., Design: A prospective clinical study., Setting: University Department of Obstetrics, Tromsø, Norway., Subjects: 18 women with untreated gestational proteinuric hypertension between 32 and 40 weeks gestation (13 primigravid) and 8 women with normal pregnancies of similar gestational age., Interventions: Fasting blood samples on two occasions, 10 min apart., Main Outcome Measures: Plasma VIP measured by radioimmunoassay., Results: Mean maternal plasma VIP was 13.9 (SEM 1.7) pmol/l in those with pre-eclampsia and 4.4 (SEM 0.5) pmol/l in normal pregnancies (P less than 0.0001)., Conclusion: The increased levels of VIP in pre-eclampsia may represent a powerful compensatory mechanism to restore vascular perfusion of various organs, including the uterus and placenta.

During the puerperium significant changes occur in the body volume homeostasis. In the present study the transcapillary fluid balance was examined antepartum in nine healthy women. The interstitial colloid osmotic pressure was measured by the 'wick' method, and interstitial hydrostatic pressure by the 'wick-in-needle' method in subcutaneous tissue on the thorax and at the ankle. From antepartum (gestational week 37-40) to postpartum (5th day), the following changes were observed: A significant increase in the colloid osmotic pressure both in plasma (mean 1.8 mmHg, P = 0.027) and in the interstitial fluid at the ankle (mean 2.9 mmHg, P = 0.008). Neither colloid osmotic pressure gradient (plasma-interstitium), interstitial hydrostatic pressure, nor haemoglobin and haematocrit changed. The observed rise in the interstitial colloid osmotic pressure must be caused by mobilization of fluid from the interstitium, probably due to a reduced capillary hydrostatic pressure. The increase in plasma colloid osmotic pressure is most likely caused by an increased albumin synthesis and/or transport of interstitial proteins back to the vascular compartment.

In 13 patients with severe pre-eclampsia mean serum concentrations of cationic trypsinogen and amylase were statistically significantly higher at 64 ng/ml and 1.6 mumol/l, respectively, than the corresponding mean serum concentrations in 30 normal pregnancies, 22 ng/ml and 1.1 mumol/l respectively. These rises exceeded the expected increased values due to the slight reduction of the renal function in the pre-eclamptic patients, and therefore indicate a concomitant injury of the pancreas.

The thromboplastin activity in blood monocytes was investigated in third-trimester pregnancies comprising 11 patients with severe pre-eclampsia, 10 with essential hypertension and 18 normal pregnancies. Thromboplastin activity in unstimulated monocytes from the severe pre-eclamptic group was on average three times that found in the normal pregnant group, but variation was wide and the differences were not statistically significant. Thromboplastin activity in endotoxin-stimulated monocytes was significantly higher in the severe pre-eclamptic group than in the other two groups (normal and chronic hypertensive). In the severe pre-eclamptic group, there was a significant negative linear correlation between thromboplastin activity of the endotoxin-stimulated monocytes and factor VII. Fibrinogen, factor VII and alpha 2-antiplasmin were significantly lower in the severe pre-eclamptic group than in the normal pregnant group, whereas no differences were observed in factors V, VIII, AT-III and prekallikrein.

Fluid transport between the plasma and interstitial fluid compartment is governed by the Starling forces, i.e. the capillary pressure (Pc), interstitial fluid hydrostatic pressure (Pi) and colloid osmotic pressure in plasma (COPp) and interstitial fluid (COPi). The COPp, COPi and Pi were measured in 10 normal pregnant women in the first and 10 women in the third trimester of pregnancy. Interstitial fluid was collected from subcutaneous tissue by implanted wicks and Pi was measured by the 'wick-in-needle' technique. The COPp was reduced from 23.2 mmHg in the first trimester to 21.1 mmHg in the third trimester. Concomitantly, COPi decreased from 13.1 to 8.4 mmHg on the thorax and from 9.6 to 5.5 mmHg at the ankle. Only small changes in Pi were observed. The more marked fall in COPi than in COPp indicates that a rise in Pc, in addition to hypoproteinaemia, contributes to increased capillary fluid filtration in pregnancy. The reduction in COPi opposes the increased filtration and thereby prevents a rise in interstitial fluid volume and oedema formation. These physiological changes imply a reduced safety margin against oedema formation in late pregnancy.

The platelet release product beta-thromboglobulin (BTG) in venous plasma, and arterial and venous catecholamines were measured in 13 severe pre-eclamptic and 13 normotensive pregnant women. In the pre-eclamptic group, BTG was significantly higher and the platelet count significantly lower than in the normotensive pregnant group. In the pre-eclamptic group, arterial concentrations were significantly higher for adrenaline, noradrenaline and dopamine, whereas in venous plasma only adrenaline and dopamine were higher. Significant positive correlations appeared in the pre-eclamptic patients between venous BTG and arterial adrenaline (r = 0.82), arterial noradrenaline (r = 0.76) and venous adrenaline (r = 0.55). In the pre-eclamptic group, BTG also highly correlated with systolic (r = 0.84) and diastolic blood pressure (r = 0.77) and heart rate (r = 0.67). These findings indicate that sympathetic nervous tone, as measured by arterial and venous plasma catecholamines, is a good predictor of in-vivo blood platelet activation. In pre-eclampsia, increased sympathetic tone may play a key role in platelet activation and consumption and thus in the activation of the coagulation system.

The fluid transport between the plasma and interstitial fluid compartment is governed by the Starling forces, i.e. the capillary pressure (Pc), interstitial fluid hydrostatic pressure (Pi) and colloid osmotic pressure in plasma (COPp) and interstitial fluid (COPi). Interstitial fluid was collected from subcutaneous tissue on the thorax and ankle by implanted wicks and Pi was measured using the 'wick-in-needle' technique. In pre-eclampsia, COPp is reduced due to hypoproteinaemia and this predisposes towards loss of fluid from the vascular compartment. An important oedema-preventing mechanism is reduction of COPi, which serves as a homeostatic buffer against increased capillary filtration. This mechanism works in moderate, but not in severe pre-eclampsia. A higher COPi was found both at the thorax (8.3 vs 7.0 mmHg) and ankle (5.9 vs 3.9 mmHg) in the group with severe pre-eclampsia compared with the group moderate pre-eclampsia, in spite of a significant reduction in COPp (15.5 vs 19.9 mmHg). These findings suggest that an increased microvascular permeability of plasma proteins to subcutaneous tissue contributes to COPp reduction in severe pre-eclampsia.