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Biomedical subjects

V M Parisi

Publications and source records attributed to V M Parisi.

At least 37 records · Page 2Linked to original sources
PubMed1992

The effect of preterm birth on umbilical cord blood gases.

Apgar scores are used routinely to assess early neonatal status, but are less accurate in the preterm neonate because of developmental immaturity. Attention has been directed to umbilical cord gases as a method of neonatal evaluation. Using a retrospective chart review of all viable preterm births (24-36 weeks' gestation) between January 1986 and December 1989, we tabulated the umbilical cord gas indices of these infants. Fetuses with lethal congenital anomalies and those with abnormal heart rate tracings on admission were excluded from the data base, leaving 1872 infants. Cord arterial blood gas values were available for analysis in 74.4% of cases and cord venous gas values in 81.8%. The mean (+/- standard deviation [SD]) arterial and venous umbilical cord blood gas values for the preterm infants, were, respectively: pH, 7.26 +/- 0.08 and 7.33 +/- 0.07; oxygen pressure, 19.0 +/- 7.9 and 29.2 +/- 9.7 mmHg; carbon dioxide pressure, 53.0 +/- 10.0 and 43.4 +/- 8.3 mmHg; bicarbonate, 24.0 +/- 2.3 and 22.8 +/- 2.1 mEq/L; and base excess, -3.2 +/- 2.9 and -2.6 +/- 2.5 mEq/L. Acidemia was defined statistically as 2 SDs or more below the population mean. The incidence of 5-minute Apgar scores below 7 in the preterm infants was 8.5% and within this group, 17.8% were acidemic (arterial pH 7.10 or lower). More than 82% of neonates with 5-minute Apgar scores less than 7 had normal umbilical cord blood gases. There was no significant difference in umbilical arterial blood gas values between preterm infants and 1924 term deliveries at our institution between 1986-1988.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1991

Epidural analgesia and cesarean section for dystocia: risk factors in nulliparas.

A retrospective study assessing the effect of epidural analgesia in labor on the incidence of cesarean section was performed. The first 500 consecutive nulliparas meeting the following criteria were included in this study: term (37 weeks or longer) and singleton gestation, cephalic presentation, spontaneous onset of labor, and 5 cm or less of cervical dilation on admission. Patients were grouped according to their rate of cervical dilation in early labor (greater than or equal to 1 cm/hr, and less than 1 cm/hr) and the timing of epidural placement (none, early, or late). There was no effect of epidural analgesia on the incidence of cesarean section for fetal distress. The incidence of cesarean section for dystocia was significantly greater (p greater than 0.000001) in the epidural group (15.6%) than in the nonepidural group (2.4%). The greatest effect of epidural analgesia on the incidence of cesarean section for dystocia was observed in nulliparas who dilated at slower rates (less than 1 cm/hr) in early labor and who had epidural analgesia placed at 5 cm or less of cervical dilation (20.6% versus 3.4%, relative risk of 6, p less than 0.0005). The increase of cesarean section for dystocia associated with epidural analgesia could not be accounted for when other possibly confounding variables were studied. Both the dilation rate prior to epidural placement and the cervical dilation at epidural placement were significantly correlated to frequency of cesarean section for dystocia (p less than 0.01). This study suggests that epidural analgesia in labor may increase the incidence of cesarean section for dystocia in nulliparas.

Adolescent↗
PubMed1990

Placental thromboxane and prostacyclin production in an ovine diabetic model.

We hypothesized that streptozocin-induced ovine diabetes would cause alterations in the placental production of thromboxane and prostacyclin. With a tissue incubation technique, we examined the placental production of thromboxane and prostacyclin in cotyledons from seven normal near-term ewes (127 +/- 3 days' gestation) and six streptozocin-induced diabetic ewes (125 +/- 3 days' gestation). Diabetic status was verified with serial fasting blood glucose assessments. Placental tissue was incubated in Dulbecco's modified Eagle's medium for 48 hours at 37 degrees C with 95% oxygen and 5% carbon dioxide. Samples were collected at 0, 1, 2, 4, 8, 20, 32, and 48 hours. Radioimmunoassay of the stable metabolites thromboxane B2 and 6-keto-prostaglandin F1 alpha were used to determine thromboxane and prostacyclin production, respectively. Placental thromboxane production was reduced in diabetic animals when compared with control animals (5.63 +/- 2.81 vs 7.32 +/- 1.37 pg/mg per hour, respectively; p less than 0.05). Prostacyclin production was also significantly reduced in the diabetic placentas compared with control placentas (11.44 +/- 4.06 vs 16.29 +/- 4.59 pg/mg per hour, respectively; p less than 0.05). We conclude that the ovine placenta produces thromboxane and prostacyclin. The ovine thromboxane production rate is comparable to that of the human placenta but the prostacyclin production rate is approximately two to three times higher. The observed decrease in the placental production of thromboxane and prostacyclin may reflect an adverse effect of hyperglycemia directly on eicosanoid production or indirectly through decreased placental cellular proliferation.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Effect of active management on latent phase labor.

The effect of active management on latent phase labor was assessed in 197 consecutive nulliparous women. Active management resulted in a significant shortening of the latent phase but had no effect on active phase labor. Patients undergoing induction of labor had latent phases that were almost identical to the accepted norm. The effect of active management may be due to early diagnosis of labor and early intervention in the form of artificial rupture of membranes and selective high-dose oxytocin infusion.

Extraembryonic Membranes↗
PubMed1990

Hemodynamic effects of leukotriene C4 in ovine fetus.

Leukotrienes are synthesized during pregnancy and produce cardiovascular effects in adults. We hypothesized that leukotriene C4 would cause vasoconstriction in the fetus and placenta. Eight near-term, unanesthetized ovine fetuses were studied before and after infusion of 10 micrograms leukotriene C4 (LTC4) into the fetal vena cava. Cardiovascular monitoring of maternal and fetal arterial pressures and heart rates was performed. Fetal blood flows were measured by the radioactive-microsphere technique. Sustained elevations in systolic and diastolic blood pressure and decreased fetal heart rate began by 1 min and returned to baseline by 30 min. Arterial pH fell from 7.33 +/- 0.01 to 7.29 +/- 0.01 at 15 min (P less than 0.05) and to 7.29 +/- 0.01 at 30 min (P less than 0.05), with a significant increase in base deficit from 0.7 +/- 0.7 to 3.5 +/- 0.7 at 15 min (P less than 0.05) and to 2.9 +/- 1.0 at 30 min (P less than 0.05). Fetal PO2 and PCO2 were unchanged. Significant decreases in blood flow and resistance were seen in the umbilical placental circulation as well as in fetal skeletal muscle and intestine. Blood flow and resistance were unchanged in the renal and adrenal vascular beds. Fetal administration of LTC4 caused no changes in maternal cardiovascular parameters. These findings represent the first in vivo studies of the effects of a lipoxygenase metabolite on fetal-placental blood flow.

Animals↗
PubMed1990

Maternal lithium therapy and polyhydramnios.

Lithium is widely used in the treatment of bipolar affective disorders, and teratogenic effects include cardiovascular abnormalities, notably Ebstein anomaly. The most common side effect in the patient taking lithium is polyuria, a form of nephrogenic diabetes insipidus. We report the case of a manic-depressive gravida on lithium therapy who developed polyhydramnios in her last trimester. Because lithium crosses the placenta, we postulate that, by a similar mechanism, lithium may cause fetal polyuria which results in polyhydramnios.

Adult↗
PubMed1989

Fetal vascular responses to prostacyclin.

Prostacyclin is a potent vasodilator produced by both maternal and fetal tissues that dilates the umbilical placental vasculature in vitro. To test the hypothesis that prostacyclin dilates the fetal placental circulation in vivo, we measured blood flow by the radioactive microsphere technique in six unanesthetized near-term ovine fetuses before and during prostacyclin infusion. Fetal mean arterial pressure fell 15% from 35 +/- 3 to 31 +/- 3 mm Hg (p less than 0.05) during prostacyclin infusion, and heart rate increased from 182 +/- 6 to 208 +/- 19 beats/min (p less than 0.05). Placental blood flow changed from 240 +/- 58 to 191 +/- 46 ml.min-1.kg-1 fetal weight (p = 0.07), whereas vascular resistance was unchanged (0.16 +/- 0.04 to 0.18 +/- 0.06 mm Hg.ml-1.min.kg fetal weight). Fetal arterial pH decreased from 7.33 +/- 0.03 to 7.28 +/- 0.02 (p less than 0.05) during prostacyclin infusion, with a significant decrease in base excess from -1.2 +/- 1.4 to -3.1 +/- 1.6 (p less than 0.05) and a trend toward hypercarbia (p = 0.07). We conclude that in vivo administration of prostacyclin to the ovine fetus does not cause fetal placental vasodilation and does cause a significant fetal acidemia. The mechanism for these unexpected observations is likely shunting of blood away from the placenta to other organs in the face of systemic vasodilation.

Animals↗
PubMed1989

Routine umbilical cord blood gas determinations?

Between 1986 and 1988, 1924 term nulliparous patients with spontaneous onset of labor were studied to assess the importance of obtaining umbilical cord blood gas levels on all deliveries. The umbilical cord arterial and venous pH values (expressed as mean +/- 2 SD) were 7.24 +/- 0.14 (n = 1694) and 7.32 +/- 0.12 (n = 1820), respectively. The incidence of newborn depression (1- or 5-minute Apgar score less than 7) was 14.1%; of these depressed newborns, the incidence of normal umbilical cord arterial pH values (greater than or equal to -2 SD) was 77.8%. Of the vigorous newborns, there was a 2.1% incidence of umbilical cord arterial blood acidemia. Umbilical cord arterial blood acidemia in vigorous newborns was not highly predictive of specific morbidity in the immediate newborn period. Regression analysis demonstrated the umbilical cord arterial pH to correlate best with the Apgar scores when compared with all other arterial or venous blood gas measurements. We reached the following conclusions: (1) that obtaining cord arterial pH values in vigorous newborns should be considered since the values will provide objective documentation or normal fetal acid base balance in 98% of infants. (2) Only a cord arterial pH determination is recommended since it reflects fetal or newborn status more accurately than all other measurements. Additional measurements increase the likelihood of abnormal results and do not contribute to neonatal management. (3) An umbilical cord blood pH value is extremely useful in ruling out the diagnosis of birth asphyxia in the depressed newborn.

Acid-Base Equilibrium↗
PubMed1989

The effect of continuous epidural analgesia on cesarean section for dystocia in nulliparous women.

Epidural analgesia in labor is generally accepted as safe and effective and therefore has become increasingly popular. However, little is known regarding the effect of epidural analgesia on the incidence of cesarean section for dystocia in nulliparous women. During the first 6 months of 1987 we studied 711 consecutive nulliparous women at term, with cephalic fetal presentations and spontaneous onset of labor. Comparison of 447 patients who received epidural analgesia in labor with 264 patients who received either narcotics or no analgesia was performed. The incidence of cesarean section for dystocia was significantly greater (p less than 0.005) in the epidural group (10.3%) than in the nonepidural group (3.8%). There remained a significantly increased incidence (p less than 0.005) of cesarean section for dystocia in the epidural group after selection bias was corrected and the following confounding variables were controlled by multivariate analysis: maternal age, race, gestational age, cervical dilatation on admission, use of oxytocin, duration of oxytocin use, maximum infusion rate of oxytocin, duration of labor, presence of meconium, and birth weight. The incidence of cesarean section for fetal distress was similar (p greater than 0.20) in both groups. There were no clinically significant differences in frequency of low Apgar scores at 5 minutes or cord arterial and venous blood gas parameters between the two groups. This study suggests that epidural analgesia in labor may increase the incidence of cesarean section for dystocia in nulliparous women.

Analgesia, Epidural↗
PubMed1989

The effect of magnesium sulfate tocolysis on the fetal biophysical profile.

The biophysical profile has proved to be a valuable tool for the assessment of fetal well-being, independent of gestational age. Magnesium sulfate is commonly used as a tocolytic agent, yet relatively little is known about its effects on the biophysical activities of the fetus. To investigate the effects of magnesium sulfate on the biophysical profile, we performed serial studies on patients who received tocolytic therapy with this agent because of preterm labor. A total of 16 women with 22 fetuses at 26 to 34 weeks' gestation in spontaneous preterm labor were studied. An initial biophysical profile was performed at the time of admission, and a second examination was performed when maternal serum magnesium levels reached 6 to 8 mg/dl. On admission all fetuses had reactive nonstress test results and 21 of 22 (95%) demonstrated sustained fetal breathing movements. With magnesium sulfate tocolysis, 50% of fetuses had nonreactive nonstress test results, and only 4 of 22 (18%) demonstrated sustained fetal breathing movements. Fetal tone, gross body movements, and amniotic fluid volume were found to be unaffected by magnesium sulfate tocolysis.

Adult↗
PubMed1989

Fetoplacental vascular responses to prostacyclin after thromboxane-induced vasoconstriction.

The vasodilator prostacyclin is produced by fetal tissues and may serve to protect umbilical blood flow. We hypothesized that prostacyclin could reverse fetoplacental vasoconstriction produced by a thromboxane mimic (U-46619). Fetal regional blood flow was measured by the radioactive microsphere technique in six unanesthetized, near-term ovine fetuses. Measurements were made in the control period, again 20 minutes after a fetal infusion of U-46619 was begun, and finally 20 minutes after prostacyclin was added to the U-46619 infusion. Mean arterial pressure rose significantly in response to U-46619 (38 +/- 1 to 51 +/- 2 mm Hg, p less than 0.01) and returned to baseline after prostacyclin (42 +/- 2 mm Hg). Renal resistance was increased from 0.16 +/- 0.01 to 0.22 +/- 0.01 mm Hg.ml-1.min.100 gm-1 (p less than 0.05) by U-46619 and decreased significantly (p less than 0.05) below baseline by addition of prostacyclin (0.10 +/- 0.02 mm Hg.ml-1.min.100 gm-1). Placental resistance also increased significantly (p less than 0.03) in response to U-46619 (from 0.15 +/- 0.01 to 0.21 +/- 0.01 mm Hg.ml-1.min.kg-1 fetal weight) but was further increased to 0.29 +/- 0.03 mm Hg.ml-1.min.kg-1 fetal weight by the addition of prostacyclin. Umbilical placental blood flow decreased significantly (p less than 0.03) when prostacyclin was added to U-46619 (315 +/- 40 to 195 +/- 30 ml.min-1.kg-1 fetal weight). Whereas U-46619 had no effect on fetal arterial blood gases, the addition of prostacyclin resulted in significant fetal acidosis (p less than 0.03). We conclude that thromboxane mimic causes fetal hypertension and renal and placental vasoconstriction. Prostacyclin reverses hypertension and renal vasoconstriction but, unexpectedly, worsens fetal placental vasoconstriction produced by thromboxane. It is likely that the observed fetal acidosis is a result of compromised placental function.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Fetal vascular responses to maternal nicardipine administration in the hypertensive ewe.

Calcium channel blockers such as nicardipine act as arterial vasodilators and are effective in the treatment of hypertension. Although they are also effective tocolytic agents, fetal effects have not been fully studied. Fifteen chronically catheterized near-term ewes were studied. Maternal and fetal cardiorespiratory parameters were measured in the control period and again 15 minutes after maternal venous infusion of angiotensin II. Nicardipine 20 micrograms/kg/min was given over 2 minutes and maternal and fetal cardiorespiratory parameters and fetal blood flow were measured 5.30 and 60 minutes later. Nicardipine reversed maternal hypertension and produced transient tachycardia. Fetuses responded initially with transient bradycardia and then developed hypercapnia and acidemia (p less than 0.03) by 60 minutes after nicardipine. Fetal placental blood flow decreased and vascular resistance increased by 5 minutes after nicardipine but returned toward control values after 30 minutes. Unexpectedly we observed the death of five fetuses by 65 minutes after nicardipine. We conclude that the administration of nicardipine in the hypertensive ewe results in significant alterations of fetal cardiorespiratory status and placental function that may lead to acidemia.

Angiotensin II↗
PubMed1989

Placental vascular responses to nicardipine in the hypertensive ewe.

Calcium channel blockers are arterial vasodilators effective in the treatment of hypertension. Therefore nicardipine, a dihydropyridine calcium channel blocker, should modulate angiotensin II-induced vasoconstriction. Regional blood flows were measured with radioactive microspheres in five chronically catheterized near-term ewes both before and 15 minutes after maternal infusion of angiotensin II at 5 micrograms/min. Nicardipine was then administered intravenously at 20 micrograms/kg/min over 2 minutes while the angiotensin II infusion was maintained. Blood flows were measured after 5 minutes. Maternal blood pressure levels were increased by angiotensin II from 83 +/- 4 mm Hg to 114 +/- 5 mm Hg, and were decreased to 70 +/- 4 mm Hg by nicardipine (p less than 0.05). Nicardipine also reversed angiotensin II-induced vasoconstriction in the renal and endomyometrial vascular beds (p less than 0.05). Unexpectedly, however, nicardipine worsened placental vasoconstriction caused by angiotensin II, as placental blood flow fell from 242 +/- 32 ml.min-1.kg-1 fetal weight to 128 +/- 7 ml.min-1.kg-1 fetal weight (p less than 0.05), and placental resistance increased from 0.48 +/- 0.04 mm Hg.ml-1.min.kg-1 fetal weight to 0.55 +/- 0.05 mm Hg.ml-1.min.kg-1 fetal weight (p less than 0.05). Nicardipine reverses angiotensin II-induced vasoconstriction systemically and in the kidney and uterus of the pregnant ewe, but does not reverse placental vasoconstriction and may significantly alter fetal cardiorespiratory status.

Angiotensin II↗
PubMed1989

Fetal placental vascular responses to prostacyclin after angiotensin II-induced vasoconstriction.

The vasodilator prostacyclin is produced by many fetal tissues and may serve to protect umbilical placental blood flow. We hypothesized that prostacyclin could reverse fetoplacental vasoconstriction produced by angiotensin II (ANG II). Studies were done in eight unanesthetized near-term ovine fetuses. After a control period, ANG II was infused into the fetal inferior vena cava at a rate of 0.5 microgram/min for 40 min. Twenty minutes after starting the ANG II infusion, an infusion of prostacyclin at a rate of 5 micrograms/min was added to the ANG II infusion. Blood flows were measured by the radioactive microsphere technique. Blood flow measurements were made during the control period, 20 min after starting the ANG II infusion, and 20 min after adding prostacyclin to the ANG II infusion. ANG II produced significant fetal hypertension and renal, intestinal, and placental vasoconstriction. Placental vascular resistance rose from 0.14 +/- 0.01 to 0.18 +/- 0.01 mmHg.min.kg fetal wt.ml-1 during the ANG II infusion period (P less than 0.05). The addition of prostacyclin to the ANG II infusion resulted in a return to control values for fetal blood pressure and renal and intestinal resistance. However, placental vasoconstriction was not reversed by addition of prostacyclin as placental vascular resistance remained significantly elevated over the control value (0.17 +/- 0.01 mmHg.min.kg fetal wt.ml-1). Although unchanged by ANG II infusion, fetal pH decreased significantly during the ANG II plus prostacyclin infusion period. We conclude that ANG II causes fetal hypertension and renal and intestinal vasoconstriction, which are reversed by prostacyclin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1988

Effects of high-dose oxytocin augmentation on umbilical cord blood gas values in primigravid women.

Active management of labor for term primigravid women with singleton, vertex presentations is associated with significant decreases in incidence of cesarean section and duration of labor, without adversely affecting major perinatal outcome variables. Concern has been expressed that high-dose oxytocin augmentation may increase the incidence of fetal compromise. With active management of labor, 43% of 1423 primigravid women received high-dose oxytocin augmentation during an 11-month period. Umbilical cord blood gas values from those who received high-dose oxytocin augmentation were compared with values in those who received no oxytocin. The mean arterial pH value in the no oxytocin group was 7.24 +/- 0.07, which is not significantly different (p greater than 0.10) from that of the oxytocin-augmented group, 7.23 +/- 0.07. Similarly, all other arterial and venous umbilical cord gas parameters were unaffected by high-dose oxytocin augmentation (p greater than 0.10). Our values were compared with other published values where labor was not managed according to the principles of active management of labor, and no differences were found. We report the largest series of cord blood pH values in primigravid women and conclude that there is no adverse effect of high-dose oxytocin augmentation or active management of labor on umbilical cord blood gas values at delivery.

Adult↗
PubMed1988

Cervical incompetence and preterm labor.

The ability of the cervix to function as a competent sphincter to retain the fetoplacental unit in utero until term is dependent on a complex set of biochemical, biophysical, and environmental events. The understanding of these interactions is limited at present and requires that cervical incompetence be a diagnosis of exclusion. Currently, differentiation of cervical incompetence from preterm labor is a major problem. Advances in ultrasonography, ambulatory uterine activity monitoring, cervical histomorphology, and biochemistry should improve the understanding of both normal and abnormal cervical and uterine function and may provide new techniques to distinguish between true cervical incompetence and preterm labor. Well-designed and strictly executed randomized clinical trials of cervical cerclage should answer the question of therapeutic efficacy for this popular technique when the diagnosis of cervical incompetence is made.

Cervix Uteri↗
PubMed1986

The role of arachidonic acid metabolites in preeclampsia.

Preeclampsia is characterized by imbalances in the production rates of several arachidonic acid metabolites. There is a considerable amount of evidence to indicate that PGI2 production is decreased in preeclampsia. PGI2 is a potent vasodilator, an inhibitor of platelet aggregation, and an inhibitor of uterine contractility. Evidence is accumulating that TX production in preeclampsia is either increased or unchanged so that the ratio of TX to PGI2 favors TX. TX opposes the actions of PGI2 in that it is a potent vasoconstrictor, a stimulator of platelet aggregation, and a stimulator of uterine contractility. Therefore, an imbalance of increased TX/decreased PGI2 production can account for the major clinical symptoms of preeclampsia. There is now preliminary evidence that the placenta produces lipoxygenase, as well as cyclooxygenase compounds. The hydroxyeicosatetranoic acids (5-HETE, 12-HETE, 15-HETE) and LTB4 have been identified as placental products. The preeclamptic placenta appears to be deficient in the 5- and 12-lipoxygenase enzymes, as indicated by placental production of 5-HETE and 12-HETE. Little is known about the regulation of arachidonic acid metabolites in normal or preeclamptic pregnancies. Steroids are known to affect cyclooxygenase product production. Progesterone, for example, inhibits PGI2 production. Although circulating and urinary concentrations of progesterone do not differ between normal and preeclamptic pregnancies, there is one report that placental progesterone concentrations are higher in preeclampsia; this may partially explain the decreased placental production of PGI2. There is a considerable amount of evidence in various tissues that regulatory interactions exist between the cyclooxygenase and lipoxygenase metabolites of arachidonic acid, but the role of these interactions in preeclampsia is not known. There is still much to be learned about the etiology of preeclampsia, but it is certain that aberrations in the production of arachidonic acid metabolites play an important role. It is likely that the effective treatment of preeclampsia will come from understanding the regulation of the arachidonic acid metabolites during pregnancy, and, therefore, the ability to specifically treat the production imbalances that characterize this disorder.

Arachidonic Acids↗