PubMed Health⌕ Search

Biomedical subjects

L L Peeters

Publications and source records attributed to L L Peeters.

At least 37 records · Page 2Linked to original sources

Hemodynamic changes in early pregnancy in chronically instrumented, conscious rats.

To explore the onset of and the interrelationship between maternal hemodynamic changes in pregnancy, serial hemodynamic measurements were performed in chronically instrumented, conscious rats using electromagnetic flow probes around the ascending aorta and arterial catheters. The rats were studied daily from day 4 to day 12 and on days 14, 18, and 20 of pregnancy. Nonpregnant (NP) rats matched for age and days postsurgery served as controls. In the pregnant (P) group, the hematocrit started to decrease by postconceptional day 6 (day of implantation) to reach a value of 9 +/- 3% below the initial level by day 8. In these 2 days, cardiac output (CO) increased by 9 +/- 4%, as a result of a rise in stroke volume (SV). No changes in mean arterial pressure were observed. In both groups, heart rate (HR) had decreased by day 7. Aortic flow acceleration and peak aortic flow, indicators of myocardial contractility, increased from day 10 on only in the P group. In this context, it should be emphasized that the results of this study do not allow differentiation between the contractile properties of the cardiac muscle and the contractile changes as a result of the altered preload and afterload. By days 12 and 18, CO had increased by 20 +/- 5 and 29 +/- 9%, respectively, above the initial value and by 25 and 40%, respectively, above the value observed in the NP group. The rise in CO after day 14 was accomplished by a concomitant increase in HR and SV and was accompanied by a further increase in myocardial performance. We conclude that hemodynamic changes can already be identified by day 8 of rat pregnancy, 2 days after implantation. The rise in CO in early pregnancy results from a selective increase in SV and is accompanied by a rise in myocardial performance.

Animals↗

The effect of labetalol on maternal haemodynamics and placental perfusion in awake near term guinea pigs.

The effect of labetalol (20 micrograms/kg/min) on maternal haemodynamics in general, and absolute placental perfusion in particular, was studied in eight chronically instrumented hypertensive guinea pigs near term. One day before drug testing, all experimental animals were subjected to haemoconcentration (haematocrit was gradually raised from 35.9 +/- 2.9 to 49.4 +/- 5.6 vol%, mean +/- S.D.) to establish a prolonged and stable state of hypertension. This procedure increased mean arterial pressure from 59.7 +/- 7.2 to 70.3 +/- 8.6 mmHg, and was paralleled by mild foreseeable systemic haemodynamic effects (redistribution of cardiac output away from intestines and brain), without consistent changes in the maternal placental blood flow. The hypotensive effect of labetalol was paralleled by a selective reduction in placental perfusion as reflected by a consistent fall in weight-specific cardiac output fraction (from 55.5 +/- 26.6 to 40.9 +/- 12.5%/100 g, P < 0.05) and blood flow (from 155 +/- 76 to 112 +/- 44 ml/min/100 g, P < 0.05) to the placentas. The concomitant placental resistance had increased consistently from 0.55 +/- 0.26 to 0.62 +/- 0.32 mmHg.min.100 g/ml, P < 0.05. We conclude that in awake late-pregnant hypertensive guinea pigs, labetalol reduces uteroplacental blood flow selectively. We speculate that the latter selective effect is secondary to the fall in blood pressure.

Animals↗

Maternal volume homeostasis in early pregnancy in relation to fetal growth restriction.

OBJECTIVE: To test the hypothesis that volume adaptation in pregnancies complicated by fetal growth restriction (FGR) is already abnormal very early in pregnancy. METHODS: In six pregnancies later complicated by FGR, volume homeostasis in the first 8 weeks was compared to that in ten normal pregnancies. Creatinine clearance, volume-dependent hormones, hemodilution-related variables, and ultrasonic cardiovascular dimensions were measured weekly between weeks 5 and 10, in the second and third trimesters, and postpartum. Differences between the two groups were analyzed by nonparametric tests. RESULTS: Very early in pregnancy, pregnancies complicated by FGR differed from normal pregnancies in the following ways: smaller left atrial diameter, smaller collapsible part of the inferior vena cava, lower serum sodium concentration, and smaller fall in serum creatinine and urea. CONCLUSION: Fetal growth restriction is preceded by defective volume adaptation very early in pregnancy. It appears that the maternal compensation mechanisms are unable to resolve the transient state of vascular underfill seen in this period in normal gestation.

Adult↗

Lack of positive correlation between placental blood flow and mean arterial pressure in the non-anaesthetised guinea pig near term; an indication for autoregulation?

The objective of the present study was to evaluate whether placental blood flow (PBF) decreases or increases, in response to a fall or rise in mean arterial pressure (MAP), respectively, in an unanaesthetised animal model with a haemochorial placenta. Such a response would support the absence of autoregulation of placental blood flow for changes in mean arterial pressure. To this end, 31 late-pregnant guinea pigs were subjected to isovolemic haemodilution, a sham procedure or isovolemic haemoconcentration, after adequate recovery from instrumentation. The percentage change from baseline in PBF (delta PBF, %), was compared between animals with a fall in MAP, in response to haemodilution or the sham procedure (MAP-fall, n = 8, mean delta MAP -11 +/- 7%) and those with a rise in MAP, following haemoconcentration (MAP-rise, n = 10, mean delta MAP +15 +/- 8%). In addition, the percentage change in the blood flow to the myocardium, gastrointestinal tract, adrenals, kidneys, brain, skin, carcass and myometrium was compared between the MAP-fall and the MAP-rise group. The direction of the change in PBF did not differ between the MAP-fall and the MAP-rise group. In this respect, the distribution of delta PBF over the two groups was comparable with that observed for the myocardium, gastrointestinal tract, adrenals, skin, carcass and myometrium. The blood flow to the kidneys and the brain varied in response to the change in haematocrit. The results of this study show that PBF varies independently from MAP. This observation supports the idea that the blood flow to the labyrinthine placenta of the awake and healthy guinea pig near term may be autoregulated for hydrostatic inflow pressure, at least over the spectrum of arterial pressures observed in the present study.

Animals↗

Obstetric antecedents of surgically treated obstetric brachial plexus injuries.

OBJECTIVE: To determine whether the anatomy of an obstetric brachial plexus lesion (OBPL) is causally related to the preceding obstetric history. DESIGN: Anatomical classification of the OBPL during reconstructive neurosurgical treatment in consecutive infants who had surgery for OBPL between 1986 and 1994 and relating these findings with the characteristics of the preceding birth. SETTING: De Wever Hospital, Heerlen, The Netherlands. SUBJECTS: All infants who had surgical treatment for OBPL between 1 April 1986 and 1 January 1994 (n = 130). RESULTS: An Erb's C5-C6 injury was preceded more frequently by a difficult breech birth (19/26 cases or 73%). In contrast, the more extensive forms of Erb's palsy classified as a C5-C7 injury or a total palsy with a C5-T1 injury were observed more frequently after complicated cephalic birth (52/59 or 88%, and 43/45 or 96%, respectively). The extent of anatomical damage as expressed by the incidence of an avulsion of one or more spinal nerves was 18/26 (69%) in Erb C5-C6, 13/59 (22%) in Erb C5-C7 and 21/45 (47%) in total C5-T1 palsy. CONCLUSION: The Erb's C5-C6 palsy, occasionally bilateral and/or complicated by phrenic nerve injury, was the most frequent form of OBPL after a breech birth. The more extensive form of Erb's palsy and the total palsy were observed more frequently after delivery in a cephalic presentation. The pure form of Erb's palsy and the total palsy were characterised by a higher incidence of nerve avulsions than the extensive form of Erb's palsy.

Birth Weight↗

Severely impaired fetal growth is preceded by maternal hemodynamic maladaptation in very early pregnancy.

OBJECTIVE: To test the hypothesis that in pregnancies complicated by intrauterine growth retardation (IUGR) maternal cardiovascular adaptation is already abnormal in the first weeks of pregnancy. SETTING: University Hospital Maastricht, Maastricht, The Netherlands. SUBJECTS: Fourteen healthy pregnant women, recruited from the subfertility clinic. Ten pregnancies were uneventful and four pregnancies resulted in the birth of growth retarded infants. METHODS: Maternal cardiovascular status was followed longitudinally by combined M-mode and Doppler echocardiography. Studies were performed weekly between the fifth and 10th week, at 14, 25 and 35 weeks and postpartum. Differences between the two groups were analyzed by nonparametric tests. RESULTS: In early pregnancy, the IUGR group differed from the normal group by a consistently smaller left atrial diameter and a cardiac output that failed to increase. Postpartum the subjects in the IUGR group had a significantly smaller left atrial diameter and faster mean circumferential fiber shortening. CONCLUSION: Maternal hemodynamic adaptation in the first weeks of pregnancy is defective in IUGR pregnancies, presumably associated with a concomitant inadequacy of the vascular filling state.

Echocardiography, Doppler↗

Value of maternal fructosamine in the screening of an unselected population for hyperglycemia-related complications in the newborn.

The relationship between the maternal serum fructosamine concentration and pregnancy outcome was studied in 765 consecutive subjects of an obstetric community hospital population. The neonatal outcome of patients with a fructosamine concentration in pregnancy below and above 2.30 mmol/L were compared. Patients with a fructosamine concentration above 2.30 mmol/L did not show an increased incidence of neonatal hypoglycemia, hyperbilirubinemia, or respiratory distress syndrome. On the other hand, they did give birth to infants with a higher birthweight ratio, a variable defined as newborn weight corrected for sex, gestational age, and parity. However, the predictive value with respect to birthweight ratio was modest: Fructosamine accounted for only 1.4% of the variation in birthweight ratio, much less than other well-known contributors to this variation, such as smoking (10%) and prepregnancy maternal (6.5%) or paternal weight (2.8%). The screening value of fructosamine to identify patients who would give birth to a macrosomic infant was limited irrespective the gestational age at measurement. It is concluded that fructosamine determined during pregnancy in an unselected obstetric population is an unsuitable screening method to trace patients with an increased risk to deliver of an infant with neonatal complications of maternal hyperglycemia.

Adult↗

Value of the fern test to confirm or reject the diagnosis of ruptured membranes is modest in nonlaboring women presenting with nonspecific vaginal fluid loss.

The strength of the fern test to differentiate between amniotic and nonamniotic fluid in vaginal discharge was determined in 51 term women in labor with ruptured membranes and compared with that in a group of 120 nonlaboring subjects, presenting with nonspecific vaginal fluid loss. Sensitivity and specificity in the laboring group were 98.0 and 88.2%, respectively, in agreement with previous reports. In contrast, in the non-laboring group sensitivity and specificity were only 51.4 and 70.8%, respectively. The result of the fern test predicted the actual state of the membranes correctly in 63% and incorrectly in 29% of these patients. In 16 or 39 subjects with ruptured membranes (approximately 40%), the outcome of the fern test was negative. The modest diagnostic strength of the fern test in the present study compared with previously reported data is at least in part due to differences in study population (laboring versus nonlaboring) and to the fact that observers were deprived of relevant clinical information. It is concluded that the fern test should be granted supportive rather than conclusive value in diagnosing ruptured membranes in nonlaboring women presenting with nonspecific vaginal fluid loss.

Amniotic Fluid↗

Measurement of anterior-posterior diameter of inferior vena cava by ultrasonography: a new non-invasive method to assess acute changes in vascular filling state.

OBJECTIVE: The aim was to determine whether measurement of the anterior-posterior diameter of the inferior vena cava (IVC) by ultrasonography, before and during deep inspiration, allows indirect information on baseline blood volume and changes in vascular filling state to be obtained in healthy subjects. METHODS: Blood volume was measured in 12 volunteers by a standard radioactive isotope method. The IVC dimensions were measured by ultrasound in various positions. In addition, in 10 male subjects the effect on the IVC dimensions of volume loading was evaluated by rapid infusion of plasma expander. During and immediately following volume loading, the IVC dimensions and blood volume were remeasured. RESULTS: Neither the baseline IVC diameters nor any combination of these variables correlated with the concomitant blood volume. Volume loading increased the anterior-posterior IVC dimensions linearly, the largest increase being observed with the maximum IVC diameter and the subject in supine position. CONCLUSIONS: It follows that ultrasonic IVC indices cannot be used as accurate indirect estimate of baseline blood volume, but provide reliable information on acute changes of the subjects' vascular filling state.

Adult↗

Renal hemodynamics and volume homeostasis in pregnancy.

Maternal hemodynamic adaptation to pregnancy consists of profound changes in various interdependent systems. Of crucial importance in the early adaptation of the volume homeostatic mechanisms to pregnancy is the resetting of the volume and osmoreceptors. This resetting may be induced by a reduction in vascular tone and leads to early changes in plasma osmolality and glomerular filtration rate. After this initial adaptation other volume-regulating mechanisms such as the renin-angiotensin-aldosterone system, pregnancy hormones, and alpha-ANP adapt to the rising blood volume. The initial adaptation results in a state of relative vascular underfill, inducing secondary compensations in the volume homeostasis. The initially increased vascular capacitance in pregnancy is compatible with the signals of vascular overfill. Contrarily, the protracted filling of this enlarged vascular bed triggers signals compatible with vascular underfill.

Adaptation, Physiological↗

Maternal cardiovascular hemodynamic adaptation to pregnancy.

Maternal cardiovascular adaptation to pregnancy involves enormous changes. Cardiac output increases in early pregnancy, initially as a result of an increased heart rate, soon followed by an increased stroke volume. Cardiac output continues to increase until midpregnancy, and remains stable afterward, with a possible small decline in the last weeks of pregnancy. Blood pressure decreases in early pregnancy, reaching a minimum in midpregnancy, then returning to baseline levels at term. Consequently, peripheral vascular resistance is reduced throughout pregnancy. Myocardial contractility seems to be increased during all trimesters of pregnancy, thus gradually provoking the development of a mild ventricular hypertrophy. The increase in preload, which develops in concert with the increment in blood volume, leads to an increase in left atrial diameter, which also begins during early pregnancy. During labor, both cardiac output and blood pressure increase. After delivery, cardiac output initially increases, but begins to decrease within the first hour to reach baseline levels 2 weeks postpartum. Most cardiovascular parameters show their greatest changes within 2 weeks postpartum. Five months postnatally, only a mild residual ventricular hypertrophy persists.

Adaptation, Physiological↗

The effect of early maternal maladaptation on fetal growth.

IUGR can develop, either in response to a reduced IGP or in response to a deficient transplacental supply of O2 and nutrients. Particularly, insight in the pathogenesis of extrinsic IUGR is important for the clinician to offer him tools for a more causal treatment. Extrinsic IUGR is usually preceded by a gradually developing uteroplacental insufficiency. Uteroplacental hypoperfusion may represent the common starting point for extrinsic IUGR and maternal systemic symptomatology (PIH, (pre)eclampsia). In addition, it may be the common endpoint of two different (subclinical) pathways: defective trophoblast differentiation ("primary") and decompensation of early-pregnancy circulatory maladaptation ("secondary"). From a theoretical point of view, the primary pathway may develop at a slower rate. Therefore, the primary pathway is more likely to result in extrinsic IUGR. In contrast, the secondary pathway assumes decompensation of an initially maladapted maternal circulation. This implies a highly variable rate of development and with it, severity of clinical symptomatology. It also indicates that the the pathogenesis, eventually leading to manifest vascular disease, is superimposed on a pre-existent inadequacy in maternal hemodynamics, renal function and/or volume homeostasis. It is understood that intertwining of these two pathways is common. Unfortunately, our current knowledge, about placentation and the concomitant early-pregnancy adjustments is poor. Current research of trophoblast differentiation and of the concomitant maternal end-organ effects in normal and pathologic pregnancy, is likely to increase our understanding of the first-trimester phenomena preceding IUGR soon.

Adaptation, Physiological↗

Increased red cell aggregation does not reduce uteroplacental blood flow in the awake, hemoconcentrated, late-pregnant guinea pig.

The effect of increased red blood cell aggregation on uteroplacental blood flow was studied in 11 awake, late-pregnant guinea pigs. The aggregation of the red cells was increased by administering high molecular weight dextran (HMWD) to the previously hemoconcentrated animal. The purpose of the hemoconcentration before HMWD was 1) to use a preeclampsia model in which the hemorheology may be impaired because of the combined effect of polycythemia, an increased red cell aggregation, and an increased plasma viscosity and 2) to potentiate the aggregation-increasing effect of HMWD. Relative to the pre-HMWD condition, arterial blood pressure and systemic vascular resistance increased by 10 and 26%, respectively. The cardiac output fraction shunted across the systemic circulation and the arterial hematocrit decreased by 30 and 4%, respectively. Neither cardiac output nor the weighted organ flows, including those to the placentas, changed in response to the rise in red cell aggregation. We conclude that an imposed increase in red cell aggregation has no appreciable effect on uteroplacental blood flow in the awake and healthy late-pregnant guinea pig. These data do not exclude the possibility that increased red blood cell aggregation potentiates the negative effects on uteroplacental blood flow, e.g. in pregnancy-induced hypertension or preeclampsia, where the placenta is not only marginally perfused but also frequently damaged histologically.

Animals↗

The effect of volume expansion on placental blood flow in awake hypovolemic rats in late pregnancy.

Symptomatic hypovolemia in preeclampsia is often treated by volume expansion. However, the effect of this treatment on placental blood flow is unclear. In the present study the hypothesis was tested that slow volume expansion, imposed on volume-depleted rats, does not compromise placental blood flow. Mild hypovolemia was induced in rats in late pregnancy by 24 hours' thirsting. The resulting gradual dehydration was associated with a 7% reduction in blood volume. These rats were then subjected to blood volume expansion by a continuous infusion with a plasma substitute. Volume expansion increased blood volume by 32% and cardiac output by 73%. The extra cardiac output was distributed to kidneys, carcass, and portal bed. Placental blood flow decreased by 31%. The pattern of response was comparable to the one previously observed in normovolemic rats. However, the magnitude of the changes was larger, probably associated with a delayed or impaired diuretic response. These data suggest that volume expansion therapy in mildly hypovolemic pregnant rats elicits an exaggerated hemodynamic response as compared with normovolemic rats, including placental compromise.

Animals↗

Nondeformable red blood cells do not interfere with uteroplacental blood flow in the awake, late-pregnant guinea pig.

The fractional entrapment of rigidified [relative to control (labeled)] red cells after the intravascular bolus injection of a cocktail of these cells, and the concomitantly induced changes in cardiac output and its distribution (microspheres) were studied in 14 awake, late-pregnant guinea pigs. In a preceding validation study in eight nonpregnant guinea pigs, it was demonstrated that with this technique reproducible data could be generated on the fractional entrapment of rigidified red cells in all organs in this species except for lungs, liver, and spleen. In response to a bolus injection with rigidified and control red cells, only the brain showed preferential entrapment of rigidified red cells, together with a small but consistent increase in blood flow. In other organs (lungs, liver, and spleen excluded), neither preferential entrapment of rigidified red blood cells nor a consistent change in blood flow could be demonstrated. The results of our study suggest that circulating nondeformable red cells have no measurable adverse effect on the perfusion of the nondiseased hemochorial placenta in the awake, late-pregnant guinea pig. This does not exclude the possibility that rigidified red cells may increase the resistance to flow in a microcirculation that has been pathologically changed by some underlying disease.

Animals↗

Hemodynamic response to volume stress in awake late-pregnant and nonpregnant rats.

The present study was designed to determine whether the often observed gestational rise in blood volume alters the hemodynamic response to volume stress relative to the nonpregnant state. Late-pregnant and nonpregnant Wistar rats, prepared with an electromagnetic flow probe around the ascending aorta and/or intravascular catheters were used for this study. One of the following sets of measurements were performed either before and after volume loading or before and after volume depletion (24 h thirst): 1) continuous monitoring of cardiac output, blood pressure, heart rate, and fluid balance (only during volume loading); 2) measurement of cardiac output and regional blood flows (microspheres); and 3) measurement of the inferior vena cava diameter (x-ray). Both rapid (bolus) and slow volume loading (infusion) led to a rise in cardiac output. The generated surplus in cardiac output was distributed to the kidneys, skeletal tissues, and intestines (only in nonpregnant rats), and was paralleled in the pregnant rats by a consistent fall in placental blood flow. Slow volume depletion had neither a consistent effect on cardiac output nor on its distribution, with even a preserved maturational rise in placental blood flow during the 24 h of thirst. Slow volume loading and depletion led to an increase and decrease of the caliber of the inferior vena cava, respectively. The nonnuterine hemodynamic response to all forms of volume stress had not changed in pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The response of the umbilical and femoral artery pulsatility indices in fetal sheep to progressively reduced uteroplacental blood flow.

Fetal artery Doppler velocimetry may provide noninvasive information on the state of fetal oxygenation. It was hypothesized that during decreasing fetal oxygenation, the pulsatility index in the femoral artery will increase, whereas the pulsatility index in the umbilical artery will not change. Decreasing fetal oxygenation was induced in ten chronically-instrumented fetal sheep by progressive occlusion of the maternal common internal iliac artery. The pulsatility index in the umbilical artery was serially measured in six fetuses (group I, n = 6) and the pulsatility index in the femoral artery was serially measured in four fetuses (group II, n = 4). Fetal arterial oxygen content decreased by 72% in group I (P less than 0.0001) and by 79% in group II (P less than 0.0001). Fetal heart rate did not change. Fetal blood pressure increased by 11% in group I (P less than 0.02) and by 15% in group II (P less than 0.005). The umbilical artery pulsatility index (group I) did not significantly change during decreasing fetal oxygenation, whereas the femoral artery pulsatility index (group II) increased by 150% (P less than 0.005). It is concluded that progressively reduced uteroplacental blood flow results in fetal hypoxaemia, which is associated with increased pulsatility index in the femoral artery, while the pulsatility index in the umbilical artery does not change.

Acid-Base Equilibrium↗

Systemic leakage of 15 micron radioactive microspheres over a period of 24 hours, in awake late-pregnant guinea pigs.

The present study was designed to determine the reliability of regional blood flow measurements with 15 microns radioactive microspheres, when 24 h have elapsed between reference sampling and sacrifice. The study was performed in 12 chronically-instrumented late-pregnant guinea pigs. The fraction of microspheres recovered from the lungs was consistently higher, by about 2% of the cardiac output after such a 24-h period, as compared to microsphere experiments performed immediately prior to sacrifice. This finding suggests dislodgement of radioactive particles from the systemic circulation between the time of completion of reference sampling and the subsequent 24 h. No correlation could be demonstrated between the change in lung fraction and the change in any organ fraction in particular. Therefore, it is highly unlikely that the microspheres accumulated in the lungs over this period originate from the placenta or any other specific organ. It is concluded that in the awake late-pregnant guinea pig, the 2% loss of microspheres from the systemic circulation during the 24 h following reference sampling, does not invalidate the cardiac output distribution derived.

Animals↗