Christine S. Thompson

Does the intravenous infusion of ritodrine or magnesium sulfate alter the hemodynamic response to hemorrhage in gravid ewes

Abstract The purpose of this study was to determine whether the intravenous infusion of ritodrine or magnesium sulfate alters the hemodynamic response to maternal hemorrhage in gravid ewes. Twenty-seven experiments were performed in 12 chronically instrumented animals at 0.8 of timed gestation. Each animal was subjected to hemorrhage (20 ml/kg over 60 minutes) during infusion of ritodrine (0.004 mg/kg/min), magnesium sulfate (4 gm/hour), or saline solution control. Infusion of magnesium sulfate increased the mean (±SEM) maternal serum magnesium concentration to 4.8 ± 0.2 mg/dl before hemorrhage and 5.3 ± 0.3 mg/dl after hemorrhage. At the end of hemorrhage maternal mean arterial pressures were 63% ± 4%, 82% ± 2%, and 79% ± 6% of baseline in the magnesium sulfate, ritodrine, and control groups, respectively. The maternal mean arterial pressure response in the magnesium sulfate group differed significantly from the maternal mean arterial pressure responses in the ritodrine and control groups ( p p = 0.0001). Fetal Po 2 was decreased significantly in the magnesium sulfate and ritodrine groups ( p

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)

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)

Does furosemide alter the hemodynamic response to rapid intravascular transfusion of the anemic fetal lamb

The purpose of this study was to define the hemodynamic response to rapid intravascular transfusion of the anemic fetal lamb and to determine whether furosemide alters that response. Sixteen experiments were performed in nine chronically instrumented gravid ewes between 0.8 and 0.9 of timed gestation. On day 1 of each experiment, each fetus was subjected to hemorrhage (40 ml/kg of estimated fetal weight) over 1 hour. On day 2, plasma was withdrawn from the stored fetal blood until the hematocrit was approximately 70%, and the packed red blood cells were returned to the fetus intravenously over 10 minutes. Each fetus received either furosemide (2 mg/kg)or control saline solution intravenously at time zero and again at 5 minutes. The order of experiments was randomly determined for each animal. Hemorrhage resulted in a similar decrease in fetal hematocrit in the two groups. The mean ± SEM fetal hematocrit before hemorrhage was 38 ± 3% in the furosemide group ( n = 8) and 36 ± 2% in the control group ( n = 8). On day 2, the mean ± SEM fetal hematocrit before transfusion was 28 ± 2% in the furosemide group and 25 ± 1% in the control group. There was no significant difference between groups in the fetal hemodynamic response to transfusion. At the end of the transfusion, the fetal central venous pressure had increased from 4.9 ± 0.5 to 6.2 ± 0.5 mm Hg in the furosemide group ( p = 0.01) and from 3.9 ± 0.2 to 5.8 ± 0.3 mm Hg in the control group ( p = 0.0001). Fetal mean arterial pressure increased from 42 ± 1 to 50 ± 1 mm Hg in the furosemide group ( p = 0.0001) and from 40 ± 1 to 46 ± 1 mm Hg in the control group ( p = 0.0007). Fetal heart rate decreased from 187 ± 2 to 169 ± 5 beats/min in the furosemide group ( p = 0.004) and from 188 ± 4 to 170 ± 5 beats/min in the control group ( p = 0.0008). Transfusion did not significantly change fetal pH in either group. At 120 minutes, the fetal PO 2 had increased from 17 ± 1 to 19 ± 1 mm Hg in the furosemide group ( p = 0.03) and from 19 ± 1 to 21 ± 2 mm Hg in the control group ( p = 0.05). We conclude that rapid transfusion of the anemic fetal lamb resulted in modest increases in fetal central venous pressure and mean arterial pressure. Second, furosemide did not significantly alter the hemodynamic response to rapid transfusion.

Intravenous administration of d-tubocurarine and pancuronium in fetal lambs

The purpose of this study was to assess the effects of intravenous administration of d-tubocurarine and pancuronium in fetal lambs. Eighteen experiments were performed in seven chronically instrumented pregnant ewes between 0.8 and 0.9 of timed gestation. Each fetus received 6 ml of study drug intravenously at 1.2 ml/min over 5 minutes (d-tubocurarine 3.0 mg/kg, pancuronium 0.5 mg/kg, or saline solution control). Pancuronium (n = 7) significantly increased both fetal heart rate and mean arterial pressure. d-Tubocurarine (n = 5) significantly decreased both fetal heart rate and mean arterial pressure. Saline solution control (n = 6) did not significantly alter fetal heart rate or mean arterial pressure. The present study suggests that pancuronium is preferable to d-tubocurarine for those intrauterine procedures when an increase in fetal heart rate is desired.

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 chronically 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 less than 0.05) and increased cardiac output (p less than 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 less than 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 less than 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 INTRAVENOUS INFUSION OF RITODRINE OR MAGNESIUM SULFATE ALTER THE HEMODYNAMIC RESPONSE TO HEMORRHAGE IN GRAVID EWES

63% 5 4%, 82% 2 2%, and 79% f 6% of baseline in the magnesium sulfate, ritodrine, and control groups, respectively. The maternal mean arterial pressure response in the magnesium sulfate group differed significantly from the maternal mean arterial pressure responses in the ritodrine and control groups (p < 0.01). Fetal pH was decreased significantly only in the magnesium sulfate group (p = 0.0001). Fetal PO, was decreased significantly in the magnesium sulfate and ritodrine groups (p -C 0.001) but not in the control group. We conclude that magnesium sulfate but not ritodrine, worsened the maternal hypotensive response to hemorrhage in gravid ewes. (AM J OBSTET GYNECOL 1988;159:1467-73.)