Factors associated with uterine artery Doppler anomalies in patients with preeclampsia.

UNLABELLED: Uterine artery Doppler anomalies are associated with unfavorable outcomes in women with preeclampsia. OBJECTIVES: To examine the association between abnormal uterine artery Doppler and severity of preeclampsia. STUDY DESIGN: Retrospective analysis of a population of 287 patients with preeclampsia who underwent a uterine artery Doppler velocimetric examination at the onset of preeclampsia, between 1996 and 2002. The population was classified into three groups: Group I had normal uterine artery Doppler findings; Group II had a high uterine artery resistance index; and, Group III had both high uterine artery resistance index and bilateral notches. RESULTS: Compared to Group I, preeclampsia occurred earlier in Group II (76.3%) (p < 0.001), and HELLP syndrome was most frequent in Group III. The frequency of fetal growth restriction (pound 3(rd) percentile) was different between groups (19.1, 32.4 and 49.7% in groups I, II and III, respectively). The perinatal death rate was significantly higher in group III than the other two groups (12.8% vs 2.9%, p < 0.01). CONCLUSIONS: In patients with preeclampsia, the presence of uterine artery Doppler anomalies (high resistance index with or without bilateral notches) was associated with unfavorable pregnancy outcomes.

The mechanisms of pain-induced pulmonary vasoconstriction: an experimental study in fetal lambs.

BACKGROUND: Nociceptive stimulation induces pulmonary vasoconstriction in fetuses and newborns. The mechanism of this response is not fully understood. As the systemic hemodynamic response to pain is mainly mediated by sympathetic stimulation, we hypothesized that pain-induced pulmonary vasoconstriction results from the activation of catecholaminergic receptors. To test this hypothesis, we studied the pulmonary vascular response to nociceptive stimuli in fetal lambs before and after alpha-adrenoceptor blockade. METHODS: Surgery was performed in fetal lambs. Catheters were placed into the ascending aorta, superior vena cava, and main pulmonary artery. An ultrasonic flow transducer was placed around the left pulmonary artery, and subcutaneous catheters were placed in the limb. The hemodynamic responses to (1) subcutaneous injection of formalin (which is used as nociceptive stimulus in experimental studies), (2) prazosin (specific alpha(1)-adrenoceptor antagonist), and (3) formalin during prazosin infusion were evaluated. Plasma cortisol and catecholamine concentrations were measured. RESULTS: Pulmonary vascular resistance (PVR) increased by 50% (P < 0.01) after the formalin test. PVR did not change after the formalin test during prazosin infusion or during prazosin infusion alone. Catecholamine and cortisol levels did not change during any of the protocols. DISCUSSION: Our results indicate that the fetal pulmonary vasoconstrictive response to pain involves alpha(1)-adrenoceptors activation. As plasma catecholamine concentrations did not change after the formalin test, we speculate that the pulmonary vascular response to nociceptive stimuli could be triggered by a local release of catecholamine induced by sympathetic stimulation.

Effects of phosphodiesterase 5 inhibitor on pulmonary vascular reactivity in the fetal lamb.

BACKGROUND: Nitric oxide released by pulmonary vascular endothelium is a potent vasodilator related to increased cyclic guanosine monophosphate (cGMP) content. Hydrolysis of cGMP is achieved predominately by cGMP-specific phosphodiesterases. Sildenafil is a selective phosphodiesterase-5 (PDE5) inhibitor. The purpose of the study is to assess the effects of sildenafil on pulmonary vascular circulation during the perinatal period. METHODS: Thirty-two pregnant ewes were operated on at the end of gestation, and fetal lambs were prepared with catheters placed into the aorta, vena cava, pulmonary artery, and left atrium. An ultrasonic flow transducer and an inflatable vascular occluder were placed respectively around the left pulmonary artery and the ductus arteriosus. Fetal lambs were randomly divided into two groups: (1) sildenafil group, infused continuously with sildenafil for 24 hours at a rate of 1 mg/h; or (2) control group, infused with saline for 24 hours. After 24 hours of infusion, we compared basal pulmonary vascular resistance and the pulmonary vascular responses to increase in fetal PaO2 and to acute ductus arteriosus compression causing "shear stress." RESULTS: Sildenafil infusion did not change mean aortic and pulmonary artery pressures, increased mean left pulmonary blood flow by 160%, and decreased pulmonary vascular resistance by 60% (p < 0.05). However, both mean flow (Q) and pulmonary vascular resistance returned to baseline values after 2 hours of sildenafil infusion. Despite similar baseline values, pulmonary vascular resistance during maternal O2 inhalation was lower in the sildenafil group than in the control group (0.21 +/- 0.03 versus 0.33 +/- 0.03 mm Hg.mL(-1).min(-1), respectively; p < 0.01). Furthermore, drop in pulmonary vascular resistance during acute ductus arteriosus compression was greater in the sildenafil group (from 0.56 +/- 0.06 to 0.26 +/- 0.04 mm Hg.mL(-1).min(-1)) than in the control group (from 0.55 +/- 0.05 to 0.39 +/- 0.03 mm Hg.mL(-1).min(-1); p < 0.01). CONCLUSIONS: Although sildenafil induces a transient pulmonary vasodilation, it mediates a sustained change in vascular reactivity, especially to birth-related stimuli in the ovine fetal lung. These data suggest that PDE5 is involved in the regulation of pulmonary vascular reactivity during the perinatal period and may potentiate birth-related pulmonary vasodilator stimuli.