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Biomedical subjects

J de Haan

Publications and source records attributed to J de Haan.

At least 55 records · Page 3Linked to original sources
PubMed1992

Leukocyte activation with increased expression of CR3 receptors during cardiopulmonary bypass.

The effects of cardiopulmonary bypass (CPB) on the expression of leukocyte adhesive receptors, ie, complement receptor type 3 (CR3), were studied in 16 patients. The CR3 expression on leukocytes was determined by time-resolved fluoroimmunoassay on a standardized number of cells isolated from blood samples taken during various times during CPB. The results demonstrated that CR3 expression on leukocytes increased immediately after the start of CPB (p less than 0.05), concomitant with an early sharp increase of plasma concentrations of C3a (p less than 0.01). After release of the aortic cross-clamp, a second peak of leukocyte CR3 expression was induced (p less than 0.05), paralleled by a significant increase of leukotriene B4 (p less than 0.05) and elastase (p less than 0.05) levels in the late period of CPB. In vitro studies with leukocytes isolated from healthy donors (n = 5) showed a dose-dependent increase of CR3 expression stimulated by zymosan-activated plasma, indicating that the rapid CR3 expression on leukocytes is likely mediated by complement activation. However, the mechanisms for the second peak of leukocyte CR3 expression during CPB remain to be further elucidated. In conclusion, CR3 expression on leukocytes increased immediately after the start of CPB and was followed by a second peak of expression in the late phase of CPB. Pharmacological blockage of these adhesive receptors might reduce the leukocyte-mediated deleterious effects of CPB.

Cardiopulmonary Bypass↗
PubMed1991

Fetal hypertension induced by norepinephrine infusion and umbilical artery flow velocity waveforms in fetal sheep.

This study was designed to examine the effects of fetal hypertension on the umbilical artery pulsatility index. Fetal arterial blood pressure and umbilical venous pressure were measured in eight sheep, 3 to 5 days after surgery. Umbilical blood flow was measured with an electromagnetic flowmeter around the common umbilical vein. Umbilical artery flow velocity waveforms were obtained either by an indwelling 5 MHz pulsed Doppler device (n = 4) or transcutaneously by a 4 MHz continuous-wave Doppler device (n = 4). Fetal blood pressure was raised by intravenous infusion of norepinephrine 10 micrograms/min during 5 minutes. Norepinephrine infusion resulted in elevated arterial and umbilical venous pressures, accompanied by a bradycardia during the first 3 minutes. Umbilical blood flow, calculated placental vascular resistance, and umbilical artery pulsatility index did not change. After atropine administration, the norepinephrine-induced elevated arterial and umbilical venous pressures were accompanied by tachycardia, increased umbilical blood flow, and no change in placental vascular resistance and umbilical artery pulsatility index. It is concluded that fetal arterial hypertension provoked by norepinephrine infusion has no effect on placental vascular resistance, umbilical blood flow, and umbilical artery pulsatility index.

Animals↗
PubMed1991

Umbilical artery pulsatility index and placental vascular resistance during acute hypoxemia in fetal lambs.

The effect of hypoxemia on the pulsatility index (PI) of the umbilical artery flow velocity waveform and placental vascular resistance was studied. Fetal hypoxemia was induced by maternal breathing of a low-oxygen gas mixture. Umbilical venous blood flow was measured with an electromagnetic flowmeter. Placental vascular resistance (PVR) was defined as the ratio perfusion pressure (mean arterial pressure minus umbilical venous pressure) and umbilical blood flow. Umbilical artery velocity waveforms were obtained by a 5-MHz pulsed Doppler device around one umbilical artery in 4 lambs and by a transcutaneous 4-MHz continuous wave Doppler transducer in 3 lambs. Fetal arterial oxygen content was lowered from 2.28 +/- 0.18 to 0.93 +/- 0.15 mM (p less than 0.05), while pCO2 and pH remained unchanged. Control values of the hemodynamic variables were compared with values during deepest hypoxemia. Fetal heart rate, mean arterial and umbilical venous pressure, PVR and the umbilical artery PI did not significantly change, whereas umbilical blood flow increased from 436 +/- 64.7 to 491 +/- 65.9 ml/min (p less than 0.05) during deepest hypoxemia. Individual regression analysis, however, showed a significant inverse correlation of umbilical venous pressure whereas PVR had a positive correlation with actual oxygen content. It is concluded that acute fetal hypoxemia slightly decreases PVR, but does not affect the umbilical artery PI in sheep. Decreasing fetal oxygenation is associated with an increase in pressure in the umbilical vein.

Animals↗
PubMed1990

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↗
PubMed1990

The response of the umbilical artery pulsatility index in fetal sheep to acute and prolonged hypoxaemia and acidaemia induced by embolization of the uterine microcirculation.

In eight chronically-instrumented sheep, embolization of the uterine microcirculation was performed to evaluate the response of the umbilical artery pulsatility index to prolonged fetal hypoxaemia and acidaemia. From four days after surgery onwards, fetal arterial oxygen content [( O2]a) was progressively reduced by administration of microspheres into the uterine circulation. Measurements included fetal [O2]a, PO2, PCO2, pH, base excess, heart rate, blood pressure and umbilical artery pulsatility index. Fetal survival varied between less than 2 and less than 8 days, while mean fetal survival was less than 4 days. From baseline condition to the last evaluation preceding the diagnosis of fetal death, [O2]a decreased from 3.10 +/- 0.36 to 0.87 +/- 0.27 mM, pH decreased from 7.36 +/- 0.03 to 7.22 +/- 0.08, base excess decreased from -0.3 +/- 1.5 to -7.3 +/- 3.2 and blood pressure increased from 35.0 +/- 7.1 to 40.7 +/- 8.7 (means +/- SD). The umbilical artery pulsatility index (1.05 +/- 0.19 at baseline condition) did not significantly change (1.08 +/- 0.12 prior to fetal death). It is concluded that a condition of prolonged hypoxaemia and acidaemia in fetal sheep, induced by repeated embolizations of the uterine circulation, is not associated with consistent changes in the umbilical artery pulsatility index.

Acid-Base Equilibrium↗
PubMed1990

Umbilical artery flow velocity waveforms and placental vascular resistance during maternal placental outflow obstruction in sheep.

This study was designed to test the hypothesis that the pulsatility index (PI) of the umbilical artery flow velocity waveform varies as a function of placental vascular resistance. Placental vascular resistance was raised by a one-minute occlusion of the maternal inferior vena cava. Occlusion of the maternal inferior vena cava resulted in a decrease in fetal heart rate from 183 +/- 7.8 beats/min to 142 +/- 8.6 beats/min at the end of occlusion (P less than 0.05). Placental vascular resistance increased from 0.113 +/- 0.021 mmHg.ml-1.min during control to 0.151 +/- 0.033 mmHg.ml-1.min (P less than 0.05) during occlusion. The pulsatility index increased from 1.05 +/- 0.05 to 1.85 +/- 0.4 (P less than 0.05) during occlusion. After parasympathetic blockade with atropine fetal heart rate did not change during occlusion. Placental vascular resistance increased from 0.091 +/- 0.014 before to 0.121 +/- 0.021 mmHg.ml-1.min during occlusion (P less than 0.05). The pulsatility index increased from 0.98 +/- 0.1 before to 1.12 +/- 0.12 during occlusion (P less than 0.05). These results support the hypothesis that, in the fetal sheep, placental vascular resistance is one of the determinants of the pulsatility index of the umbilical artery.

Animals↗
PubMed1989

Selective hepatobiliary transport of nordeoxycholate side chain conjugates in mutant rats with a canalicular transport defect.

Canalicular transport of bilirubin diglucuronide, dibromosulfophthalein and several glutathione conjugates is deficient in mutant TR- rats. In contrast, transport of cholyltaurine (taurocholate), a conjugated bile acid, is normal. Previous studies using normal rats have shown that C23 nor-dihydroxy bile acids are conjugated with sulfate or glucuronide during hepatic transport in contrast to the natural C24 bile acids, which are amidated with glycine or taurine. Studies were performed to test the hypothesis that (a) in the TR- rat, nordeoxycholate would be conjugated with glucuronate or sulfate just as in the normal rat, and (b) that such conjugates would have defective biliary secretion. [C23-14C]Nordeoxycholate was administered intravenously to bile fistula rats (TR- and normal), and the biliary recovery of metabolites was assessed by chromatography and mass spectrometry. In both groups of rats, the major biotransformation product of nordeoxycholate was the side chain (23-ester) glucuronide. Conjugation on the nucleus with sulfate and glucuronide at the 3-position (ethereal linkage) also occurred, as well as amidation at the C23 carboxylic acid group. In the mutant rats, biliary secretion of the 3-sulfate and 3-glucuronide conjugates was less than 10% and 1%, respectively, of that of normal rats, whereas biliary secretion of the 23-ester glucuronide and the 23-taurine amidate, as well as unchanged nordeoxycholate, was not decreased. Canalicular secretion of nor-bile acid 3-ether glucuronides and 3-sulfates appears to involve the "bilirubin transport system," which is deficient in mutant rats. Canalicular secretion of unconjugated, amidated or esterified nordeoxycholate is mediated via another pathway, probably the "bile acid transport system."(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Umbilical artery flow velocity waveforms during acute hypoxemia and the relationship with hemodynamic changes in the fetal lamb.

The contributions of the variables of the fetal circulation to changes in the pulsatility index of the umbilical artery flow velocity waveform have not been assessed. Acute fetal hypoxemia was induced by 60 to 90 seconds of total occlusion of the maternal common internal iliac artery in six sheep. Mean fetal PO2 levels decreased from 26.0 to 18.3 mm Hg (p less than 0.01) after occlusion of uterine blood flow. Fetal heart rate decreased from 188 to 121 beats per minute at the end of occlusion (p less than 0.05). Placental vascular resistance did not change during the heart rate deceleration. The pulsatility index increased from 0.86 during the control period to 1.27 at the end of occlusion (p less than 0.05). After fetal parasympathetic blockade with atropine, fetal heart rate and placental vascular resistance did not change during occlusion. The pulsatility index did not change during occlusion after parasympathetic blockade. It is concluded that the changes in the umbilical artery pulsatility index during late decelerations in the fetal heart rate pattern appear to be primarily associated with changes in fetal heart rate and bear no relationship with placental vascular resistance.

Acute Disease↗
PubMed1989

Uterine vascular resistance during compression of the umbilical arterial and/or venous circulation in sheep.

Total umbilical cord occlusion and selective occlusion of the umbilical arteries and veins is associated with changes in uterine blood flow. In the present study, the resistance to uterine blood flow during selective occlusions of the umbilical arteries and/or veins was analysed in five chronically instrumented pregnant sheep in the last third part of pregnancy. An occluding device which allows separate occlusion of umbilical veins and arteries was applied to the umbilical cord. Median uterine artery blood flow was measured using an electromagnetic flow meter. Maternal pressures were measured in a branch of the uterine artery and vein. Two occlusions of the umbilical veins and/or arteries with a duration of 30-60 s were performed in each animal. Selective occlusion of the umbilical arteries resulted in a small increase in uterine blood flow from 637 +/- 79 ml/min during control toward 664 +/- 77 ml/min at the end of occlusion (p less than 0.05). Uterine perfusion pressure (uterine arterial pressure - uterine venous pressure) did not change. No changes were observed in calculated uterine vascular resistance (Poiseuille equation). Selective occlusion of the umbilical veins on the other hand caused a decrease in uterine blood flow from 617 +/- 75 ml/min during control to 546 +/- 69 ml/min at the end of occlusion (p less than 0.001), and a return to control value at 1 min after occlusion. The uterine perfusion pressure increased from 40.1 +/- 6.8 mmHg during control to 42.8 +/- 7.0 mmHg at the end of occlusion (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Detection of Chlamydia trachomatis, Mycoplasma hominis and Ureaplasma urealyticum in pregnant Dutch women.

A prospective study was performed to determine the prevalence of endocervical infection by Chlamydia trachomatis and vaginal colonization by Mycoplasma hominis and Ureaplasma urealyticum in pregnant women seeking routine obstetrical care in two clinics in the southern part of the Netherlands. C. trachomatis was detected using the direct immunofluorescence staining technique. For the genital mycoplasmata, generally accepted culture methods were used. Evaluable samples were obtained from 691 of 770 women in the first trimester of pregnancy. C. trachomatis was detected in 2.3%, M. hominis in 5.2% and U. urealyticum in 23.9% of the women. The isolation percentages of C. trachomatis and U. urealyticum were almost equally distributed in the different age groups. The prevalence of all three micro-organisms did not seem to be related to parity. Smoking and alcohol consumption seemed to influence the isolation rate of M. hominis and U. urealyticum.

Adult↗
PubMed1989

Hepatobiliary transport of glutathione and glutathione conjugate in rats with hereditary hyperbilirubinemia.

TR- mutant rats have an autosomal recessive mutation that is expressed as a severely impaired hepatobiliary secretion of organic anions like bilirubin-(di)glucuronide and dibromosulphthalein (DBSP). In this paper, the hepatobiliary transport of glutathione and a glutathione conjugate was studied in normal Wistar rats and TR- rats. It was shown that glutathione is virtually absent from the bile of TR- rats. In the isolated, perfused liver the secretion of glutathione and the glutathione conjugate, dinitrophenyl-glutathione (GS-DNP), from hepatocyte to bile is severely impaired, whereas the sinusoidal secretion from liver to blood is not affected. The secretion of GS-DNP was also studied in isolated hepatocytes. The secretion of GS-DNP from cells isolated from TR- rat liver was significantly slower than from normal hepatocytes. Efflux of GS-DNP was a saturable process with respect to intracellular GS-DNP concentration: Vmax and Km for efflux from TR- cells was 498 nmol/min.g dry wt and 3.3 mM, respectively, as compared with 1514 nmol/min.g dry wt and 0.92 mM in normal hepatocytes. These results suggest that the canalicular transport system for glutathione and glutathione conjugates is severely impaired in TR- rats, whereas sinusoidal efflux is unaffected. Because the defect also comes to expression in isolated hepatocytes, efflux of GS-DNP from normal hepatocytes must predominantly be mediated by the canalicular transport mechanism, which is deficient in TR- rats.

Amino Acids↗
PubMed1988

Comparison of blood velocity waveform indices recorded by pulsed Doppler and continuous wave Doppler in the umbilical artery.

A comparison was made between the AB ratio, resistance index (RI), and pulsatility index (PI), calculated from tracings obtained by pulsed Doppler (PD) and continuous wave (CW) Doppler devices in 14 uncomplicated singleton pregnancies. The AB ratio, RI, and PI were a slightly higher for the CW Doppler compared to the PD system, although not significantly (p = 0.18, p = 0.21, and p = 0.44, respectively). The difference in signal to noise ratio (S/N ratio) between the PD and CW Doppler systems was felt to be the reason for the discrepancy in the calculated velocity waveform indices.

Blood Flow Velocity↗
PubMed1988

The blood flow velocity waveform index in the fetal thoracic aorta and its ability to detect fetal compromise in the small for gestational age fetus.

In a prospective longitudinal study of 96 patients, mean values of blood velocity waveform indices of the fetal thoracic aorta are established with a combined linear array real-time and pulsed Doppler transducer. The course of the various blood velocity waveforms is elucidated. The most striking finding is the restricted variability of the pulsatility index (PI), resistance index (RI), A/B ratio, acceleration time (AcT) and acceleration time percentage (AcTP) during the last trimester of pregnancy. In 17 proven and evaluable SGA infants the various blood velocity waveform indices were compared with the established mean values. Fourteen of these 17 (82%) infants were proven to be intrauterine growth-retarded (IUGR). Only 3 of these 14 (21%) showed a significant increase in PI values.

Aorta, Thoracic↗
PubMed1988

Variability of PI calculations.

In obstetrics the pulsatility index (PI) may be a useful parameter for the determination of fetal well-being. Although the PI is unambiguously defined, calculation from the measured data can be difficult. In order to study the comparability of PI values found by several investigators and with different methods tape recordings of Doppler signals of fetal vessels were used. The tapes were processed by several centres in Europe and the results were compared. Comparability is poor, although for the umbilical artery the results are in reasonable agreement. The method used has its drawbacks but shows that one must be careful in comparing results from different centres.

Aorta, Abdominal↗
PubMed1988

Death from chemotherapy in gestational trophoblastic disease.

Multiple cytotoxic drug administration is the generally accepted treatment of patients with a high-risk stage of choriocarcinoma. Based on this principle a 27-year old woman, classified as being in the high-risk group (Goldstein and Berkowitz score: 11), was treated with multiple cytotoxic drugs. The multiple drug schema consisted of: Etoposide 16.213, Methotrexate, Cyclophosphamide, Actomycin-D, and Cisplatin. On the first day of the schedule, moderate high doses of Methotrexate, Etoposide and Cyclophosphamide were administered. Within 8 hours after initiation of therapy the patient died with a clinical picture resembling massive pulmonary obstruction due to choriocarcinomic tissue plugs, probably originating from the uterus. Formation of these plugs was probably due to extensive tumor necrosis at the level of the walls of the major uterine veins, which resulted in an open exchange of tumor plugs to the vascular spaces; decrease in tumor tissue coherence secondary to chemotherapy may have further contributed to the formation of tumor emboli. In view of the close time association between the start of chemotherapy and the acute onset of massive embolism other explanations, such as spontaneous necrosis, must be considered less likely. Patients with large pelvic tumor loads are, according to existing classifications, at high risk to die and to develop drug resistance. Notwithstanding these facts our findings suggest that these patients might benefit from relatively mild initial treatment, especially true for patients not previously exposed to this drug. Close observation of the response status both clinically and with beta-hCG values may indicate whether and when more agressive combination chemotherapy should be started.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Umbilical artery blood velocimetry: a prospective longitudinal study in search of the intrauterine growth-retarded fetus.

In a longitudinal prospective study involving 125 patients, blood velocity waveforms in the umbilical artery were recorded and analyzed from the 15th week of gestation until term to evaluate the predictive value of blood velocity parameters with regard to fetal growth retardation. Measurements were performed with a combined real-time linear array and 2-MHz pulsed Doppler technique. The mean values (+/- 2 S.D.) of the A/B ratio, resistance index (RI) and pulsatility index (PI) were calculated from the 15th to the 40th week of gestation. The degree of intrauterine growth retardation was related to postnatal catch-up growth. Three groups of patients were compared with regard to blood velocity waveform indices. Group NL-I/II: waveform indices (WI) within 2 S.D. of the population mean. Group EL-II: consistently WIs above 2 S.D. of the population mean. Significant differences with regard to neonatal growth variables were found between these groups. In spite of the fact that these differences in growth variables were statistically significant, no clear relationship was found between the velocity waveform indices and true intrauterine growth retardation, defined by a non-birthweight criterion. It seems that umbilical artery velocimetry cannot predict true intrauterine growth retardation.

Birth Weight↗