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Biomedical subjects

C D Rudolph

Publications and source records attributed to C D Rudolph.

36 records · Page 2Linked to original sources
PubMed1991

No-enema therapy for idiopathic constipation and encopresis.

Idiopathic constipation and encopresis of childhood are thought to occur when children volitionally withhold stool. Withholding may be prompted by social pressures or by episodes of painful defecation. Repetitive withholding may result in colonic dilatation and colorectal dysfunction. Therapy involves removal of impacted stool, stool softening, and behavioral therapy. The use of enemas in this therapy is widespread but may be counterproductive. A retrospective review of patients treated without enemas revealed 45 patients whose course could be followed for six months. Ninety-eight percent of these had successful initial cleanouts without enemas; 94% had continued success at six months. These results, comparable with other treatment programs, demonstrate that therapy without enemas is a reasonable alternative in the treatment of childhood constipation and encopresis.

Child↗
PubMed1991

Effects of ductus venosus obstruction on liver and regional blood flows in the fetal lamb.

The ductus venosus allows highly oxygenated blood returning from the umbilical-placental circulation to bypass the liver, and is believed thereby to facilitate preferential distribution of this blood to the fetal brain and heart. To examine this hypothesis, we developed a model that allows acute obstruction of the ductus venosus in chronically catheterized fetal lambs. In seven fetal lambs, a Swann-Ganz catheter was inserted into the inferior vena cava and the balloon tip advanced into the ductus venosus. Control measurements were obtained 1-2 d after surgery, before and during inflation of the balloon in the ductus venosus. At each sample time, radioactive microspheres were injected to determine organ blood flow and the distribution of umbilical venous blood flow. During balloon inflation, the percentage of umbilical venous return passing through the ductus venosus was reduced from 38 +/- 15% to 1 +/- 0.5%. Umbilical-placental blood flow was unchanged from control values of 181 +/- 33 mL/min/kg. Total liver blood flow increased from 346 +/- 98 to 553 +/- 105 mL/min/100 g. Pressure in the inferior vena cava did not change, but umbilical venous pressure increased from 7.2 +/- 2.7 to 8.7 +/- 3.5 mm Hg. Total vascular resistance across the liver and ductus venosus increased from 0.013 +/- 0.006 to 0.020 +/- 0.011 during ductus venosus obstruction. Fetal heart rate, arterial blood pressure, and descending aortic pH and blood gases were unchanged, as was oxygen content in the descending aorta and carotid artery. Organ blood flows, combined ventricular output, and oxygen delivery were also unchanged. In five animals, these studies were repeated during maternal hypoxemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Hemodynamic responses to alpha-adrenergic blockade during hypoxemia in the fetal lamb.

The mechanisms responsible for the increase in umbilical venous and hepatic vascular resistance during hypoxemia are poorly understood. To assess the relative importance of alpha-adrenergic receptors, we produced an acute, severe hypoxemia in chronically instrumented fetal sheep. While fetal arterial oxygen saturation was maintained at the same level, we then injected phentolamine, a selective alpha-adrenoreceptor blocker. We found that the hypoxemia-induced vasoconstriction of the umbilical veins and hepatic vasculature was reversed by alpha blockade. Thus, alpha-adrenergic stimulation is necessary to maintain vasoconstriction of the umbilical veins and hepatic vasculature during acute fetal hypoxemia. Furthermore, alpha-adrenergic stimulation is responsible for the hypoxemia-induced vasoconstriction of the gut, spleen, and lower carcass. Thus, the alpha-adrenergic system mediates important fetal hemodynamic adaptations to acute hypoxemia. However, the alpha-adrenergic system is not responsible for the hypoxemia-induced constriction of the renal vasculature.

Adrenergic alpha-Antagonists↗
PubMed1991

Cortisol induces perinatal hepatic gluconeogenesis in the lamb.

To examine the influence of a prenatal increase in plasma cortisol concentration on perinatal initiation of hepatic gluconeogenesis, we infused cortisol into seven fetal sheep at 137-140 days gestation. 14C-Lactate provided tracer substrate for estimation of gluconeogenesis. We measured hepatic blood flow using radionuclide-labeled microspheres. After delivery, fetal arterial blood glucose concentration (1.33 +/- 0.4 mmol/l) increased transiently, but returned to fetal levels within 1 h after delivery. Substantial hepatic gluconeogenesis was induced in the fetus after cortisol infusion, averaging 23.4 +/- 12.2 mumol/min/100 g liver (7.8 +/- 4.4 mumol/min/kg fetal weight). Fetal hepatic glucose output was 44.4 +/- 17.7 mumol/min/100 g liver. Hepatic glucose output did not change after delivery; estimated gluconeogenesis decreased immediately, then increased by 6 h after delivery. Lactate supply to the liver fell substantially, from 1.1 +/- 0.4 mmol/min/100 g in the fetus to 0.24 +/- 0.09 at 1 h after delivery. Lactate flux across the liver decreased from 75.3 +/- 23 mumol/min/100 g in the fetus to 20.2 +/- 15.7 at 1 h after delivery. Hepatic lactate flux was significantly related to gluconeogenesis (r = 0.734, P = 0.0001). We conclude that cortisol induces substantial hepatic gluconeogenesis in fetal sheep near term. After delivery, there appears to be a transient decline in gluconeogenesis from lactate, which may be secondary to limited hepatic oxygen and substrate supply. Onset of gluconeogenesis in the fetus fails to sustain increases in either fetal or postnatal blood glucose concentrations.

Animals↗
PubMed1991

Effects of maternal fasting on hepatic gluconeogenesis and glucose metabolism in fetal lambs.

In unstressed, normoglycaemic fetal lambs, the liver produces little glucose, and gluconeogenesis is insignificant. Indirect measurements have suggested that the fetus may produce glucose endogenously during hypoglycaemia induced by prolonged maternal starvation. In eight fetal lambs we directly measured total and radiolabelled substrate concentration differences across the liver to determine whether the fetal liver produces glucose after four days of fasting-induced hypoglycaemia. Simultaneously we measured umbilical glucose uptake and fetal glucose utilization. Glucose concentrations in ewes (1.78 +/- 0.44 mmol.-1) and fetuses (0.61 +/- 0.17 mmol.l-1) were decreased. Fetal glucose utilization rate (21.7 +/- 8.9 mumol.min-1.kg-1) was not significantly different from umbilical glucose uptake (17.2 +/- 8.9 mumol.min-1.kg-1). Hepatic glucose production (8.9 +/- 17.2 mumol.min-1.100 g-1) and gluconeogenesis (6.1 +/- 4.4 mumol.min-1.100 g-1) were present, but could account for only 13% and 8% of fetal glucose requirements, respectively. To determine whether glucose output by the fetal liver was limited by substrate availability, we infused lactate, acetate, and acetone into the umbilical veins of four fasted animals, increasing hepatic substrate delivery. Hepatic glucose output did not increase during infusion of gluconeogenic substrates, indicating that substrate availability did not limit gluconeogenesis. We conclude that the gluconeogenic pathway is intact in late-gestation fetal lambs and that the fetal liver is capable of gluconeogenesis. However, the primary change in fetal metabolism during maternal starvation is the reduction in fetal glucose utilization, obviating the need for substantial hepatic glucose production. The factors stimulating this modest increase in fetal hepatic glucose production remain to be elucidated.

Animals↗
PubMed1991

Cardiovascular responses to acute, severe haemorrhage in fetal sheep.

In adults, the responses to acute haemorrhage vary greatly depending on the amount of blood lost. While many studies have documented fetal responses to mild haemorrhage, fetal responses to severe haemorrhage are not known. In this study we examined the effect of acute, severe haemorrhage in fetal lambs. Despite the severity of haemorrhage, we found that mean arterial blood pressure was restored within 2 min, and heart rate was restored within 30 min. This restoration of blood pressure and heart rate was facilitated by an increase in peripheral vascular resistance mediated in part by secretion of catecholamines and plasma renin. In addition, about 40% of the shed blood volume was restored within 30 min by fluid from either the fetal interstitium or placenta. The PO2 of umbilical venous blood increased from 33 +/- 9 mmHg to 49 +/- 17 mmHg 2 min post-haemorrhage, and to 47 +/- 15 mmHg 30 min post-haemorrhage. However, this increase was not sufficient to offset the fall in both haemoglobin concentration and umbilical-placental blood flow, so that oxygen delivery decreased from 21.1 +/- 5.5 ml/min per kg to 9.1 +/- 5.2 ml/min per kg 2 min post-haemorrhage, and 14.1 +/- 9.2 ml/min per kg 30 min post-haemorrhage. Because of this decrease in oxygen delivery, oxygen consumption fell and a metabolic acidemia ensued. Nevertheless, oxygen delivery to the heart and brain was maintained because hepatic vasoconstriction diverted more of the well oxygenated umbilical venous return through the ductus venosus. Although the fetus was able to tolerate acute loss of 40% of blood volume, larger volumes of haemorrhage resulted in fetal death.

Animals↗
PubMed1990

Venous and hepatic vascular responses to indomethacin and prostaglandin E1 in the fetal lamb.

Evidence is accumulating that prostaglandins affect the tone of the ductus venosus. Therefore prostaglandins might alter the distribution of umbilical venous return between the ductus venosus and liver. We have examined the effect of indomethacin and prostaglandin E1 on the vascular resistance of the umbilical-placental circulation, ductus venosus, and liver in 14 chronically instrumented fetal lambs. We found that indomethacin caused a nearly twofold increase in the vascular resistance of both the ductus venosus and liver. Prostaglandin E1, administered 70 minutes after indomethacin at a dose of 0.41 +/- 0.09 (SEM) micrograms/min per kilogram of fetal weight, decreased umbilical-placental blood flow, increased the vascular resistance of the umbilical arteries and placenta, and reversed the elevation of the vascular resistances of the ductus venosus and liver. Because both indomethacin and prostaglandin E1 affected the resistances of the ductus venosus and liver to the same extent, it is unlikely that prostaglandins of the E series mediate the change in distribution of umbilical venous return between the ductus venosus and liver during fetal stress.

Alprostadil↗
PubMed1990

Hypersensitivity reaction in an infant fed hydrolyzed lactalbumin contained in a semielemental formula.

Following introduction of milk protein formula feedings, a 6-month-old male developed profuse, watery diarrhea progressing to shock, requiring cardiopulmonary resuscitation. Reinstitution of enteral feedings with a formula containing hydrolyzed lactalbumin (Travasorb STD) resulted in recurrence of diarrhea with fever. Intestinal and rectal biopsies showed only nonspecific inflammatory changes. He was discharged on an elemental formula (Vivonex). Twenty-three months later, while admitted for evaluation of hypophosphatemic rickets, immunologic testing using the lymphocyte migration inhibition factor (LIF) test demonstrated positive reactions, especially to alpha-lactalbumin (56% inhibition) and whole cow's milk (22%, normal of less than 20% inhibition). Skin tests revealed sensitivity to cow's milk and eggs. Soy formula also produced diarrhea and bloody stools. Protein hydrolysate formulas, touted as hypoallergenic diets, are useful in infants with intolerance to milk protein. This is the first documented case of an immunological reaction to the hydrolyzed whey protein, lactalbumin. Although protein hydrolysate formulas are effective treatment in most infants with milk protein intolerance, allergic reactions are possible. Caution and close observation should be exercised in immunologically sensitized infants rechallenged with any formula.

Food Hypersensitivity↗
PubMed1990

Venous responses to hypoxemia in the fetal lamb.

The factors regulating umbilical venous return and its distribution between the ductus venosus and liver are poorly understood. This study was designed to determine where the major changes in resistance to umbilical venous return occur in response to fetal hypoxemia. In eight chronically-instrumented fetal lambs, during control and hypoxemic periods, we measured pressure in the descending aorta, extra-abdominal umbilical vein, portal sinus, and inferior vena cava; we also measured blood flow using radionuclide-labeled microspheres. During the control period, the umbilical arteries and placental vasculature accounted for 82% of total resistance to umbilical-placental blood flow, the umbilical veins for 11%, and the ductus venosus and liver for 7%. Hypoxemia increased resistance in the umbilical veins more than twofold, but did not affect resistance in the umbilical arteries or placenta. Although combined liver/ductus venosus resistance did not change, hepatic vascular resistance increased, and ductus venosus resistance decreased. We conclude that the major increase in resistance to umbilical venous return in response to hypoxemia resides in the umbilical veins. This increased resistance may improve maternal-fetal blood gas exchange by increasing the fetal surface area in the placenta.

Animals↗
PubMed1989

Effect of acute umbilical cord compression on hepatic carbohydrate metabolism in the fetal lamb.

Although the liver plays a central role in glucose homeostasis in the adult, its importance in fetal glucose homeostasis during acute reductions of substrate delivery is unknown. To examine this, we studied eight fetal lambs at 121 +/- 2 d gestation. We placed catheters in the descending aorta, inferior vena cava umbilical vein and the left (n = 6) or right (n = 2) hepatic vein, and a balloon occluder around the umbilical cord. At least 4 d after surgery, before and during umbilical cord compression, we measured blood oxygen saturation, glucose, lactate, and Hb concentrations, and blood flows using the radiolabeled microsphere technique. Gluconeogenesis was assessed by infusion of [U14C]lactate. Reducing umbilical flow by 50-60% from a control value of 181 +/- 20 mL/min/kg (mean +/- SD) caused a dramatic decrease in hepatic blood flow from 332 +/- 99 to 94 +/- 77 mL/min/100 g (p less than 0.05). Oxygen delivery to the fetus fell by 50% and that to the liver by 73%. However, hepatic O2 consumption was maintained by increased extraction. Glucose delivery to the liver fell from 67 +/- 24 to 20 +/- 13 mg/min/100 g (p less than 0.001), but lactate delivery did not change. In spite of the maintenance of lactate delivery, net hepatic lactate uptake fell significantly from 3.3 +/- 1.7 to 1.4 +/- 0.9 mg/min/100 g (p less than 0.05). This could account, in part, for the increase of blood lactate concentration from 16 +/- 4 to 27 +/- 7 mg/dl.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Changes in ovine hepatic circulation and oxygen consumption at birth.

The umbilical vein provides the majority of hepatic blood flow during fetal life. After birth, liver blood flow is derived from the hepatic artery and portal vein, but ductus venosus patency can alter portal venous blood flow to the liver. To characterize changes in hepatic blood flow and oxygen metabolism in the immediate perinatal period, we studied liver and ductus venosus blood flow in seven fetal sheep before and after birth using the radionuclide-labeled microsphere method. Hepatic blood flow fell from 423 +/- 117 (mean +/- SD) mL/min/100 g liver in the fetus to 144 +/- 73 by 2 h after delivery. Although portal venous blood flow increased progressively from 2 to 10 h (137 +/- 48 to 305 +/- 140 mL/min/100 g), because of increasing ductus venosus shunt flow, total hepatic blood flow did not change. Hepatic arterial flow was 46 +/- 24 mL/min/100 g at 2 h, providing 35% of total hepatic blood flow, and did not change over the next 8 h. Hepatic oxygen delivery fell after birth from 58 +/- 25 mL/min/100 g liver in the fetus to 21 +/- 11 at 2 h and then remained constant. Hepatic oxygen consumption was 7.3 +/- 2.6 mL/min/100 g liver in the fetus and ranged from 3.2 +/- 1.5 to 4.1 +/- 1.8 mL/min/100 g liver during the 10 h after birth. Loss of the umbilical-placental circulation at birth substantially reduces hepatic blood flow. Hepatic arterial flow does not increase to compensate for decreases in total hepatic blood flow. The persistent ductus venosus shunt compromises portal venous supply to the liver.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of cortisol on hepatic gluconeogenesis in the fetal sheep.

To determine whether the prenatal surge in cortisol induces the onset of gluconeogenesis in the fetal sheep, we performed studies in eight fetal sheep of 124 +/- 3 days gestational age. Catheters were inserted chronically in the descending aorta, inferior vena cava, and hepatic and umbilical veins, allowing the measurement of substrate flux across the liver and placenta. Cortisol was infused over a 48-h period, raising plasma cortisol concentrations from 3.5 +/- 2.5 ng/ml to 78 +/- 22 ng/ml at 24 h and 111 41 ng/ml at 48 h. At 24 and 48 h, [14C]lactate was infused into the inferior vena cava, and blood samples were obtained to measure plasma concentrations and specific activities of glucose and lactate. Comparison of the cortisol-treated group with an untreated control group of animals revealed no differences in blood gases, haemoglobin concentrations, or glucose and lactate levels. Similarly, there were no differences between groups in liver oxygen consumption, glucose and lactate flux, or gluconeogenesis from lactate. In two animals we demonstrated hepatic glucose production from lactate. One of these was in active labor at the time of study, and one aborted within hours of the study. We conclude that the prenatal cortisol surge alone is not responsible for the onset of hepatic gluconeogenesis in the perinatal period. However, cortisol may have a permissive action, promoting hepatic gluconeogenesis in response to other hormonal stimuli.

Animals↗
PubMed1989

Perinatal onset of hepatic gluconeogenesis in the lamb.

Hepatic gluconeogenesis does not occur in the unstressed fetal sheep. After birth, in addition to glycogenolysis, the newborn lamb must eventually initiate gluconeogenesis to maintain glucose homeostasis. The regulation and time course of this transition have not been defined. We studied six animals in an acute preparation before and after delivery to determine hepatic lactate and glucose uptake, hepatic gluconeogenesis from lactate, and plasma catecholamine and cortisol concentrations. After a priming dose, continuous infusion of [14C]lactate provided tracer substrate for calculations of gluconeogenesis in the fetus and then for ten hours after delivery in the newborn lamb. The radionuclide-labelled microsphere method was used to measure hepatic blood flow. Appreciable gluconeogenesis was not present during the fetal period. Following delivery, the newborn lambs began to produce significant quantities of glucose from lactate at 6 h of age (1.37 +/- 0.84 mg.min-1.100 g-1 min-1 x 100 g-1 liver), when gluconeogenesis from lactate accounted for 22% of hepatic glucose output. Despite the onset of gluconeogenesis, postnatal lambs had blood glucose concentrations that remained less than fetal levels of 23.4 +/- 12.1 mg/dl for the duration of the 10-h study. Plasma norepinephrine concentration was 1380 +/- 1145 pg/ml in the fetus and fell by 2 h after birth. Plasma epinephrine concentrations were highest at 15 min after birth (205 +/- 262 pg/ml), but remained quite low for the remainder of the study. Plasma cortisol concentrations did not vary over the course of study, ranging from 40 to 50 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Lactate uptake by the fetal sheep liver.

Lactate is produced by the sheep placenta and is an important metabolic substrate for fetal sheep. However, lactate uptake and release by the fetal liver have not been assessed directly. We measured lactate flux across the liver in 16 fetal sheep at 129 (120-138) days gestation that had catheters chronically maintained in the fetal descending aorta, inferior vena cava, right or left hepatic vein, and umbilical vein. Lactate and hemoglobin concentrations and oxygen saturation were measured in blood drawn from all vessels. Umbilical venous, portal venous, and hepatic blood flow were measured by injecting radionuclide-labeled microspheres into the umbilical vein while obtaining a reference sample from the descending aorta. We found net hepatic uptake of lactate (5.0 +/- 4.4 mg/min per 100 g liver). A large quantity of lactate was delivered to the liver (94.2 +/- 78.1 mg/min per 100 g), so that the hepatic extraction of lactate was only 7.7 +/- 6.5%. Hepatic oxygen consumption was 3.18 +/- 3.3 ml/min per 100 g, and the hepatic lactate/oxygen quotient was 2.07 +/- 1.54. There was no significant correlation between hepatic lactate uptake and hepatic lactate or glucose delivery, hepatic oxygen consumption, hepatic blood flow, hepatic glucose flux, total body oxygen consumption, arterial pH, oxygen content, or oxygen saturation. There was, however, a significant correlation between hepatic lactate uptake and umbilical lactate uptake (r = 0.74, P less than 0.005) such that net hepatic lactate uptake was nearly equivalent to that produced across the umbilical-placental circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Analysis of the actions of angiotensin on the central nervous system of conscious dogs.

Angiotensin II (ANG II) acts on the brain to elevate blood pressure (BP), stimulate drinking, increase the secretion of vasopressin and corticotropin (ACTH), and inhibit the secretion of renin. The present studies were designed to evaluate the possible physiological significance of these effects. The experiments were performed in conscious dogs with small catheters chronically implanted in both carotid and both vertebral arteries. ANG II was infused into both carotid or both vertebral arteries in doses of 0.1, 0.33, 1.0, and 2.5 ng.kg-1.min-1. Intravertebral ANG II produced dose-related increases in BP that were generally accompanied by increases in heart rate. Intracarotid angiotensin also increased BP but did not change heart rate. Intracarotid ANG II stimulated drinking and, at the highest dose only, increased the secretion of vasopressin, ACTH, and corticosteroids. Intravertebral and intracarotid ANG II suppressed plasma renin activity (PRA). In a parallel series of experiments, the effects of intravenous ANG II, in doses of 2, 5, 10, and 20 ng.kg-1.min-1, were studied. These infusions produced dose-related increases in BP and water intake and suppressed PRA. Only the highest dose of ANG II increased vasopressin or corticosteroid secretion. Analysis of these results in terms of calculated or measured changes in plasma ANG II concentration indicate that the central cardiovascular and dipsogenic actions of angiotensin, as well as the suppression of PRA, can be elicited by concentrations of the peptide that are within the physiological range. On the other hand high, probably supraphysiological, levels of ANG II are required to increase vasopressin or ACTH secretion.

Adrenal Cortex Hormones↗
PubMed1980

Sites at which clonidine acts to affect blood pressure and the secretion of renin, growth hormone and ACTH.

To further define the sites in the brain at which clonidine acts to lower blood pressure, inhibit renin secretion, inhibit ACTH secretion, and stimulate growth hormone secretion, small doses of this drug were infused into the vertebral arteries, into the carotid arteries and intravenously in pentobarbital-anesthetized dogs. Because injections of radioactive microspheres demonstrated that vertebral blood reached the hypothalamus, intravertebral and intracarotid infusions were also carried out after occlusion of the basilar artery in the midpontine region. Intracarotid clonidine, 2 microgram/kg, decreased plasma ACTH and corticoids and increased plasma growth hormone, whereas the same dose had no effect on these hormones when given intravenously or when given intravertebrally after occlusion of the basilar artery. Intravertebral clonidine lowered blood pressure to a greater degree than intracarotid and intravenous clonidine. The reduction in heart rate produced by clonidine was essentially the same whether the drug was administered via the intravenous, intracarotid, or intravertebral route. Intracarotid and intravertebral clonidine decreased plasma renin activity whereas in this dose intravenous clonidine did not. However, there was no renin response to intracarotid and intravertebral clonidine when the basilar artery was occluded. The data support the conclusion that clonidine acts rostral to the pons to decrease ACTH secretion and increase growth hormone secretion, whereas it acts on the medulla or adjacent hindbrain to lower blood pressure. In the dose used, clonidine appears to affect heart rate by a peripheral rather than a central action. The data confirm the observation that clonidine acts on the brain to inhibit renin secretion, and establish that the renin-inhibiting site is different from the blood pressure-lowering site. However, they do not permit localization of the renin-lowering site within the brain.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

Study of the placental transfer of cisapride in sheep. Plasma levels in the pregnant ewe, the fetus, and the lamb.

The placental transfer of cisapride, a new prokinetic agent, was studied in a sheep model. The pharmacokinetics of cisapride were studied in the lamb, the pregnant ewe, and the fetus by obtaining blood samples from chronically implanted arterial catheters. Comparable pharmacokinetic parameters were found in the lamb and the adult sheep: half-life, 1.39-1.83 hr; total plasma clearance, 1998-2160 ml/kg/hr; AUC, 92.6-100.1 ng.hr/ml. Cisapride plasma concentrations after continuous infusion were predicted correctly based on the parameters obtained after iv bolus. There was a materno-fetal transfer of cisapride following a single iv bolus administered to the mother. Cisapride crossed the placenta within 5 min and equilibrated with maternal plasma within 20 to 30 min after dosing. The average fetal-to-maternal plasma concentration ratio was 0.71. The amniotic fluid also contained measurable amounts of cisapride. The protein binding of cisapride in maternal and fetal plasma is 89.0% and 88.4%, respectively; the free fraction is 4 times larger than in humans. Cisapride crosses the ovine placental barrier. The sheep placenta is less permeable than the human placenta, but the higher free fraction of cisapride facilitates placental transfer.

Amniotic Fluid↗