Heat shock protein expression in umbilical artery smooth muscle.
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Postpartum vasospasm in the umbilical arteries may be due to impaired vasorelaxation secondary to alterations in the expression of heat shock proteins. The contractile responses of pre- and full-term bovine umbilical artery smooth muscles were determined in a muscle bath. Heat shock protein expression was determined in bovine and human arterial tissues using western blotting with specific antisera. Full-term bovine and human umbilical artery smooth muscle was refractory to relaxation induced by the nitric oxide donor, sodium nitroprusside. This impaired vasorelaxation was associated with the expression of the inducible form of the heat shock protein, HSP70i, and increases in the expression of the small heat shock protein, HSP27. Small heat shock proteins have been implicated in modulating contraction and relaxation responses in vascular smooth muscles. Thus, alterations in heat shock protein expression may play a role in umbilical artery vasospasm. (+info)
Strong induction of members of the chitinase family of proteins in atherosclerosis: chitotriosidase and human cartilage gp-39 expressed in lesion macrophages.
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Atherosclerosis is initiated by the infiltration of monocytes into the subendothelial space of the vessel wall and subsequent lipid accumulation of the activated macrophages. The molecular mechanisms involved in the anomalous behavior of macrophages in atherogenesis have only partially been disclosed. Chitotriosidase and human cartilage gp-39 (HC gp-39) are members of the chitinase family of proteins and are expressed in lipid-laden macrophages accumulated in various organs during Gaucher disease. In addition, as shown in this study, chitotriosidase and HC gp-39 can be induced with distinct kinetics in cultured macrophages. We investigated the expression of these chitinase-like genes in the human atherosclerotic vessel wall by in situ hybridizations on atherosclerotic specimens derived from femoral artery (4 specimens), aorta (4 specimens), iliac artery (3 specimens), carotid artery (4 specimens), and coronary artery (1 specimen), as well as 5 specimens derived from apparently normal vascular tissue. We show for the first time that chitotriosidase and HC gp-39 expression was strongly upregulated in distinct subsets of macrophages in the atherosclerotic plaque. The expression patterns of chitotriosidase and HC gp-39 were compared and shown to be different from the patterns observed for the extracellular matrix protein osteopontin and the macrophage marker tartrate-resistant acid phosphatase. Our data emphasize the remarkable phenotypic variation among macrophages present in the atherosclerotic lesion. Furthermore, chitotriosidase enzyme activity was shown to be elevated up to 55-fold in extracts of atherosclerotic tissue. Although a function for chitotriosidase and HC gp-39 has not been identified, we hypothesize a role in cell migration and tissue remodeling during atherogenesis. (+info)
Thromboatheromatous complications of umbilical arterial catheterization in the newborn period. Clinicopathological study.
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Severe catheter-related thromboatheromatous lesions were found at necropsy in 33 of 56 infants who had umbilical arterial catheters passed during life. In infants dying within 8 days of insertion of the catheter, varying degrees of thrombosis of the aorta and its major branches were seen. With increasing thrombosis and aging of the thrombus, fatty deposits were seen first within the thrombus, and then in the intima and media. In addition there was evidence of proliferation of medial smooth muscle cells and of disruption of the medial architecture below the thrombus, characterized by the presence of abundant mucopolysaccharide. In infants who survived longer, varying degrees of organization of the thrombus could be traced, leading eventually to raised fibrous plaques with lipid and occasionally calcification. The lesions in the older infants were similar in many respects to experimental thromboatheromatous lesions produced in rabbits, and to some lesions of artheroma occurring spontaneously in humans. A wide variety of embolic phenomena were found, with features suggesting asynchrony of embolic episodes. The presence of thrombotic lesions could not be related to birthweight, Apgar scores at 1 and 5 minutes, age at catheterization, duration of catheterization, underlying disease process, age at death or the presence of hypothermia, acidosis, or anomalies in coagulation tests. There is a need for less hazardous methods of monitoring arterial oxygen tension. (+info)
Circulatory changes induced by isovolumic increase in red cell mass in fetal lambs.
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AIM: To verify whether extra uterine changes in total peripheral vascular resistance and cardiac output, caused by raised haematocrit, occur in fetal life and if they can be documented using conventional ultrasound techniques. METHODS: An exchange transfusion with packed red cells was performed on five fetal lambs at 140 days of gestation (weight 3.44, SD 0.48 kg); three others were used as controls. The haematocrit was raised from 44 +/- 3 to 64 (SD2)%. RESULTS: Body temperature, blood gas, and pH remained within normal limits. Blood viscosity increased from 5.3 (0.3) to 9.6 (1.6) cps. Combined cardiac output fell to 30% of its initial value. The pulsatility index (PI) remained unchanged in the umbilical artery (0.66, SD 0.1) and descending aorta (1.3, SD 0.3). A significant positive correlation was found between haematocrit and PI only in the carotid artery (r = 0.67, p < 0.01). CONCLUSION: In the fetus, as in adults, an increase in blood viscosity is associated with a fall in cardiac output. However, the low resistance and the relative inertia of the placental vascular bed blunt the velocimetric changes that could be induced in the lower body vascular system by an increase in resistance. Such changes were observed only in the carotid artery. These results could be of interest in the Doppler monitoring of human fetuses at risk of an abnormal increase in their haematocrit. (+info)
Characteristics of blood flow in intrauterine growth-restricted fetuses with hypercoiled cord.
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OBJECTIVE: To clarify the characteristics of fetoplacental blood flow of growth-restricted fetuses with hypercoiled umbilical cord. SUBJECTS: Eight growth-restricted fetuses with hypercoiled cord. METHODS: Flow velocity waveforms of the umbilical cord artery and vein, fetal abdominal aorta and fetal inferior vena cava were analyzed. RESULTS: The resistance index in the umbilical artery in the hypercoiled cases was lower than that in normal fetuses. Early-diastolic reversed flow was observed in the abdominal aorta in some cases. In all cases, umbilical venous pulsation was observed in the entire cord until delivery. In one case, fetal heart failure occurred, resulting in pre-mature delivery. An atrophic type of single umbilical artery was observed in four cases. CONCLUSION: Fetal blood flow disturbance caused by a hypercoiled umbilical cord may be a cause of growth restriction. (+info)
Prenatal diagnosis of a lean umbilical cord: a simple marker for the fetus at risk of being small for gestational age at birth.
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OBJECTIVE: The purpose of this study was to investigate whether the prenatal diagnosis of a 'lean' umbilical cord in otherwise normal fetuses identifies fetuses at risk of being small for gestational age (SGA) at birth and of having distress in labor. The umbilical cord was defined as lean when its cross-sectional area on ultrasound examination was below the 10th centile for gestational age. METHOD: Pregnant women undergoing routine sonographic examination were included in the study. Inclusion criteria were gestational age greater than 20 weeks, intact membranes, and singleton gestation. The sonographic cross-sectional area of the umbilical cord was measured in a plane adjacent to the insertion into the fetal abdomen. Umbilical artery Doppler waveforms were recorded during fetal apnea and fetal anthropometric parameters were measured. RESULTS: During the study period, 860 patients met the inclusion criteria, of whom 3.6% delivered a SGA infant. The proportion of SGA infants was higher among fetuses who had a lean umbilical cord on ultrasound examination than among those with a normal umbilical cord (11.5% vs. 2.6%, p < 0.05). Fetuses with a lean cord had a risk 4.4-fold higher of being SGA at birth than those with a normal umbilical cord. After 25 weeks of gestation, this risk was 12.4 times higher when the umbilical cord was lean than when it was of normal size. The proportion of fetuses with meconium-stained amniotic fluid at delivery was higher among fetuses with a lean cord than among those with a normal umbilical cord (14.6% vs. 3.1%, p < 0.001). The proportion of infants who had a 5-min Apgar score < 7 was higher among those who had a lean cord than among those with normal umbilical cord (5.2% vs. 1.3%, p < 0.05). Considering only patients admitted in labor with intact membranes and who delivered an appropriate-for-gestational-age infant, the proportion of fetuses who had oligohydramnios at the time of delivery was higher among those who had a lean cord than among those with a normal umbilical cord (17.6% versus 1.3%, p < 0.01). CONCLUSION: We conclude that fetuses with a lean umbilical cord have an increased risk of being small for gestational age at birth and of having signs of distress at the time of delivery. (+info)
Early prenatal diagnosis of cord entanglement in monoamniotic multiple pregnancies.
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OBJECTIVES: Cord entanglement is a severe complication in monoamniotic multiple pregnancies. Three cases were reviewed to determine how early ultrasound diagnosis might improve counselling and management. METHODS: In two monoamniotic twin and one dichorionic diamniotic triplet pregnancies, cord entanglement was detected between 10 and 18 gestational weeks by color Doppler and pulsed Doppler velocimetry. Pregnancies were followed up on a weekly basis with special observation of fetal behavior and use of color Doppler velocimetry. RESULTS: In Case 1, a monoamniotic twin pregnancy with cord entanglement close to the umbilical insertions was diagnosed at 10 weeks. Longitudinal follow-up showed intrauterine death of both twins at 15 weeks. In Case 2, entanglement of the umbilical cords of two monoamniotic triplets within a dichorionic diamniotic triplet pregnancy was diagnosed at 10 weeks. The pregnancy continued uneventfully until 35 weeks when cord entanglement was confirmed at Cesarean section. All triplets have since developed normally. In Case 3, monoamniotic twins were diagnosed at 18 weeks. Color Doppler detected side-by-side insertion of the umbilical cords and Doppler velocimetry suggested an entanglement at the chorionic plate. The pregnancy was complicated by polyhydramnios. Cesarean section at 36 weeks confirmed cord entanglement at the chorionic plate. Postnatal computer angiography and morphological examination of the placenta showed the presence of superficial artery-to-artery and vein-to-vein anastomoses and of deep arteriovenous shunts. The development of the twins was uneventful. CONCLUSIONS: Diagnosis of cord entanglement is feasible early in gestation. Future protocols are proposed to document the gestational age at detection, the location, and the Doppler flow patterns and to facilitate the assessment of short- and long-term development. (+info)
Abnormal ductus venosus blood flow: a clue to umbilical cord complication.
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We report a case of umbilical cord complication causing, fetal hypoxemia and acidemia. At 30 weeks of gestation, the patient was referred because of slightly increased amniotic fluid volume and a non-reactive cardiotocogram. Biometry was appropriate for gestational age. Umbilical artery and fetal aortic Doppler findings were normal, whereas diastolic blood flow velocities in the middle cerebral artery were increased and the ductus venosus showed severely abnormal flow velocity waveforms with reversal of flow during atrial contraction. Since other reasons for fetal hypoxemia could be excluded, careful examination of the umbilical cord was performed. Traction of the hypercoiled umbilical cord due to its course around the fetal neck and shoulders was suspected. Cesarean section confirmed the sonographic findings and fetal blood gases revealed fetal acidemia. This case indicates that investigation of fetal venous blood flow may also help to identify fetal jeopardy due to reasons other than increased placental vascular resistance. (+info)