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G R Saade

Publications and source records attributed to G R Saade.

At least 73 records · Page 4Linked to original sources

Simulated airplane flight increases plasma lactate in fetal rabbits.

We studied the effect of 9 h of simulated airplane cabin conditions at cruising altitude (8,000 feet; inspired oxygen equivalent to 15% O2 at sea level) on fetal plasma lactate in near-term pregnant rabbits. Controls (n = 19) spent 9 h at sea level (21% O2). Study group I (n = 21) experienced airplane cabin conditions. Study group II (n = 17) was studied at 8,000 feet with the inspired O2 concentration normalized to sea level. Study group III (n = 19) remained at sea level breathing 15% O2. Before ending each exposure, fetal blood sampling for lactate was performed under ultrasound guidance. Maternal lactates were obtained before and after sampling fetuses. Wilcoxon signed rank test, analysis of variance, and Bonferroni's method were used as appropriate. P < 0.05 denoted statistical significance. Study group I (altitude/hypoxia) had higher fetal lactates than controls (sea level/normoxia) and study group II (altitude/normoxia). Fetal lactates in study group I (altitude/hypoxia) were higher than in study group III (sea level/hypoxia). Maternal lactates were lower after fetal sampling. Fetal lactic acidemia was observed after 9 h of airplane cabin conditions. This was attributed to the combined effect of the lowered oxygen concentration and the decrease in atmospheric pressure.

Acidosis, Lactic↗

Preeclampsia may cause both overperfusion and underperfusion of the brain: a cerebral perfusion based model.

BACKGROUND: The hypothesis was that low cerebral perfusion pressure is more common in women with mild preeclampsia as compared to those with severe preeclampsia, while high cerebral perfusion pressure is more common in women with severe preeclampsia than in women with mild preeclampsia. DESIGN: Prospective, observational study. SETTING: University teaching hospitals. METHODS: Transcranial Doppler ultrasound was used to measure the blood velocity in the middle cerebral arteries of 54 patients with mild preeclampsia and 44 patients with severe preeclampsia. Blood pressure was measured simultaneously. Cerebral perfusion pressure was calculated and plotted on the same axes as data from 63 normal pregnant women. Data outside of the 95% prediction limits were regarded as abnormal. All studies were prior to labor, and before volume expansion or treatment. ANALYSIS: Student's t-test, Mann Whitney U test, and Fisher's exact test as appropriate with two-tailed p<0.05. MAIN OUTCOME MEASURE: The number of patients in each group with cerebral perfusion pressure values outside the normal 95% prediction limits. RESULTS: Almost the same number of women with mild (21/54=39%) and severe (15/44=34%) preeclampsia had measurements within the normal range (p=0.78). Mild preeclamptic women were more likely to have low (28/54=52%) rather than high cerebral perfusion pressure (p<0.001), while severe preeclamptics were more likely to have high cerebral perfusion pressure (26/44=59%) than low (p<0.001). CONCLUSIONS: In preeclampsia the brain can be normally perfused, underperfused and over-perfused. Although many women with mild preeclampsia will have underperfusion (52%), and a significant number of women with severe preeclampsia will have overperfusion (59%), many preeclamptic women have cerebral perfusion within the normal range.

Adult↗

Endothelium-dependent and -independent mechanisms of vasorelaxation by corticotropin-releasing factor in pregnant rat uterine artery.

Corticotropin-releasing factor (CRF), a potent vasorelaxant, is increased tremendously during human pregnancy. Placenta is the main source for this increase. CRF is thought to be important in modulating vascular resistance and uteroplacental blood flow during pregnancy. Here we investigated pathways mediating a vasorelaxant effect of CRF in the uterine artery. Two-millimeter segments of uterine artery (o.d. 300-400 microm) from day 18 pregnant rats were mounted in a small vessel myograph and precontracted with norepinephrine, and relaxation responses to CRF were studied. CRF relaxed the uterine artery in a concentration-dependent manner. Relaxation of uterine artery by CRF was abolished completely by alpha-helical CRF 9-41 (CRF antagonist, 1 micromol) and partially by removal of endothelium, Nomega-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor, 0.1 mmol), 6-anilino-5,8-quinolinedione (guanylate cyclase inhibitor, 10 micromol), or thiopental/miconazole (cytochrome P-450 inhibitors, 0.3 mmol/30 micromol), but remained unaffected by indomethacin (cyclo-oxygenase inhibitor, 10 micromol). Relaxation was also inhibited when depolarizing solution (K+, 120 mmol) was used for precontraction. In deendothelized preparations, relaxation was not inhibited by 9-tetrahydro-2-furanyl-9H-purin-6-amine (adenylate cyclase inhibitor, 0.2 mmol), glibenclamide (adenosine triphosphate-dependent K+ channel blocker, 10 micromol), tetrabutyl ammonium (nonspecific K+ channel blocker, 1 mmol), nitrendipine (voltage-gated Ca++ channel blocker, 1 micromol), or when vessels were precontracted with depolarizing solution. CRF causes vasorelaxation by receptor-operated, endothelium-dependent and -independent pathways. The endothelium-dependent relaxation is mediated by nitric oxide-cyclic guanosine monophosphate pathway and endothelium-derived hyperpolarizing factor but not prostacyclin. However, cyclic adenosine monophosphate, K+ channels, or Ca++ channels are not involved in endothelium-independent vasorelaxation by CRF.

Animals↗

The effects of nitric oxide on the contractility of isolated uterine and aortic rings from pregnant rats.

OBJECTIVE: The object was to compare the effects of nitric oxide on isolated uterus and aorta of pregnant rats. STUDY DESIGN: Rings of uterus and thoracic aorta without endothelium from Sprague-Dawley rats at mid and late gestation were used for isometric tension recording. The concentration-response curve for diethylamine/nitric oxide was studied in the presence or absence of oxyhemoglobin (10(-5) mol/L), or oxyhemoglobin was added after the response to diethylamine/nitric oxide. RESULTS: Diethylamine/nitric oxide concentration dependently inhibited uterine contractions, and the effect was attenuated by previous treatment with oxyhemoglobin at mid gestation (n = 8). The effects were negligible at late gestation (n = 8). The relaxation of aortic rings by diethylamine/nitric oxide and its attenuation by previous treatment with oxyhemoglobin were similar at mid (n = 6) and late (n = 6) gestation. The sensitivity of aortic rings to diethylamine/nitric oxide is significantly higher than that of uterine rings. Oxyhemoglobin partly restored inhibited diethylamine/nitric oxide phenylephrine tension in aortic rings and had no effect on diethylamine/nitric oxide-inhibited uterine rings. CONCLUSIONS: Uterine smooth muscle is less sensitive to nitric oxide than is aortic smooth muscle. Nitric oxide sensitivity of rat uterus but not aorta decreases toward term.

Animals↗

Both soluble guanylate cyclase and particulate guanylate cyclase regulate myometrial contractility.

OBJECTIVE: Our purpose was to compare the effects of agents stimulating particulate and soluble guanylate cyclase with spontaneous rat uterine contractions at midgestation and term. STUDY DESIGN: Uterine rings from midgestation (day 13) and term nonlaboring (day 22) rats were positioned in organ chambers for isometric force recording. Rings were treated with increasing concentrations of atrial natriuretic peptide, permeable analogs of cyclic guanosine monophosphate, and diethylamine/nitric oxide. RESULTS: Atrial natriuretic peptide was more effective in inhibition of uterine contractions than diethylamine/nitric oxide. The 50% inhibitory concentrations were -7.4 +/- 0.12 and -7.38 +/- 0.11 for atrial natriuretic peptide and -5.68 +/- 0.09 and -4.23 +/- 0.12 for diethylamine/nitric oxide at midgestation and term, respectively. Pretreatment of uterine rings with atrial natriuretic peptide significantly attenuated inhibition of spontaneous contractions by diethylamine/nitric oxide at midgestation. CONCLUSIONS: Uterine spontaneous contractions are influenced by both soluble and particulate guanylate cyclase; the former, but not latter, is gestational age dependent.

Animals↗

Uterine activity during pregnancy and labor assessed by simultaneous recordings from the myometrium and abdominal surface in the rat.

OBJECTIVES: The aim of this study was to analyze records of uterine electrical activity made from the abdominal surface of pregnant and laboring rats to examine whether similar quantitative information can be extracted as from direct recording from the uterine muscle. STUDY DESIGN: Electrical activity during pregnancy (nonlabor, days 18 to 22), term labor (day 22), and preterm labor (onapristone injected on day 18, delivery on day 19) was measured with use of electrodes attached to the uterine wall and to the abdominal surface. The fast Fourier transform and wavelet transforms were obtained for representative electromyographic bursts. Power spectra were generated. Intrauterine pressure was also measured. RESULTS: (1) Several parameters have been identified for use in following up the progressive increase in uterine activity that occurs in preparation for and during labor. Analyses of amplitude, frequency, and percent time active represent a convenient method for objectively determining the efficiency of uterine contraction. (2) Most of the changes in these parameters appear in the last 24 hours before delivery. (3) Although the uterine electromyographic signals on the abdominal surface are attenuated, the abdominal surface signals are generally similar to the signals obtained from the uterine muscle during pregnancy and during preterm and term labor. (4) The characteristics of onapristone-induced preterm labor are generally similar to those of spontaneous term labor. CONCLUSIONS: Recording of uterine electromyographic activity from the abdominal surface may be useful in following the progression of pregnancy and in predicting and diagnosing labor.

Abdomen↗

In vivo effects of corticotropin-releasing factor in pregnant rats.

OBJECTIVES: Our purpose was to study the effects of corticotropin-releasing factor on (1) maternal blood pressure, (2) uterine vasculature, and (3) parturition in pregnant rats. STUDY DESIGN: Infusion minipumps containing vehicle, corticotropin-releasing factor, or alpha-helical corticotropin-releasing factor 9-41 (corticotropin-releasing factor receptor antagonist) were inserted subcutaneously in timed pregnant rats on day 16 of gestation. Systolic blood pressure was measured daily by the tail-cuff method. The time of onset of labor was determined and the newborn pups were weighed. Circulating levels of corticotropin-releasing factor were measured in untreated controls by radioimmunoassay. Relaxant responses to corticotropin-releasing factor were studied in isolated segments of uterine artery from late (day 18) and term (day 22) pregnant rats mounted in a wire myograph. RESULTS: The blood pressure was decreased by corticotropin-releasing factor and increased by alpha-helical corticotropin-releasing factor 9-41 (p < 0.05). The time of onset of labor was not affected by either treatment. Pup weight was decreased by corticotropin-releasing factor (p < 0.05). Circulating levels of corticotropin-releasing factor (immunoreactive) were not changed in pregnancy. In vitro, corticotropin-releasing factor caused relaxation of the uterine artery in a concentration-dependent manner and the relaxation was decreased at term compared with late pregnancy (p < 0.05). CONCLUSIONS: Endogenously produced corticotropin-releasing factor lowers blood pressure during pregnancy in rats. It is a relaxant of uterine vasculature and this effect is decreased at term. It does not play an essential role in the initiation of labor in rats.

Animals↗

Ultrasonographic measurement of crown-rump length in high-order multifetal pregnancies.

The objective of the study was to evaluate the crown-rump length (CRL) in high-order multifetal pregnancies (three or more fetuses). The records of patients who underwent multifetal pregnancy reduction were reviewed. The following parameters were defined: the mean CRL (CRLMEAN) and the difference between the largest and smallest CRL (CRLRANGE) for each pregnancy. CRLMEAN was plotted versus gestational age (GA) and the line of best fit was derived. The residual for each CRL (CRLRES) was calculated by subtracting the value predicted by the regression line from the individual CRL (CRLIND). Regression lines for single-tons with confirmed GA from four previously reported studies were used for comparison. A total of 82 patients were included (29 triplets, 38 quadruplets and 15 quintuplets; mean GA 10.7 +/- 0.78 weeks). CRLMEAN correlated with GA (CRLMEAN = 38.88 - 8.78(GA) + 0.82(GA)2; R = 0.83; R2 = 0.70). This second-degree polynomial remained within the range for singletons. No significant differences in maternal age, GA and CRLMEAN were noted between the patients with different numbers of fetuses. The median CRLRANGE was largest in quintuplets, followed by quadruplets and triplets. The CRLRANGE correlated poorly with GA. The mean CRL in multifetal pregnancies increases with GA similarly to that in singletons. The variability of individual measurements increases with the number of fetuses and CRLs are lower in quintuplets.

Adult↗

Effect of gestational age on in-vitro responses of pregnant rat aorta.

The hypothesis that the changes in vascular reactivity seen during pregnancy are determined by the gestational age was examined. Experiments were designed to investigate changes in vascular responses with progression of pregnancy. The contractile responses to potassium and phenylephrine (in the presence and absence of N(omega)-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor) and the relaxant responses to acetylcholine and sodium nitroprusside were measured in isolated aortic rings from pregnant rats at various stages of gestation and from non-pregnant female rats. Potassium-evoked contractile response was higher early in pregnancy and was decreased at term (P < 0.05). The contractile response to phenyllephrine was decreased and the relaxant response to acetylcholine was increased in early pregnancy (P < 0.05). Inhibition of nitric oxide synthase caused an increase in the contractile response to phenylephrine in all the groups, but the attenuation of the response in early pregnancy was maintained (P < 0.05). There was a small decrease in the maximal relaxant response to sodium nitroprusside at term (P < 0.05). It was concluded that the effects of pregnancy on the responses of rat aorta in vitro vary at different stages of gestation. Vascular resistance may be lowered by changes in vascular reactivity in early gestation and by a decrease in the contractile potential of the vasculature during the later stages.

Analysis of Variance↗

Instrumentation for the diagnosis of term and preterm labour.

The problems associated with labor during pregnancy are among the most important health issues facing physicians. Understanding the role of the uterus and cervix in labor and developing methods to control their function is essential to solving problems relating to labor. At the moment, only crude, inaccurate and subjective methods are used to assess changes in the uterus and cervix that occur in preparation for or during labor. In the past several years, we have developed noninvasive methods to quantitatively evaluate the uterus and cervix based respectively on recording of uterine electrical signals from the abdominal surface (uterine EMG) and measurement of light-induced cervical collagen fluorescence (LIF) with an optical device (Collascope). The methods are rapid and allow assessment of uterine contractility and cervical ripening. Studies in rats and humans indicate that uterine and cervical function can be successfully monitored during pregnancy using these approaches and that these techniques might be used in a variety of conditions associated with labor to better define management. The potential benefits of the proposed instrumentation and methods include a reducing the rate of preterm delivery, improving maternal and perinatal outcome, monitoring treatment, decreasing cesarean section rate and improving research methods to understand uterine and cervical function.

Animals↗

Effect of chronic treatment with 17beta-estradiol and progesterone on endothelium-dependent and endothelium-independent relaxation in isolated aortic rings from ovariectomized rats.

OBJECTIVE: Our purpose was to study the influence of chronic treatment with sex hormones on endothelium-dependent and endothelium-independent relaxation of rat aortic rings. STUDY DESIGN: Rings of aortas, with and without endothelium, from rats treated with sex hormones or vehicle for 10 days were mounted in organ baths for isometric tension recording. Indomethacin (10(-5) mol/L) and N(omega)-nitro-L-arginine methyl ester (10(-4) mol/L), alone or in combination, were used to block cyclooxygenase and nitric oxide synthase, respectively. Mean data of contraction induced by potassium chloride (60 mmol/L), the relaxation by acetylcholine (10(-6) mol/L) in potassium chloride-contracted rings, tension induced by phenylephrine, and the negative logarithm of the concentration of acetylcholine or 3-morpholinosydnonimine producing a 50% relaxation, and area under the curve were calculated. RESULTS: Treatment with 17beta-estradiol (10 microg/rat/day) decreased the tension induced by 60 mmol/L potassium chloride and increased the relaxation by acetylcholine in the rings with endothelium precontracted with potassium chloride. Contraction induced by potassium chloride and relaxation induced by acetylcholine were not influenced by the treatment with progesterone (2 mg/rat/day) or estrogen-progesterone combination. Treatment with estradiol, progesterone, or both hormones had no effect on tension developed in intact rings in response to phenylephrine and did not influence endothelium-dependent relaxation to acetylcholine or endothelium-independent relaxation to 3-morpholinosydnonimine in rings contracted with phenylephrine. The inhibition by N(omega)-nitro-L-arginine methyl ester of endothelium-dependent relaxation by acetylcholine was attenuated after the treatment with the sex hormones. CONCLUSIONS: Chronic treatment with sex hormones did not increase production or release of endothelium-derived relaxing factor and did not change the sensitivity of rat aortic smooth muscle to nitric oxide. The treatment slightly counteracted the inhibition of endothelium-dependent relaxation produced by nitric oxide synthase blocker.

Acetylcholine↗

The relaxation responses to corticotropin-releasing factor in rat aorta are endothelium dependent and gestationally regulated.

OBJECTIVE: Our purpose was to examine the hypothesis that the relaxant response to corticotropin-releasing factor is endothelium dependent and changes during pregnancy. STUDY DESIGN: Relaxant responses to cumulative concentrations of corticotropin-releasing hormone were measured in rings of thoracic aorta, precontracted with phenylephrine, from pregnant and nonpregnant female rats. Each group consisted of 5 to 10 rats. RESULTS: The relaxation induced by corticotropin-releasing factor in aortic rings from nonpregnant rats decreased after deendothelization and treatment with N omega-nitro-L-arginine methyl ester (a nitric oxide synthase inhibitor), LY-83,583 (a guanylate cyclase inhibitor), or alpha-helical corticotropin-releasing factor 9-41 (a corticotropin-releasing factor antagonist). The percent decrease in relaxation at 1 nmol/L of corticotropin-releasing factor was about 88% with deendothelization, 100% with N omega-nitro-L-arginine methyl ester, 76% with LY-83,583, and 100% with alpha-helical corticotropin-releasing factor 9-41. The responses to corticotropin-releasing factor in intact rings from rats in early pregnancy were not significantly different from those in the nonpregnant female rats, but the responses were decreased during the later stages of gestation (percent decrease in relaxation at 1 nmol/L of corticotropin-releasing factor about 71% at day 20 and 98% at term). The relaxation induced by corticotropin-releasing factor during pregnancy was also inhibited by deendothelization, N omega-nitro-L-arginine methyl ester, or LY-83,583. CONCLUSIONS: The relaxant response to corticotropin-releasing factor in the rat aorta is endothelium dependent and is mediated by the nitric oxide-cyclic guanosine monophosphate pathway. The receptor involved in this effect is alpha-helical corticotropin-releasing factor 9-41 sensitive. This inhibitory response is unchanged during early pregnancy but reduced toward the end of gestation.

Animals↗

The effect of intrauterine transfusion on fetal bilirubin in red cell alloimmunization.

OBJECTIVE: To evaluate the change in fetal serum bilirubin levels in response to intrauterine transfusion for red cell alloimmunization. METHODS: The records of 37 patients who underwent more than one intrauterine transfusion were reviewed. The following indices were extracted: pre- and post-transfusion fetal hematocrit, total and direct serum bilirubin, reticulocyte count, Kleihauer-Betke test results, volumes of intravascular and intraperitoneal transfusions, and the source used for transfusion. The data were compared for interval 1 (transfusion 1 to 2) and interval 2 (transfusion 2 to 3). The rates of change in bilirubin, reticulocyte count, and percent fetal cells on the Kleihauer-Betke test were defined as the differences between the initial values of one transfusion and the initial values of the next transfusion divided by the number of days between transfusions. Analysis of variance, sign-rank test, and linear regression analysis were used when appropriate. P < .05 was significant. RESULTS: The median number of intrauterine transfusions for each patient was 3 (range 2-8). Gestational ages ranged from 22 to 37 weeks. Total bilirubin remained above the 97.5 percentile for gestational age in all but five patients. There was a significant decrease in reticulocyte count and fetal cells on the Kleihauer-Betke test, and an increase in hematocrit with serial intrauterine transfusions. Bilirubin increased significantly after the first intrauterine transfusion (3.9 versus 5.0 mg/dL) and remained elevated thereafter. CONCLUSION: Fetal total serum bilirubin remains elevated with repeated intrauterine transfusions in fetal alloimmunization. Total bilirubin should not be used to evaluate fetal hematologic responses to the transfusions.

Adult↗

Human immunodeficiency virus (HIV)-related pulmonary complications in pregnancy.

With changes in the demographics of human immunodeficiency virus (HIV) infection, women and children are becoming the fastest growing group of newly infected patients. With longer survival after HIV infection, more women infected with HIV are becoming pregnant. Pulmonary disease is one of the most common presenting conditions in an AIDS-defining illness. Pneumocystis carini pneumonia and tuberculosis are the most common disorders that herald the onset of AIDS. They are also the most frequently encountered HIV-related pulmonary complications during pregnancy. Others have been rarely reported during pregnancy and include fungal infections (Cryptococcus neoformans, Histoplasma capsulatum, and Coccidioides immitus), bacterial infections (Haemophilus influenzae and Streptococcus pneumoniae along with Pseudomona aeruginosa), viral infections (CMV), opportunistic neoplasms (Kaposi's sarcoma, lymphoma) and miscellaneous conditions peculiar to HIV-infected individuals (nonspecific interstitial pneumonitis, lymphoid interstitial pneumonitis, isolated pulmonary hypertension, and pulmonary edema secondary to cardiac disease or drug abuse). Most of the data regarding the pulmonary complications of HIV infection come from studies in nonpregnant patients. The extent to which pregnancy affects the course of respiratory disease in HIV infection and vice versa is not well documented. Clinical presentation is usually not altered by pregnancy. Except for minor modifications mainly related to potential fetal effects, the diagnostic work-up and management are similar to those in the nonpregnant patient. The most important effect of pregnancy on these conditions remains the delay in diagnosis and treatment. A high index of suspicion should, therefore, be maintained. In addition, most prophylactic measures recommended in nonpregnant HIV-infected individuals also apply to pregnant women.

Bacterial Infections↗

The direct action of 17 beta-estradiol in isolated omental artery from nonpregnant and pregnant women is related to calcium antagonism.

OBJECTIVE: Our purpose was to study the mechanism by which 17 beta-estradiol modulates contractile activity in isolated rings of omental artery from nonpregnant and pregnant patients. STUDY DESIGN: Rings of omental artery with intact endothelium from nonpregnant and pregnant women were mounted in organ chambers for isometric tension recording. The concentration-relaxation relationship to 17 beta-estradiol (10(-7) mol/L to 3 x 10(-5) mol/L) was studied in rings contracted with 60 mmol/L potassium chloride (in both the absence and the presence of tamoxifen, 10(-6) mol/L). The effect of 17 beta-estradiol (10(-5) mol/L) on the contraction induced by 60 mmol/L potassium chloride and on the concentration-contraction relationships to both norepinephrine (10(-9) mol/L to 10(-5) mol/L) and calcium ion (0.05 mmol/L to 2.5 mmol/L in calcium-free depolarizing solution) were studied in the presence and absence of tamoxifen (10(-6) mol/L). The maximal contraction, negative logarithm of the concentration producing 50% relaxation or 50% contraction to the reference 60 mmol/L potassium chloride contraction, and the area under the curve were calculated. Data analysis was by one-way analysis of variance, Newman-Keuls test, and two-sample tests as appropriate. Probability values less than 0.05 in a two-tailed test were considered statistically significant. RESULTS: 17 beta-Estradiol relaxed omental arteries contracted with 60 mmol/L potassium chloride, and this effect was potentiated by tamoxifen in both groups. Incubation of the omental arteries with 17 beta-estradiol inhibited contractions induced by 60 mmol/L potassium chloride in rings from both groups of patients, and tamoxifen did not antagonize this effect in either group. Rings of omental artery from the nonpregnant patients (expressed as percentage of the reference potassium chloride contraction) showed greater contraction than rings from the pregnant women when exposed to norepinephrine, a statistically significant difference. 17 beta-Estradiol decreased the norepinephrine-induced contraction in omental arteries from nonpregnant but not pregnant women in a statistically significant way. Tamoxifen did not influence the effect of norepinephrine for either group. 17 beta-Estradiol inhibited calcium ion-induced contraction similarly in rings of omental artery from both nonpregnant and pregnant patients. Tamoxifen potentiated estradiol-induced inhibition in arteries from pregnant patients. CONCLUSIONS: 17 beta-Estradiol inhibits norepinephrine-induced contractions in omental arteries from nonpregnant but no pregnant patients. The inhibition of the ter sion developed after exposure to potassium chloride, norepinephrine, and calcium ion is caused by a calcium channel blocking action.

Adult↗

Effects of estradiol-17 beta and progesterone on isolated human omental artery from premenopausal nonpregnant women and from normotensive and preeclamptic pregnant women.

OBJECTIVE: Our purpose was to study the direct vascular effects of estradiol-17 beta and progesterone on isolated omental artery from premenopausal nonpregnant women and from normotensive and preeclamptic pregnant women. STUDY DESIGN: Omental artery rings from normotensive premenopausal nonpregnant women and from normal and preeclamptic pregnant women were mounted in Krebs-bicarbonate solution in organ baths for isometric tension recording. The endothelium was removed from some of the rings, and all were contracted with potassium chloride (60 mmol/L) and then exposed to cumulative concentrations of estradiol-17 beta and progesterone. Concentration response curves were constructed and relaxation was expressed as percent change from the reference 60 mmol/L potassium chloride contraction. Data analysis was by repeated-measures analysis of variance, Newman-Keuls test, and the unpaired Student t test as appropriate. A two-tailed p < 0.05 was considered statistically significant. RESULTS: Both hormones studied caused vasorelaxation in omental arteries from all three groups of patients. Of the two, estradiol-17 beta was more effective, regardless of the presence or absence of endothelium. Removal of the endothelium shifted the estradiol-17 beta concentration-response curve to the right in the normal pregnant artery but not in nonpregnant or preeclamptic vessels. Removal of the endothelium shifted the progesterone concentration-response curve to the left in arteries from preeclamptic patients. CONCLUSIONS: Estradiol-17 beta and progesterone have direct in vitro vasodilator activity that appears to be linked, in part, to the endothelium in human omental artery from normal and hypertensive women in different hormonal states.

Adult↗

Effects of selected vasoconstrictor agonists on isolated omental artery from premenopausal nonpregnant women and from normal and preeclamptic pregnant women.

OBJECTIVE: Our purpose was to compare the responsiveness of omental resistance arteries from nonpregnant women and from normotensive and preeclamptic pregnant women to selected contractile agonists. STUDY DESIGN: Omental artery rings with intact endothelium from normotensive premenopausal nonpregnant women and from normal and preeclamptic pregnant women were mounted in Krebs-bicarbonate solution in organ baths for isometric tension recording. After the presence of endothelium was confirmed, cumulative concentrations of norepinephrine, serotonin, U46619, and endothelin-1 were added. Concentration-response curves were constructed and expressed as percentage of a reference 60 mmol/L potassium chloride contraction. Data analysis was by repeated-measures analysis of variance. Newman-Keuls test, and paired or unpaired Student t test, as appropriate. Statistical significance was by two-tailed p<0.05. RESULTS: Endothelin-1 and U46619 increased tension similarly in all three groups. Norepinephrine increased tension in nonpregnant vessels to a greater extent than in either preeclamptic or pregnant vessels (nonpregnant 114.3 +/- 5.42% vs pregnant 65.2 +/- 10.5%, p<0.05). Nonpregnant omental artery developed significantly greater tension than did pregnant tissue at three concentrations of norepinephrine (10(-5) mol/L, 3 x 10(-5) mol/L, 10(-4) mol/L), and preeclamptic vessels developed more tension than that from normal pregnant vessels at 3 x 10(-6) mol/L (p=0.06) and 10(-5) mol/L (p<0.05). There was a negligible change in tension with increasing concentrations of serotonin in the vessels from nonpregnant women; serotonin-induced contraction in the omental arteries from normotensive pregnant women and preeclamptic patients was <6% of the potassium chloride reference contraction, but this was significantly (p<0.05) different from that of the nonpregnant women. CONCLUSIONS: Omental artery segments from nonpregnant, normotensive pregnant and preeclamptic women contract similarly to endothelin-1 and U46619 but exhibit variable responses to norepinephrine and serotonin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗