Blood Volume in Newborn Piglets: Effects of Time of Natural Cord Rupture, Intra-Uterine Growth Retardation, Asphyxia, and Prostaglandin-Induced Prematurity

Pediatr. Res. 15: 53-57 (1981) asphyxia natural cord rupture blood volume prostaglandin F 2 intra-uterine growth retardation

137 OTWIN LINDERKAMP, , KLAUS BETKE, MONIKA GUNTNER, GIOK H. JAP, KLAUS P. RIEGEL, AND KURT WALSER Department of Pediatrics and Department of Veterinary Gynecology, University of Munich, Munich, Federal Republic of Germany

Summary (27, 29, 32). Placental transfusion is accelerated by keeping the infant below the placenta (19, 27), by uterine contractions (32), Blood volume (BV), red cell mass (RCM; Cr-51) and plasma 125 and by respiration of the newborn (19). Placental transfusion is volume ( 1-labeled albumin) were measured in lOS piglets from prevented by holding the infant above the placenta (19, 27), by 28 Utters shortly after birth. Spontaneous cord rupture in healthy maternal hypotension ( 17), by tight nuchal cord ( 13), and by acute piglets occurred during delivery (n • 25) or within 190 sec of birth intrapartum asphyxia (5, 12, 13). Intra-uterine asphyxia results in (n • 82). Spontaneous and induced delay of cord rupture resulted prenatal transfusion to the fetus (12, 13, 33). In a time-dependent Increase in BV and RCM. BV (x ± S.D.) at It is to be assumed that blood volume in newborn mammals is birth was 72.5 ± 10.5 ml/kg (RCM, 23.6 ± 4.6 ml/kg) In the 25 similarly influenced by placental transfusion as in the human piglets with prenatal cord rupture and 110.5 ± 12.9 ml/kg (RCM, neonate. Indeed, late clamping of the umbilical cord markedly 38.4 ± 7.0 ml/kg) In 17 piglets with late spontaneous cord rupture. increases the blood volume of the newborn lamb (34). Prenatally The mean blood volume of all the 107 healthy piglets with spon induced hypoxia in the lamb results in placental transfusion to taneous cord rupture was 90.2 ± 12.7 ml/kg (RCM, 30.1 ± 4.8 the fetus before birth (18, 35). Moreover, maternal hypotension ml/kg). RCM was significantly (P < 0.05) Increased In nine piglets impedes placental transfusion to the lamb (7). with Intra-uterine growth retardation (RCM, 35.8 ± 11.2 ml/kg) No animal studies have been found in the literature concerning and In 13 with metabolic acidosis but without signs of asphyxia naturally occurring factors which might affect neonatal blood (RCM, 35.8 ± 6.7 ml/kg). In five piglets with cord wrapping, volume such as the time of spontaneous cord rupture, intra-uterine prenatal cord rupture, and acute asphyxia, BV (57.8 ± 7.3 ml/kg) growth retardation, acidosis, asphyxia, or cord wrapping. In the was significantly decreased. In five other piglets with prenatal cord present study, we measured the blood volume of 164 naturally rupture and acute asphyxia, BV (67.9 ± 10.0 ml/kg) corresponded born, full-term piglets and 41 premature piglets. to that of the normal piglets with prenatal cord rupture. However, delay of cord rupture to 60 sec after birth did not Increase BV (66.0 ± 11.8 ml/kg) in four piglets with acute asphyxia. Forty-one ANIMALS premature piglets delivered 6 days before normal term had their Two hundred five vaginally delivered newborn piglets from 28 cords ruptured prenatally or within 5 sec of birth. Their hematocrit litters were included in the study. They were products of healthy at birth (0.337 ± 0.028 liters/liter) was significantly decreased nulliparous German landrace sows with accurately timed gesta compared to the normal full-term piglets with corresponding time tion. All piglets were delivered while the sow was in lateral of cord rupture (0.384 ± 0.033 liters/liter). RCM in 18 piglets with recumbency. The time taken for the umbilical cord to rupture prostaglandin-Induced prematurity (18.9 ± 3.4 ml/kg) was signifi after delivery was recorded. cantly lower than In 23 piglets whose births had been Induced by One hundred fifty-four piglets were born at term with a gesta ovarectomy of their mothers (RCM, 22.1 ± 3.2 ml/kg). tional age of 114 to 116 days. The full-term piglets were divided into four main groups. Speculation Group I consisted of 128 normal piglets. In 25 of these piglets (group Ia), the cords had broken before birth, this frequently There is a great variabillty of placental transfusion in piglets occurs in piglets (22). In 82 piglets, cords ruptured spontaneously (average, 24%; range, 0 to 60% of fetal blood volume) because 6 to 190 sec after delivery (groups Ib to If). In 11 piglets, the intact natural cord rupture occurred at any time from sub partu to 3 min cords were ruptured by one of us within 5 sec of birth (group Ig). after birth. This impUes that hypo- or hypervolemia per se, in the In l 0 piglets, cord breakage was prevented by holding them tight otherwise well adapted newborn, must not represent a pathologic on the floor close the introitus vaginae without drawing the condition. On the other hand, in the newborn with abnormal umbilical cord. Their cords were ruptured at 3 min after birth adaptation to extra-uterine life, abnormal blood volume may be (group lh). carefully considered as either cause or consequence of maladap Group II were nine piglets with intra-uterine growth retarda tation requiring appropriate treatment. tion. Their weights ranged from 570 to 800 g. Two had their cords broken before birth, and seven by us within 5 sec of birth. Thirteen apparently healthy piglets with severe metabolic aci Neonatal blood volume largely depends on the direction and dosis at birth (base excess below -10 mmoles/liter), but without magnitude of perinatal transfer of blood between the fetus and signs of asphyxia, were assigned to group III. Time of cord the placenta. The effects of various factors on blood volume in the severage varied between prenatal and 3 min after birth (Fig. 3). human neonate have been extensively studied. In normal newborn Group IV consisted of 14 severely asphyxiated piglets. They infants, blood volume increases with the time of cord clamping showed no respiratory efforts. Heart rate was below 100 beats/ 54 LINDERKAMP ET AL. min (normal values measured in 20 normal piglets shortly after piglets. The labeled compounds were injected via a peripheral birth, 213 ± 41 beats/min). Muscle tone was flaccid, and skin vein. Six blood samples of 1.0 ml were taken from an umbilical color was pallid or cyanotic. The viability score adapted from the venous catheter at 5, 10, 20, 30, 45, and 60 min after injection of Apgar score (21) was below 5. The asphyxiated piglets were the tracers and analyzed for hematocrit and for radioactivity in a resuscitated by pharyngeal suction, bagging with 100% oxygen well-type scintillation counter (Frieseke & Hoepner, Erlangen inhalation, and cardiac massage immediately after cord rupture. Bruck, Federal Republic of Germany). The counts of the tracers Five asphyxiated piglets had their cords wrapped around the body were retropolated to the time of their injection. Inasmuch as 1251- or a limb (group IVa). Their cords had broken before delivery. labeled human albumin is a heterologous protein, plasma volume The other nine piglets were either born with ruptured cord (group measurements in nine piglets were also made with Evans blue (II) IVb; n ,. 5) or the cords were ruptured by us at 60 sec after birth which combines with autologous albumin in vivo. No significant (group lYe; n = 4). Thus asphyxia was often associated with cord difference was found in any of the parameters measured with the entanglement and prenatal cord rupture. This agrees with the two markers (Table 1). Mixing time of labeled albumin and red ftndings of Randall (23, 25). cells, disappearance rate of labeled albumin, body /venous hema Forty-one piglets were delivered at 109 days of gestation. In two tocrit ratio, and the errors of analyzing the counts of a single sows, termination of pregnancy was induced by ovarectomy per blood sample taken 10 min after injection of 51 Cr-labeled red cells formed at 107 days of gestation. The sows were anesthetized with and 5 min after injection of 1261-labeled albumin and Evans blue Metomidat-HCI (2.5 mg!kg) (Hypnodil) and Azaperon (0.6 mgl were calculated as previously described (10, II). The results of the kg) (Stresnil) intravenously. In addition, low spinal anesthesia was methodological studies are summarized in Table I. obtained with 10 ml of 2% lidocain. Farrowing began 41 and 42 Based on these studies, plasma volume in the other 125 piglets hr, respectively, after ovarectomy (group V; n = 23). In three sows, was measured by analyzing a single blood sample 5 min after the parturition was induced by intramuscular administration of 10 mg injection of 1251-labeled albumin, and blood volume and red cell of prostalene (Synchrocept; Syntex, Den Haag, Netherlands), mass were calculated from plasma volume, hematocrit, and the which is an analogue of prostaglandin F2o (6). The drug was given body /venous hematocrit ratio of 0.84. at 108 days of gestation and farrowing initiated 24 to 29 hr Blood volume was measured 60 min after birth because the later (group VI; n = 18). Four piglets of the group V and four of procedure of tagging red cells with 51Cr in vitro required 50 min. the group VI were severely asphyxiated, had viability scores (21) Blood volume at birth was calculated from hematocrit, red cell below 5, and required vigorous resuscitation. The birth weights of mass, and the body /venous hematocrit ratio of 0.84. This proce the premature piglets (Table 2) corresponded to their gestational dure appears reasonable as studies in human neonates (29) and in age (I). The premature piglets had their cords broken sponta piglets (3, 8) have shown that red cell mass and body /venous neously before birth or by us within 5 sec of birth. hematocrit ratio remain stable during early postnatal life. Eight full-term and two premature piglets were stillborn and could not be resuscitated. Twenty-nine full-term and two prema RESULTS ture piglets not observed by one of us at birth were excluded from the study. One growth-retarded piglet whose cord was not severed The nonasphyxiated full-term piglets were moderately hyper immediately after birth and two piglets falsely assigned to the capnic and acidemic (Table 2). The asphyxiated piglets showed growth-retarded group were also excluded. severe metabolic and respiratory acidosis. In the normal piglets, red cell mass and blood volume at birth MATERIALS AND METHODS were markedly influenced by the time of cord severage (group I; Fig. I). There were no significant differences in any of the Blood samples were taken from the anterior vena cava imme parameters between the piglets in which the cords had ruptured diately after birth or cord rupture, respectively, and analyzed for before delivery (group Ia) and those which cords were severed by acid-base parameters (Combi-Analysator K-0, Eschweiler, Kiel, us within 5 sec of birth (group lg). The first significant increase in Federal Republic of Germany) at 39°C and for hematocrit using red cell mass and blood volume was observed 5 to 15 sec after a microhematocrit centrifuge (12,000 g; Hawksley, London). The hematocrit was corrected for 3% of trapped plasma which was measured in 20 piglets using 1251-labeled albumin (Table 1). Plasma volume and red cell mass were measured independently using 1251-labeled human serum albumin and 51 Cr-labeled autol ogous red cells ( 10) in 73 normal and seven asphyxiated full-term

Table I. Methodological studies in piglets Normal Asphyxiated '' 'Cr red blood cells (73) 1 (7) Mixing time (min) 7.9 ± 3.5 13.7 ± 5.3 2 Error-10 mn (%) 2.2 ± 1.3 3.6 ± 2.4" '"''!-labeled albumin ('"'I) (73) (7) Mixing time (min) 5.3 ± 1.8 6.4 ± 3.2 Disappearance (%/h) 31.6 ± 12.4 40.8 ± 14.22 Error-5 min(%) 2.0 ± 2.9 2.8 ± 2.5 b/v hematocrit ratio 0.84 ± 0.08 0.82 ± 0.12 Evans blue (EB) (9 ) Mixing time (min) 5.7 ± 1.5 Disappearance (%/h) 35.2 ± 9.6 Error-5 min (%) 2.9 ± 3.0 fl. PV 4(EB-' 2''1) (%) 2.2 ± 2.9 Trapped plasma(%) 2.8 ± 0.6 (20) o•enalal 5 10 15 30 60 120 240 1 Numbers in 'parentheses, number of animals. TIME OF CORD-RUPTURE sec 2 P < 0.005 compared with the normal piglets. Fig. I. Blood volume and red cell mass in normal piglets studied 3 p < 0.05. immediately after cord rupture is related to the time of spontaneous cord • PV, plasma volume. rupture. Table 2. Acid-base values, hematocrit, blood volume, red cell mass, and plasma volume in piglets at birth and 60 min after birth Time of Base excess.o cord rupture Body wt Pco2, (mmoles/li- Hcto BVo RCMso Hctso BVso PVoo Group n (sec) (g) pHo' (Torr) ter) (liter/liter) (ml/kg) (ml/kg) (liter/liter) (ml/kg) (ml/kg) Normal piglets2 a 25 (14)" Prenatal 1192 ± 232 4 7.276 ± 0.053 55.1 ± 10.2 -2.2 ± 3.7 0.386 ± 0.034 72.5 ± 10.5 23.6 ± 4.6 0.338 ± 0.061 83.7 ± 8.0 60.1 ± 7.9 b 26 (10) 5-15 1206 ± 284 7.265 ± 0.059 53.1 ± 9.0 -3.8 ± 3.0 0.391 ± 0.044 82.9 ± 13 .75 27.0 ± 4.15 0.365 ± 0.044 88.3 ± 8.6 61.3 ± 6.9 5 5 5 5 .C 22 (15) 16-30 1209 ± 233 7.285 ± 0.066 52.5 ± 8.5 -3.1 ± 3.4 0.394 ± 0.032 91.7 ± 13 .9 30.6 ± 3.9 0.392 ± 0.051 93.9 ± 8.4 63.3 ± 7.7 .d II (7) 31-60 1263 ± 180 7.273 ± 0.072 55.5 ± 9.9 -2.6 ± 3.0 0.406 ± 0.031 101.1 ± 15.45 34.4 ± 5.5 5 0.409 ± 0.055 5 100.2 ± 9.65 65.8 ± 7.8 .e 6 (5) 61-120 1217 ± 232 7.272 ± 0.064 52.7 ± 8.8 -4.0 ± 2.5 0.394 ± 0.031 112.2 ± 10.05 37.2 ± 4.7" 0.418 ± 0.0345 105.7 ± 6.45 68.5 ± 3.55 f 17 (12) 121-190 1212 ± 190 7.258 ± 0.042 56.5 ± 9.8 -2.8 ± 2.6 0.411 ± 0.0405 110.5 ± 12.9'' 38.4 ± 7.05 0.437 ± 0.0465 103.9 ± 10.85 65.5 ± 8.6 ig II (II) <5 1150 ± 210 7.236 ± 0.070 58.2 ± 8.1 -4.2 ± 3.3 0.380 ± 0.032 77.0±7.8 24.6 ± 3.3 0.348 ± 0.043 84.3 ± 7.5 59.7 ± 6.0 C:l lh 10 (10) 180 1145 ± 233 7.244 ± 0.063 59.7 ± 10.8 -2.0 ± 3.8 0.403 ± 0.046 108.9 ± 12.1 " 37.1 ± 7.9" 0.428 ± 0.0665 103.6 ± 7.7" 63 .5 ± 5.3 r 0 0 II Growth retardation 9 (7) <5 700 ± 85 7.267 ± 0.071 54.3 ± 9.0 -3.3 ± 3.4 0.43 1 ± 0.047 6 96.9 ± 19.6" 35.8 ± 11.2" 0.425 ± 0.0906 98.7 ± 12.8" 62.9 ± 6.8 0 < 7 7 7 0 III Metabolic acidosis 13 (5) Prenatal-184 1192 ± 243 7.125 ± 0.064 57.0 ± 12.1 -12.2 ± 2.2 0.439 ± 0.030 97.1 ± 16.4 35.8 ± 6.7 0.437 ± 0.040 97.2 ± 12.1 61.4 ± 6.9 re

IV asphyxia ("r1 IVa Cord wrapping 5 (2) Prenatal 1151±275 7.090 ± 0.037 85.2 ± 10.1 -8.2 ± 3.3 0.411 ± 0.035 57.8 ± 7.3" 20.0 ± 3.6 0.307 ± 0.057 78.2 ± 10.1 58.2 ± 9.5 z IVb No cord wrapping 5 (3) Prenatal 1270 ± 440 7.070 ± 0.054 82.4 ± 16.1 -8.4 ± 4.9 0.425 ± 0.042 67.9 ± 10.0 24.3 ± 4.9 0.340 ± 0.054 85.2 ± 8.3 60.9 ± 6.8 z IVc No cord wrapping 4 (2) 60 1313 ± 336 7.120 ± 0.052 78.3 ± 6.6 -6.3 ± 5.7 0.417 ± 0.031 66.0 ± 11.8" 23.0 ± 3.38 0.333 ± 0.053" 82.9 ± 12.1" 59.9 ± 11.8 ("r1

C:l 0 V Premature :;o Va Ovarectomy 19 (2) <5 1039 ± 205 7.243 ± 0.063 60.3 ± 6.2 -2.2 ± 3.8 0.355 ± 0.0306 75.1±8.9 22.4 ± 3.3 0.325 ± 0.030 81.7 ± 8.8 59.3 ± 6.6 z Vb Ovarectomy + as- 4 (2) <5 1088 ± 75 7.080 ± 0.042 79.5 ± 7.5 -8.0 ± 2.5 0.370 ± 0.036 67.2±3.1 20.9 ± 2.9 0.313 ± 0.049 79.9 ± 5.0 59.0 ± 6.2 "1:1 phyxia Ci r ...,("r1 6 9 6 6 9 VIa Prostaglandin 14 (3) ..::5 1079 ± 127 7.284 ± 0.047 57.3 ± 8.2 -3.4 ± 3.0 0.308 ± 0.028 ' 74.3 ± 14.3 19.2 ± 3.7 0.272 ± 0.039 ' 83.7 ± 7.4 64.5 ± 5.8 VJ Vlb Prostaglandin + as- 4 (2) <5 950 ± 283 7.132 ± 0.045 73.5 ± 8.5 -6.0 ± 3.1 0.315 ± 0.0236 68.2 ± 10.5 18.0 ± 2.8" 0.281 ± 0.046 76.7 ± 3.1 58.6 ± 4.5 phyxia 1 0, at binh; Hct, hematocrit; BV, blood volume. RCM. red cell mass; 60, min after birth; PV, plasma volume. 2 Normal piglets are divided into subgroups with respect to the time of cord rupture. 3 Numbers in parentheses, numbers of liuers. 'Mean± S.D. s.o Significance of differences of hematocrit, blood volume, red cell mass, and plasma volume was calculated by analysis of variance. 5 P < 0.05 if compared to Ia. 6 P < 0.05 if compared to Ia + Ig. 7 P < 0.05 if compared to Ia to I g. " P < 0.05 if compared to ld + le. 9 P < 0.05 if compared to Va. 56 LINDERKAMP ET AL. birth. This was followed by continuous gain up to 108 sec. There ml/kg.------, was no significant further rise during the third min. Hematocrit at 140 birth was little affected by the time of cord severage. The growth-retarded piglets (group II) whose cords were rup BLOOD VOLUME tured at birth showed high values for hematocrit, red cell mass, 120 and blood volume which increased as birth weight decreased (Fig. 2). The piglets with metabolic acidosis but without signs of as 100 phyxia (group III) had increased hematocrit and red cell mass values when compared to the whole group I. Red cell mass was above the mean values of group I in all cases and above i + S.D. eo· in eight of 13 cases (Fig. 3). Both red cell mass and blood volume increased with the time of cord severage. The five asphyxiated full-term piglets in which the cord was 60 wrapped around the body or a limb and had ruptured before RED CELL MASS delivery (group IVa) showed significantly decreased blood vol umes at birth compared to group Ia. The other five asphyxiated 40 piglets with prenatal cord rupture (group IVb) had similar blood volume values to group Ia. There was apparently no gain in blood 20 in the four asphyxiated piglets whose cords were ruptured 60 sec after birth (group IV c). The premature piglets (groups V and VI) had their umbilical cords ruptured before birth or by one of us within 5 sec of birth. prenatal <5 5 10 15 30 60 120 240 Therefore, their data have been compared with those of groups Ia TIME OF CORD- RUPTURE sec and Ig. In both groups of premature piglets, the hematocrit at Fig. 3. Blood volume and red cell mass in full-term pi.slets with meta birth was significantly decreased. The lowest hematocrits were bolic acidosis related to the time of cord rupture. Lines, x ± S.D. of the found in the piglets with prostanglandin-induced births (group normal piglets. VI). Their red cell mass was also significantly lower than in the normal piglets. Blood volume was similar in the premature and DISCUSSION normal piglets. Asphyxia did not affect blood volume, red cell mass, or hematocrit in both groups of premature piglets. The work presented here shows that there are evident similari The postnatal changes in blood volume and hematocrit de ties in the effects of perinatal factors on blood volume in newborn pended on the blood volume at birth. In piglets with blood piglets and in human neonates. Blood volume and red cell mass volumes below 90 ml/kg at the time of cord severage, blood in the normal piglets strongly depended on the time of cord volume increased, and in those with blood volumes above 110 ml/ severage. The rise in blood volume most likely resulted from kg, blood volume decreased shortly after birth, resulting in cor placental transfusion because there are no blood pools in the responding changes in hematocrit (Table 2). The slight increase in newborn piglet (8). Blood volume in the piglets with prenatal cord hematocrit with prolongation of the time of cord rupture, in group rupture probably corresponded to the fetal blood volume. Post I indicates that these volume shifts occur very rapidly. Plasma natal placental transfusion took place in a rapid and steady volume was about 60 ml/kg in all groups at 60 min after birth. manner and was completed within 2 min of birth. In the human neonate, placental transfusion occurs in a stepwise manner and is completed at 3 min (32). The fmal gain in blood volume from the placenta averaged 52% of fetal blood volume in the piglets. This agrees with the fmdings in the human neonate (29, 32) and in the newborn lamb (34). Naturally born lambs receive a mean placental transfusion of 23% of fetal blood volume (34). This is the ftrst study showing the effect of different times of natural cord rupture on neonatal blood volume. Natural cord rupture in the newborn piglets took place before delivery or within 190 sec of birth. Sometimes the cords in piglets may remain intact up to 12 min (22). Thus, there is no more or less defmed time of natural cord rupture in the piglet, and placental transfusion varies from 0 to 60% of fetal blood volume. Intra-uterine growth retardation in the piglet has been attributed to a small placenta and a low blood flow to the maternal placenta (31 ), resulting in fetal undernutrition and hypoxemia. Hypoxemia in tum usually entails polycythemia (20). A high incidence of polycythemia has also been shown among human infants with intra-uterine growth retardation (26). DeRoth and Downey (4) found the hematocrit in growth-retarded 15- to 30-hr-old piglets only slightly increased compared to normal piglets. However, their results are not comparable to our data because suckling of the newborn piglet results in rapid and marked plasma expansion (15). The piglets with metabolic acidosis, but without clinical signs of asphyxia, may have suffered from asphyxia in utero and re covered until birth. Normal viability at birth has occasionally been found in spite of severe intra-uterine asphyxia (12, 13, 21). Fig. 2. Blood volume, red cell mass, and hematocrit in piglets with It cannot be ruled out that the increase in red cell mass in the intra-uterine growth retardation related to body weight. piglets of this group was caused by increased erythropoiesis as in BLOOD VOLUME IN NEWBORN PIGLETS 57

Accuracl, of blood volume estimations in critically ill infants and children the growth-retarded piglets. However, chronic hypoxemia usually 12 results in growth retardation, and the body weights of the acidemic using !-labelled albumin and "Cr-labelled red cells. Eur. J. Pediatr.. 125: 143 (1977). piglets were in the range of those of the normal piglets (Table 2). II. Linderkamp. 0., Mader, T., Butenandt. 0., and Riegel, K. P.: Plasma volume It appears more likely that they had received some placental estimation in severely ill infants and children using a simplified Evans blue transfusion in utero. Prenatal transfer of blood to the fetus has method. Eur. J. Pediatr., 125: 135 (1977). been demonstrated in lambs with prenatally induced hypoxia ( 18, 12. Linderkamp, 0., Versmold, H. T .. Fendel, H., Riegel, K. P., and Betke. K.: Association of neonatal respiratory distress with birth asphyxia and deficiency 35) and in human newborns with intra-uterine asphyxia (12, 13, of red cell mass in premature infants. Eur. J. Pediatr., 129: 167 (1978). 33). It is explained by hypoxia-induced vasoconstriction of the 13 . Linderkamp, 0., Versmold, H. T., Messow-Zahn, K., Miiller-Holve, W., Riegel, placental vascular bed ( 18). The increased hematocrit at birth K. P., and Betke, K.: The effect of intra-partum and intrauterine asphyxia on (Table 2) may also be explained by contraction of the vascular placental transfusion in premature and full-term infants. Eur. J. Pediatr .. I 27: 91 (1978). bed ( 14, 18) leading to transvascular escape of plasma and he 14. Mann, L. 1.: Effects of hypoxia on umbilical circulation and fetal metabolism. moconcentration. The increased hematocrit in the growth-re Am. J. Physiol., 218: 1453 ( 1970). tarded and acidemic piglets did not result from enlargement of 15. McCance, R. 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Gy ical cord loops around the body (13) as pressure on the cord necol., 128: 197 (1977). preferentially obstructs the umbilical vein. The second mechanism 18. Oh. W., Omori, K., Emmanouilides. G. C., and Phelps, D. L.: Placenta to lamb may be responsible for the deprivation of placental transfusion to fetus transfusion in utero during acute hypoxia. Am. J. Obstet. Gynecol., I 22: 316 ( 1975). the acutely asphyxiated piglets, which cords were ruptured 60 sec 19. Philip, A. G. S., and Teng, S. S.: Role of respiration in effecting placental after birth. Acute asphyxia increases fetal arterial pressure and transfusion at ceaserean section. Bioi. Neonate, 31:219 (1977). umbilical blood flow (14). Moreover, lack of respiratory efforts in 20. Pickart, L. R., Creasy, R. K., and Thaler, M. M.: Hyperfibrinogenemia and the newborn has been shown to impede placental transfusion ( 19, polycythemia with intrauterine growth retardation in fetal lambs. Am. J. Obstet. 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