Maternal Mean Arterial Pressure Research Articles

Pregnancy-Induced Hypertension Is Associated with Changes in Maternal and Umbilical Blood Antioxidants

Seventeen pregnancies with pregnancy-induced hypertension (PIH) and 28 control pregnancies were analyzed with regard to maternal and fetal blood antioxidants and lipid peroxidation products (conjugated dienes). In PIH, maternal blood levels of conjugated dienes were higher than in normal pregnancy. Also the activities of platelet and plasma glutathione peroxidase (GSHPx) were higher in PIH. In umbilical cord blood, the appearance of conjugated dienes, the concentration of vitamin E and the activity of erythrocyte GSHPx were lower than the corresponding maternal values. There was no difference between PIH and normal pregnancy in the appearance of conjugated dienes in cord blood, but erythrocyte GSHPx and plasma vitamin A were lower in PIH. Cord blood plasma vitamin A showed a negative correlation to maternal mean arterial pressure. We suggest that lipid peroxidation is involved in the pathogenesis of maternal PIH, and it may also have effects on the vascular function and antioxidant status of the fetus.

The effect of smoking on the resistance index of the umbilical artery and the middle cerebral artery

23 healthy smokers with uneventful singleton pregnancies underwent Doppler-flow measurements of the foetal umbilical artery and middle cerebral artery before and ten minutes after smoking one cigarette. In both arteries the resistance indices (RI) did not change significantly. Maternal mean arterial blood pressure and heart rate increased significantly after the smoking of the cigarette. Neither the group with an RI increase of greater than or equal to 5% in the foetal umbilical artery (n = 7) nor the group with an increase of the RI in the foetal umbilical artery and, at the same time, a decrease of the RI in the arteria cerebri media (n = 5), showed a significant difference concerning maternal haemodynamic parameters and the number of cigarettes smoked before and during pregnancy. The results suggest, that the smoking of one cigarette in uneventful pregnancy does not produce acute haemodynamic effects in the foetus.

Does Calcium Chloride Help Restore Maternal Blood Pressure and Uterine Blood Flow During Hemorrhagic Hypotension in Hypermagnesemic Gravid Ewes?

Magnesium sulfate worsens maternal hypotension and fetal oxygenation during hemorrhage in gravid ewes. The purpose of this study was to determine whether calcium chloride administration is a useful adjunct to blood transfusion during hemorrhagic hypotension in hypermagnesemic gravid ewes. Sixteen experiments were performed in eight chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included (a) T = 0: magnesium sulfate 4 g IV; (b) T = 5: infusion of magnesium sulfate 4 g/h IV; (c) T = 90: maternal hemorrhage 20 mL/kg over 55 min; (d) T = 147: calcium chloride 10 mg/kg or normal saline (NS-control) 0.1 mL/kg IV; (e) T = 160: transfusion of collected maternal blood over 55 min. Magnesium sulfate alone slightly decreased maternal mean arterial pressure (P = 0.002) and increased uterine blood flow (P = 0.0001) in both groups before hemorrhage. During hemorrhage, maternal mean arterial pressure, cardiac output, and uterine blood flow, and fetal PO2 and pH all decreased sharply (P = 0.0001). Cardiac output increased (P = 0.0005) modestly just after the intravenous bolus of calcium chloride. Maternal mean arterial pressure was significantly higher (P = 0.03) during transfusion in the calcium chloride group than in the NS-control group, but only after mean arterial pressure was near baseline measurements. Maternal uterine blood flow and fetal PO2 and pH responses over time were similar in the two groups. We conclude that intravenous administration of calcium chloride (10 mg/kg) transiently increased cardiac output during hemorrhagic hypotension and slightly increased mean arterial pressure during transfusion in hypermagnesemic gravid ewes.(ABSTRACT TRUNCATED AT 250 WORDS)

Epidural Anesthesia Worsens Uterine Blood Flow and Fetal Oxygenation during Hemorrhage in Gravid Ewes

Recent studies suggest that epidural anesthesia initiated before hemorrhage may improve survival and acid-base status in laboratory animals. However, studies of hemorrhagic shock in nonpregnant animals may not be applicable to less severe hemorrhage in pregnant animals. The purpose of this study was to determine whether epidural anesthesia alters maternal and fetal hemodynamic and acid-base responses to hemorrhage in gravid ewes. Twenty-four experiments were performed in twelve chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included: 1) T = 0 min: normal saline 500 ml intravenously; 2) T = 15 min: epidural administration of 0.5% bupivacaine (epidural group) or normal saline (control group); 3) T = 30 min: epidural administration of additional 0.5% bupivacaine (epidural group only) if the sensory level of anesthesia was below T10; 4) T = 45 min: maternal hemorrhage 20 ml/kg over 55 min; and 5) T = 110 min: transfusion of collected maternal blood over 55 min. At 45 min (i.e., 30 min after the epidural injection of bupivacaine), epidural bupivacaine resulted in a median sensory level of T9 in the epidural group. At that time, maternal mean arterial pressure was less (P less than 0.05) in the epidural group than in the control group (14 +/- 2% below baseline versus 4 +/- 1% above baseline, respectively). Maternal mean arterial pressure, heart rate, cardiac output, and uterine blood flow, and fetal PO2 and pH all were significantly less during hemorrhage (P less than 0.05) in the epidural group than in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute effects of captopril, an angiotensin-converting enzyme inhibitor, on the pregnant ewe and fetus.

After control measurements had been made, 15 chronically catheterized pregnant ewes (gestational age 123-141 days) were given 15 mg of captopril intravenously followed by an infusion of 6 mg/h. These doses blocked the pressor responses of both ewes and fetuses to 5 micrograms of angiotensin I. After captopril, maternal mean arterial pressure fell from 94 +/- 3.5 to 88 +/- 3.6 (SE) mmHg (P less than 0.0001) and pulse interval fell (P = 0.008). Maternal flow to the cotyledons fell from 766 +/- 118 to 525 +/- 77 ml/min (P = 0.002), as did flow to the remainder of the maternal placenta, i.e., the caruncles and their underlying myoendometrium (control flow 188 +/- 35 ml/min, flow 10-15 min after captopril 166 +/- 36.1 ml/min; P = 0.021). Flow to the rest of the myometrium did not change. Fetal arterial pressure fell from 46.9 +/- 1.6 to 44.1 +/- 1.6 mmHg (P less than 0.009), and fetal placental blood flow fell from 639.9 +/- 93.2 to 413.1 +/- 53.9 ml/min (P = 0.025). Flow to the fetal membranes declined also, from 53.2 +/- 6.5 to 35.6 +/- 3.3 ml/min (P less than 0.005). Maternal and fetal renal blood flows and fetal adrenal blood flows were unchanged. Fetal arterial PO2 was initially 19.5 +/- 0.8 mmHg; after captopril, it was 17.7 +/- 0.9 mmHg (P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Hydralazine does not restore uterine blood flow during cocaine-induced hypertension in the pregnant ewe.

Cocaine abuse is widespread, and its use by the parturient has potential significant adverse effects in both the mother and the newborn. This study was undertaken in gravid ewes to determine the effects of treatment of cocaine-induced hypertension with hydralazine (Apresoline) on the maternal and fetal cardiovascular systems, catecholamine response, blood gas and acid-base status, and uterine blood flow (UBF). Twenty-one experiments were performed in 15 chronically instrumented ewes near term gestation. After a 30-min control period, cocaine was given intravenously to all ewes for 55 min to induce and maintain increased maternal mean arterial pressure (MMAP) and reduced UBF. The sheep were randomly assigned to receive either cocaine alone (n = 11, control group) or hydralazine (n = 10, treatment group), starting 15 min after the cocaine administration. Both drugs were discontinued 55 min after the start of the cocaine administration, followed by a 35-min recovery period. In the control group, cocaine administration resulted in a 31 +/- 13% (SD) increase in MMAP (P less than 0.05) and a 26 +/- 21% reduction in UBF (P less than 0.05). In the treatment group, the initial cocaine administration resulted in a similar increase in MMAP and decrease in UBF. Hydralazine therapy restored MMAP toward baseline after 20 min of administration, but UBF remained reduced (37 +/- 17%) throughout therapy (P less than 0.05) and recovery (18 +/- 13%) (P less than 0.05). The maternal heart rate increased maximally by 121 +/- 33% (P less than 0.05) after the administration of hydralazine, compared with a 14 +/- 21% increase (P less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Does Magnesium Sulfate Alter the Maternal Cardiovascular Response to Vasopressor Agents in Gravid Ewes?

Magnesium sulfate (MgSO4) attenuates the maternal compensatory response to hemorrhage in gravid ewes, perhaps by decreasing the response to endogenous vasopressors. The purpose of this study was to determine whether MgSO4 alters the cardiovascular response of gravid ewes to vasopressor agents. Sixteen gravid ewes underwent a series of experiments consisting of administration of two exogenous and two endogenous vasopressors, each with and without a concurrent MgSO4 infusion. Dose-response curves were constructed for phenylephrine (an alpha 1-adrenergic agonist), ST-91 (an alpha 2-adrenergic agonist), angiotensin II, and arginine vasopressin (AVP). MgSO4 significantly attenuated the increase in maternal mean arterial pressure and systemic vascular resistance and the decrease in cardiac output during ST-91 infusion but not during phenylephrine, angiotensin II, or AVP infusions. MgSO4 significantly attenuated the increase in uterine vascular resistance during phenylephrine, ST-91, and angiotensin II infusions and the decrease in uterine blood flow during phenylephrine and angiotensin II infusions. MgSO4 also appeared to attenuate the decrease in uterine blood flow during ST-91 infusion (P = 0.067). The present study suggests that MgSO4 antagonizes the effects of alpha 1-adrenergic agonists, alpha 2-adrenergic agonists, and angiotensin II on the uterine vasculature, thus providing a level of protection for the fetus in situations of maternal stress.

Fetal and maternal plasma atrial natriuretic factor responses to angiotensin II infusion

Plasma atrial natriuretic factor and angiotensin II have opposing actions in the regulation of body fluid homeostasis and systemic blood pressure. Angiotensin II infusions stimulate atrial natriuretic factor release in some, but not all, studies in adult mammals. To examine the response during the perinatal period, graded intravenous angiotensin II infusions were administered to four chronically instrumented pregnant ewes and fetuses (132 ± 1 days of gestation). Fetuses received successive 20-minute intravenous angiotensin II infusions at 25, 50, and 100 ng/kg/min. After a 90-minute recovery, maternal ewes received successive 20-minute angiotensin II infusions (5, 10, and 25 ng/kg/min). During the fetal infusions, mean (± SEM) fetal arterial blood pressure (47 ± 2 to 61 ± 2 mm Hg, p < 0.05) and heart rate (155 ± 16 to 196 ± 36 beats/min, p < 0.05) increased, although there was no change in maternal measured parameters. In response to the maternal infusion, maternal mean arterial blood pressure increased (92 ± 7 to 110 ± 8 mm Hg, p < 0.05) and maternal heart rate decreased (136 ± 4 to 125 ± 2 beats/min, p < 0.05) without change in fetal parameters. Fetal plasma atrial natriuretic factor levels (210 ± 27 to 664 ± 250 pg/ml, p < 0.05) significantly increased during the fetal angiotensin II infusions in spite of no change in maternal plasma atrial natriuretic factor (85 ± 21 to 124 ± 22 pg/ml) during the maternal angiotensin II infusions. These findings indicate that similar increases in systemic blood pressure in response to angiotensin II infusions stimulate increased fetal, but not maternal, plasma atrial natriuretic factor. (AM J OBSTET GYNECOL 1991;165:1635-41.)

Effects of Acute Hypercapnia on Maternal and Fetal Vasopressin and Catecholamine Release

Although fetal asphyxia, i.e. hypoxemia, acidosis, and hypercapnia, increases plasma arginine vasopressin (AVP) greater than 40-fold, hypoxemia and metabolic acidosis occurring independently cause only 5-fold and 2-fold increases, respectively. To determine the effects of hypercapnia on AVP release, we examined the effects of acute hypercapnia on AVP secretion in six pregnant sheep and their fetuses at 135 +/- 4 d (chi +/- SD), exposing the ewe successively to room air, 30% O2, 30% O2 plus 10% CO2, 30% O2, and room air, and monitoring uterine blood flow, as well as maternal and fetal mean arterial pressure, heart rate, arterial blood gases, and plasma AVP and catecholamines. Oxygen exposure had no effect on the ewe or fetus. During O2 plus CO2 exposure, the ewes and fetuses developed hypercapnia in the absence of hypoxia, arterial CO2 tension increasing to 8.38 +/- 0.87 kPa (62.9 +/- 6.5 mm Hg) and 10.0 +/- 0.61 kPa (75.2 +/- 4.6 mm Hg) (p less than 0.001), respectively, at 30 min of exposure. Although fetal heart rate and mean arterial pressure were unchanged, maternal values rose 61 and 30% (p less than 0.001), respectively. At 30 min of O2 + CO2 exposure, maternal norepinephrine increased from 2.23 +/- 0.74 to 8.52 +/- 3.97 nmol/L (p = 0.15) and fetal epinephrine increased from 0.27 +/- 0.10 to 2.271 +/- 0.90 nmol/L (p = 0.01); plasma AVP was not significantly increased in the ewe or fetus, although levels rose from approximately 45 to 127 +/- 48 and 137 +/- 64 pmol/L (p = 0.10), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Intravaginal Prostaglandin E2Gel and Cardiovascular Changes in Hypertensive Pregnancies

Prostaglandin E2 (PGE2) and its analogues may be potent vasodilators, and intravaginal PGE2 is known to be absorbed rapidly into the maternal circulation. This study investigated any cardiovascular effects from intravaginal PGE2 on 42 hypertensive pregnant women requiring preinduction cervical ripening. Declines in maternal diastolic, systolic, and mean arterial pressures were apparent during the first half hour. This trend was mild, was reversible without treatment, and did not influence the fetal heart rate baseline or patterns. Fear of clinically significant changes should not be a concern, but monitoring during the first hour is recommended.

Maternal and fetal effects of labetalol in pregnant ewes.

Labetalol has been advocated to rapidly decrease blood pressure in preeclamptic women and to blunt the hemodynamic response to tracheal intubation. To assess labetalol's actions in a setting of uterine vasoconstriction, saline or labetalol (1 mg/kg) was infused into maternal venous catheters in 12 pregnant ewes receiving continuous maternal intravenous infusions of norepinephrine. Norepinephrine increased maternal mean arterial pressure (MAP) to 120 +/- 4% of control and decreased uterine blood flow to 45 +/- 6% of control. Labetalol, but not saline, altered these parameters: it decreased MAP to 101 +/- 3% and increased uterine blood flow to 70 +/- 7% of prenorepinephrine values. In the second protocol, to assess the degree of labetalol-induced fetal adrenergic blockade, 7 pregnant ewes received, on separate days, saline or labetalol (0.3, 1.0, 3.0 mg/kg) via a maternal venous catheter. Maternally administered labetalol produced minor (less than 12%) decreases in maternal and fetal MAP, without significantly altering heart rate (HR). At each labetalol dose, the degree of alpha- and beta-adrenergic blockade, determined by phenylephrine and isoproterenol challenge, was greater in the ewe than in the fetus. In the near-term pregnant ewe, intravenous (iv) bolus administration of labetalol ameliorated the effects of increased circulating norepinephrine on maternal MAP, uterine blood flow, and fetal pH and arterial O2 tension (PaO2), and produced less adrenergic blockade in the fetus than in the mother.

Magnesium Sulfate Decreases Maternal Blood Pressure but Not Uterine Blood Flow during Epidural Anesthesia in Gravid Ewes

The purpose of this study was to determine whether administration of magnesium sulfate decreased maternal blood pressure during epidural anesthesia in gravid ewes. Twenty-two experiments were performed in 11 chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included: 1) T = 0: magnesium sulfate 4 g intravenously over 5 min followed by an infusion of magnesium sulfate at 4 g/h, or normal saline iv followed by an infusion of normal saline alone; 2) T = 135 min: 500 ml normal saline intravenously over 12 min; and 3) T = 150 min: epidural administration of 2% lidocaine. The initial bolus of magnesium sulfate slightly decreased maternal mean arterial pressure (MAP) but increased uterine artery blood flow (UBF). The increase in UBF was accompanied by an increase in fetal PaO2 at 145 min in the magnesium sulfate group but not in the control group. At 165 min (i.e., 15 min after the epidural injection of lidocaine), epidural lidocaine resulted in a median sensory level of T-10 in the magnesium sulfate group and T-11 in the control group. During epidural anesthesia, maternal MAP was lower (P = 0.001) in the magnesium sulfate group than in the control group. At 165 min, maternal MAP was 18 +/- 3% below baseline (P = 0.0001) in the magnesium sulfate group but did not differ significantly from baseline in the control group. Maternal cardiac output and UBF did not differ from baseline after epidural injection of lidocaine in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of magnesium on maternal blood pressure in pregnancy‐induced hypertension A randomized double‐blind placebo‐controlled trial

The effects of magnesium were compared with those of placebo in a randomized double-blind controlled study of 58 patients with pregnancy-induced hypertension, of whom 27 received magnesium and 31 placebo. Twenty patients in each group were nulliparas. The treatment comprised 48 h of either intravenous magnesium or placebo infusion followed by daily oral magnesium or placebo tablets until one day after delivery. Magnesium supplementation significantly reduced maternal mean arterial blood pressure (MAP). The gestational age at delivery was the same in both groups, whereas the relative fetal birth weight among nulliparas was reduced in the placebo group. Unbalanced analyses of variance suggested an influence of magnesium supplement on birth weight. The infants in the magnesium supplemented group spent fewer days in the neonatal intensive care unit. There were no perinatal deaths. Magnesium appeared to be beneficial in the management of pregnancy-induced hypertension. The better outcome associated with magnesium supplementation may not have been due to reduction of MAP and further studies are needed to clarify whether magnesium influences birth weight.

Fetal umbilical artery Doppler response to graded maternal aerobic exercise and subsequent maternal mean arterial blood pressure: Predictive value for pregnancy-induced hypertension

Predictive tests for the identification of women at high risk of the development of preeclampsia are critical to allow the most appropriate preventive measures. Preeclampsia is a vasospastic condition of pregnancy characterized by early and enhanced vascular reactivity to endogenous pressor agents. Exercise tolerance testing with cycle ergometry to induce hemodynamic response measured with duplex Doppler A/B ratio of the umbilical artery could unmask latent vascular pressor hypersensitivity. Our prospective cohort study was designed to test the efficacy of the American College of Obstetricians and Gynecologists exercise in pregnancy guidelines for the low-risk atheletic, physically active, or sedentary patient. The pattern of fetal response to material exercise testing at 28 weeks' gestation was compared with subsequent maternal mean arterial blood pressure and the development of pregnancy-induced hypertension and preeclampsia. Doppler A/B ratio during the recovery period was assessed as below baseline (18) or elevated above resting baseline values (12). Third-trimester blood pressure pattern was assessed to be elevated in 11 patients, 10 of whom had elevated recovery A/B ratios. The Fisher exact test results were (p = 0.00002) positive predictive value, 83%; negative predictive value, 94%; sensitivity, 91%; and specificity, 89%. Preeclampsia developed in four patients; all had elevated recovery A/B ratios. Fisher exact test results were (p = 0.01806) positive predictive value, 33%; negative predictive value, 100%; sensitivity, 100%; and specificity, 69%.

Magnesium sulfate and promethazine do not interact to cause hypotension in gravid ewes

The purpose of this study was to determine whether magnesium sulfate and promethazine interact to cause hypotension in gravid ewes. Fifteen experiments were performed in five chronicaly instrumented animals between 125 and 130 days of timed gestation (term = 145 days). In one group of experiments each animal received magnesium sulfate (4 gm intravenous bolus followed by 4 gm/hr intravenous infusion) then promethazine (50 mg intravenously). In a second group each animal received magnesium sulfate then saline solution as a control. In a third group each animal received saline solution then promethazine. Infusion of magnesium sulfate increased the mean ( ± SEM) serum magnesium concentration to 5.7 ± 0.6 and 6.6 ± 0.6 mg/dl in the magnesium sulfate-promethazine and magnesium sulfate—saline solution groups, respectively. Magnesium sulfate slightly decreased maternal mean arterial pressure (p < 0.05) and increased cardiac output (p < 0.05) in both the magnesium sulfate-promethazine and magnesium sulfate-saline solution groups. Otherwise there were no significant changes in maternal mean arterial pressure or cardiac output in any group. Promethazine increased maternal heart rate (p = 0.0001) in both the magnesium sulfate-promethazine and saline solution-promethazine groups. Magnesium sulfate increased uterine blood flow (p < 0.01) in both the magnesium sulfate-promethazine and magnesium sulfate-saline solution groups, but promethazine blunted the increase in uterine blood flow associated with magnesium sulfate. Similarly, magnesium sulfate decreased uterine vascular resistance (p < 0.01) in both the magnesium sulfate-promethazine and magnesium sulfate-saline solution groups, but promethazine eliminated the decrease in uterine vascular resistance associated with magnesium sulfate. Maternal and fetal arterial blood gas and acid-base values did not change in any group, except that there was a small, near-significant decrease (p = 0.06) in fetal pH 10 minutes after promethazine was given in the magnesium sulfate-promethazine group. We conclude that magnesium sulfate and promethazine did not interact to cause maternal hypotension in normovolemic gravid ewes. However, promethazine increased maternal heart rate and blunted the increase in uterine blood flow associated with magnesium sulfate.

Does Ritodrine Worsen Maternal Hypotension during Epidural Anesthesia in Gravid Ewes?

The purpose of this study was to determine whether prior administration ritodrine worsens maternal hypotension during epidural anesthesia in gravid ewes. Twenty-four experiments were performed in nine chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included the following: 1) at time-zero, intravenous (iv) administration of ritodrine, 0.004 mg.kg-1.min-1, or normal saline (NS) for 2 h; 2) at 120 min discontinuation of ritodrine, and administration of a 500 ml iv bolus of NS over 15 min; and 3) at 135 min epidural injection of 2% lidocaine or NS. There were three groups of experiments: 1) iv ritodrine-epidural lidocaine (n = 9); 2) iv NS-epidural lidocaine (n = 8); and 3) iv ritodrine-epidural NS (n =7). Epidural injection of lidocaine resulted in a median sensory level of T9 in both the ritodrine-lidocaine and NS-lidocaine groups. At 165 min (i.e., 30 min after the epidural injection of lidocaine), maternal mean arterial pressure was 19 +/- 3% below baseline (P = 0.0001) in the ritodrine-lidocaine group and 22 +/- 7% below baseline (P = 0.0001) in the NS-lidocaine group (NS between groups). At 120 min ritodrine had increased maternal cardiac output 45 +/- 6% above baseline (P = 0.0001) in the ritodrine-lidocaine group and 39 +/- 6% above baseline (P = 0.0001) in the ritodrine-NS group. Cardiac output remained above baseline (P less than 0.01) after epidural injection of lidocaine in the ritodrine-lidocaine group. In contrast, in the NS-lidocaine group cardiac output was 13 +/- 5% below baseline (P = 0.005) at 150 min. Fetal arterial pH did not change significantly in either the ritodrine-lidocaine or ritodrine-NS group.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternal and Fetal Cardiovascular Responses of the Normotensive and Hypertensive Pregnant Sheep to Parenteral Labetalol

Chronic and pregnancy-induced hypertension complicate 13% of all human pregnancies. Although several antihypertensive agents have been investigated for use during pregnancy, limited experimental information is available on the effects of labetalol (an α1- and β1- adrenergic blocking agent) on uterine blood flow. This study was designed to test the hypothesis that labetalol safely lowers blood pressure in the normotensive and hypertensive pregnant ewe without adversely affecting uterine blood flow or fetal blood pressure and heart rate. Twelve normotensive and three renal hypertensive pregnant ewes were chronically catheterized to study the effects of bolus intravenous injections of labetalol (12.5 mg to 200 mg) on maternal and fetal blood pressure, heart rate, and uterine blood flow. All doses of labetalol produced significant reductions in both maternal mean arterial pressure and uterine blood flow (p < 0.05). Cardiac output responses were measured only at the 12.5 and 25 mg dose of labetalol, but showed...

EFFECT OF ADRENALINE ON PLACENTAL TRANSFER OF BUPIVACAINE IN THE PERFUSED IN SITU RABBIT PLACENTA

Following general anaesthesia, each of 18 pregnant rabbits received an i.v. infusion, at a declining rate, of 0.125% bupivacaine, either plain solution followed by adrenaline (1.25 micrograms ml-1)-containing solution (n = 10) or vice versa (n = 8). All solutions contained antipyrine as an index of placental exchange. In each rabbit, a single fetal sac was opened, the umbilical vessels were cannulated and the placenta was perfused in situ with buffered Krebs solution containing Dextran. Bupivacaine and antipyrine concentrations were measured in effluent perfusate (fetal) and in maternal plasma sampled simultaneously. Mean maternal arterial pressure and mean placental perfusion pressure were not altered by adrenaline. Fetal:maternal concentration (F:M) ratios of antipyrine decreased significantly (P less than 0.05) during the second half of the experiment. In contrast, F:M ratios of bupivacaine were unchanged during the time course of the experiment and unaltered by the addition of adrenaline. It is concluded that neither adrenaline nor minor alterations in maternal placental flow affect placental transfer of bupivacaine.

Transplacental Passage and Hemodynamic Effects of Esmolol in the Gravid Ewe

Ostman, P. L.; Chestnut, D. H.; Robillard, J. E.; Weiner, C. P.; Hdez, M. J. Author Information

The effect of intravenously administered 2-chloroprocaine upon uterine artery blood flow velocity in gravid guinea pigs.

The purpose of the present study was to assess the effect of intravenously administered 2-chloroprocaine upon uterine artery blood flow velocity (UBFV) in gravid guinea pigs. Ten experiments were performed in ten chronically instrumented animals between 0.7 and 0.9 of timed gestation. Each animal received four solutions of 2-chloroprocaine in random order: 1) 0.67 mg/kg; 2) 1.34 mg/kg; 3) 2.0 mg/kg; and 4) 1.34 mg/kg, with epinephrine 0.2 microgram/kg. Six animals received a fifth solution, 0.2 ml of saline control. 2-Chloroprocaine 1.34 mg/kg significantly increased maternal mean arterial pressure (MMAP) at 30 s after injection, and 2-chloroprocaine 2.0 mg/kg significantly increased MMAP through 2 min. 2-Chloroprocaine 1.34 mg/kg, with epinephrine 0.2 microgram/kg, also significantly increased MMAP through 2 min. No other solution significantly altered MMAP. 2-Chloroprocaine 2.0 mg/kg significantly decreased UBFV at 30 s after injection. 2-Chloroprocaine 1.34 mg/kg, with epinephrine 0.2 microgram/kg, significantly decreased UBFV through 2 min. No other solution significantly altered UBFV. The authors conclude that iv administration of 2-chloroprocaine with epinephrine significantly decreased UBFV in pregnant guinea pigs. In contrast, only the largest dose (i.e., 2.0 mg/kg) of 2-chloroprocaine alone transiently decreased UBFV. These data suggest that, in doses up to 1.34 mg/kg, 2-chloroprocaine alone may not decrease uterine blood flow when used as a marker for intravenous injection in obstetric patients.