Book - Physiology of the Fetus 5
|Embryology - 24 Aug 2019 Expand to Translate|
|Google Translate - select your language from the list shown below (this will open a new external page)|
العربية | català | 中文 | 中國傳統的 | français | Deutsche | עִברִית | हिंदी | bahasa Indonesia | italiano | 日本語 | 한국어 | မြန်မာ | Pilipino | Polskie | português | ਪੰਜਾਬੀ ਦੇ | Română | русский | Español | Swahili | Svensk | ไทย | Türkçe | اردو | ייִדיש | Tiếng Việt These external translations are automated and may not be accurate. (More? About Translations)
Windle WF. Physiology of the Fetus. (1940) Saunders, Philadelphia.
1940 Physiology of the Fetus: 1 Introduction | 2 Heart | 3 Circulation | 4 Blood | 5 Respiration | 6 Respiratory Movements | 7 Digestive | 8 Renal - Skin | 9 Muscles | 10 Neural Genesis | 11 Neural Activity | 12 Motor Reactions and Reflexes | 13 Senses | 14 Endocrine | 15 Nutrition and Metabolism | Figures
|Historic Disclaimer - information about historic embryology pages|
|Embryology History | Historic Embryology Papers)|
Chapter V Fetal Respiration
The Mechanism of Gaseous Exchange
THE placenta is the organ kor respiration in the fetus. Its maternal portions develop somewhat in advance of the parts contributed by the fetus with the result that the maternal vascular bed in the placenta reaches a large size while that of the fetus is almost negligible. At the time the fetus is vers! small the maternal blood leaving the placenta is red because it has given up little oxygen to the fetus.1-2 As development oft the fetus proceeds more and more oxygen is taken up in the placenta and the maternal veins leaving it become darker and darker, containing little oxygen indeed at the end of gestation. This is illustrated in experiments designed to prevent pregnancy in one uterine horn of the rabbit. The oxygen content ok uterine vein blood remains constant throughout gestation on the nowpregnant side but declines progressively on the pregnant side (Fig. 22).
Fig. 22. Percentage saluration ok blood from thsze uterine veins during pregnancy in the rabbit. Notppxegnant uterine horn (a) , Pregnant horn (b). Birkh indicated by the double line. Two series ok experiments shown (0 and X) . (Barcroft, et al.: Jour. Physiol» Vol. 83, 1934.)
One can picture the placental circulation rather simply. A well oxygenated stream ok the mother’s blood enters the placenta and comes into intimate contact with the fetal blood stream, poor in oxygen. The two do not mix, but the degree ok contact dikkers in various mammals. 0ne might thinlc that the two streams should come into equilibrium in respect to the tensions ok their blood gases, the ketal umbilical vein blood being as saturated or unsaturated as the uterine vein blood of the mother, and that the umbilical vein blood ok the fetus should become progressively darker as gestation proceeds towards its termination. Actually this does not happen. The umbilical vein blood which courses toward the fetus is observed to be of much brighter color at term than that leaving the placenta on the maternal side. 0ne explanation of this lies in an anatomical arrangement of the fetal and maternal vessels of the placenta. Mossmans has found that the fetal and maternal capillary streams, instead of coursing parallel to one another, actually flow in opposite directions in the rabbit placenta. A similar arrangement has been observed in the cat, dog, and other animals, but may not be present in all species. Thus the fetal blood has the opportunity to come into equilibrium, not with maternal venous blood, but with that at the arterial end o«f the maternal capillary bed. This mechanism is illustrated diagrammatically in Fig. 23.
Fig. 23. The exchange ok oxygen and carbon dioxide in the placenta. lk the maternal and ketal Capillary streams course in the same directions U) , blood returning to the ketus will be as venous as that returning to the mother. But ik the streams course in opposite directions (B) , it will come into equilibrium with that ok the mother’s arterial blood. (Redrawn from Mossmam Am. J. Anat» Vol. 37, 1926.)
The placenta reaches its maximum size while the fetus is still growing at a rapid rate. Nevertheless the volume of fetal blood traversing it increases in proportion to the weight of the fetus.4 An increase in fetal blood pressure throughout pregnancy helps regulate the amount of blood passing through the placenta per minute. On the maternal side of the placenta, there is a somewhat smaller increase in the volume of How, except at the end of gestation when it appears to be reduced (see Table 8, p. 32).
The fetus is provided with another mechanism to enable it to obtain oxygen readily in the placenta. Its hemoglobin difkers from that of the mother’s blood and the diiference is such in most species that oxygen is taken up with greater ease at the low partial pressures which occur in the placenta. The total amount of oxygen taken up by the fetus increases progressively as the total number of corpuscles and their number per cubic centimeter of blood increase. The amount of oxygen utilized per gram of rissue remains nearly constant throughout the latter part of gestation in the sheeps at approximately o.oo43 cc. per minute.
The Oxygen Capacity of the Blood
A number of attempts have been made in recent years to shed light upon the question of fetal respiration by analyzing the blood on both sides of the placenta for oxygen and carbon dioxide since the original study of Cohnstein and Zuntzs several important investigations have been undertalcen in the goat, sheep and human fetus and newborn.7-17 The hemoglobin of healthy adult systemic blood leaving thesheart is approximately saturated (95 to 97 per cent) with oxygenJs The blood contains on the average about 19 volumes of this gas per ioo cc. in the human female. The amount of oxygen carried in each cubic centimeter of the mother’s blood in the latter part of gestation is somewhat less than this. The amount of oxygen which the fetal blood can take up at any partial pressure does not depend entirely upon the capacity of the mother’s blood for oxygen but upon other factors which will become evident when the nature of the maternal and fetal dissociation curves are considered. Before discussing these relationships it will be of interest to compare the capacities of maternal and fetal bloods as found experimentally. Results obtained at the end of gestation in human subjects are summarized in Table l1. 13, 15, 17
Table 11 Avniuen Oxronn Gar-zerrt- ots III-rat. Arn) Mast-annu- Bhoov n: Max«
Fetal Maternal l (vol. Yo) (vol. Z) Adult (non-pregnant) . . . . . . . . . . . . . . . . . . . . . . . . . 19 . 00
At 8 moaths (1 caesakequ Section) . . .. ...I 18.14 17420
At term (1 caesarean Section) . . . . . . . . . . . . 20.9 15.6
At normal birth 4 cases) . . . . . . . . . . . . . . . . . 2042 15 . 82
At normal birth 15 eases). . . . . . . . . . . . . . . . 20.8 15 .4
Ät normal birth ksc enges) . . . . . . . . . . . . . . .. 2l.28-2l.6«
At normal birth 80 cis-see) . . . . . . . . . . . . . . . . 21.92
Umbilical artery and umbilieal vein blood.
It will be seen that the capacity of the mother’s blood to carry oxygen at the end of gestation is low in comparison with normal non-pregnant individuals. This may be related to changes in the reaction of the blood (reduced allcalinity) , decrease in number of maternal corpuscles in each cubic centimeten and other factors. A marked decline in the oxygen content of cats’ blood during the latter part of gestation has been observed.19
The capacity of the human fetal blood is higher than that of the mother and is about the same as that of the average normal adult male. One might expect the fetal blood, which contains larger red corpuscles and considerably more hemoglobin than the adult, to be able to take up even. gcegter quantities of oxygen.
However, it has been shown that human full-term fetal hemoglobin in dilute solutions takes up oxygen, gram for gram, less readily than does that of the adult.20- The increased amount of hemoglobin little more than compensates for this deficiency. This observation is in contrast with the determinations in other mainmals.
Oxygen capacities have been determined in lower anima1s by a number of investigators, but most of the data are insullicient to -demonstrate the relation to adults of the same species. The studies in sheep and goats have shown that the mother’s blood carries more oxygen per cubic centimeter than that of the fetus. 6-8
Fig. 24. Comparison of oxygen capacities ok mater-nat (o) and fetal (x) blood in the goat. (Batcrokt: Proc. Roy. Soc. London, Vol. us, 1935)
Recent experiments in the ox and horseU suggest that the feta1 blood at term has a slightly greater capacity than that of the mother and is therefore comparable with that of man. The relationship between oxygen capacities in mothers and fetuses which Barcrofts found in the goat is illustrated in Fig. 24. It will be seen that the fetal values increase as the maternal values decrease with the approach of birth. Thiscan be correlated with changing hemoglobin values .
Roos and Romijn folslowed the changes in oxygen capacity during the Erst few days after normal birth in cows and their calves. 11 They found greater values for blood of the calves at birth than at 73H to 835 months gestation. The oxygen capacity of the mother cows akter delivery was greater, not only than those in late pregnanczz but also greater than the normal non-pregnant cows. The data are surnmarized in Table 12.
Avuxuou Oxrow ckrzerrr or Bpoov or· Pisa-us, Ort-stumm un) Morgen m srnu O:
calves cows ee. 0-X100 ee. blood ee. 0-X100 ee. blood II norkpregnant eows . . . . . . . . . . . . . . . . . . . . . . 14.6 8 caesarean Sections at 7å to 85 rnonths gestation . . . . . . . . . . . . . . . . . . . . . . . . . 12 . 6 12 .2 5 cows and 6 calves one hour or less after birtb . . . . . . . . . . . . . . . . . . . . . . . . . . . . . I8.3 15 .8
The usekulness of a Special fetal type ok hemoglobin becomes apparent when the oxygen dissociation curves ok ketal and maternal blood are eompared. conditions under which the fetal blood takes up oxygen are not nearly so advantageous as those oceurring in tlie adult lungs. An oxygen tension of about ioo mm. Hg is kound in the lungs but the tension, although not delinitely determined, is considerably reduced in the placenta. Furthermore, the surface area of the human chorionic villi has been estimated to be only about half that of the lung alveoli at birth.22
Fig. 25. Oxygen dissoeiation curves ok (a) ketal and (b) maternal blood ok the goat at 18 to 19 weeks' gestation. Brolcen lines indicate limits of normal non-pregnant adult goat blood. (Barcrokt, et a1.: Jour. Physiol. Vol. Es, 1934.)
Oxygen dissociation curves of maternal and fetal blood at the time of birth have been prepared by a number of investigators,11s I2s 1«3-23- 24s 25 but Barcroft and his colleaguess are the only ones who have compared the curves at different times during prenatal life. They studied the goat. It was found that the curve for maternal blood is displaced to the right of the normal adult curve from ten weeks on to birth, while that of the fetus gradually shifts to the left between the 1oth and the 18th or rgth weeks and then returns at full term to approximately the position characterizing normal adult blood. The shape of the fetal cjurve difkers in important respects from that of the mother. It is steeper at low oxygen pressures and crosses the maternal curve at about 7o mm. Hg. These results are illustrated in Figs. 25 and 26.
Fig. 26. Oxygen dissociation curves ok the blood of a newborn goat (lekt) and the mother (right). Broken lines indicate limits of normal nonspregnant adult goat blood. (Barcrokt, et a1.: Jour. Physiol» Vol. 83, 1934.)
Oxygen dissociation curves for the human at full term are shown in Fig. 27. Here ioo the maternal curve 1ies to the right of that of the normal nowpregnant woman and the fetal curve is almost within the range of the non-pregnant woman, but lies to the 1eft of the maternal curve and is of a different shapeJEI some investigators24 have found variations in human fetal oxygen dissociation curves at bitt-h; the extremesare of two types, one of which is displaced farther to the left than the other and is less deflected, crossing the maternal curve at higher oxygen tensions (85 mm. I—Ig) than the other (7o mm. Hg).
Fig. 27. Oxygen dissociation curves of the blood of the human fetus at bit-m, its mother, and notkpregnant human adult. (Eastman, et al.: Johns Hopkins Hosp. Ball» Vol. 53. 1933.)
There is general agreement that the shift of the maternal oxygen dissociation curve to the right is due to a reduced allcalinity of the maternal blood. If this is the only factor governing the shift, the amount of displacement of the maternal curve must be deiinitely limited, for the reaction of the blood can not be greatly altered toward the acid side and still maintain normal health.
The shape of the fetal oxygen dissociation curve was found to be very different from that of the mother by most investigators. Roos and Romijn 11 have obtained the most strilcing demonstration of this difkerence in the fetal calf. They found that the fetal blood can attain 5o per cent saturation with oxygen at an oxygen pressure of 11.5 mm. Hg, whereas that of the maternal blood becomes only about 8 per cent saturated at this tension. The maternal curve lies within the rather wide range of the normal non—pregnant cow, but the fetal curve is so far to the left that go per cent saturation with oxygen is reached when the mother’s blood is less than 7o per cent saturated. Because the carbon dioxide dissociation curves of the fetus and mother almost coincide in the ox, the leftward displacement of the fetal oxygen dissociation curve cannot be explained on the basis of blood pH changes during pregnancy It must be explained by a different type of hemoglobin in the fetus.
What is the signilicance of the observations outlined above? They show that there are species’ differences, that the blood of some animals at birth is able to take up oxygen at approximately the same tension as that. in the adult, but in others the fetal blood near term still takes it up with greater avidity than the adult and gives it up less readily. They demonstrate a mechanism which must be of inestimable value to successful intrauterine life. The spread between maternaf and fetal oxygen dissociation curves indicates that oxygenation of the fetal blood is facilitated at the partial pressures which are physiologic in the placenta; the fetal blood can takeup oxygen at a tension which causes the mother’s blood to lose oxygen. It also makes the giving up of oxygen to the tissues of the fetus less easily efkectedz but this is not a serious obstacle to the fetus in utero which is relatively inactive and can get along with a slower tissue respiratioxr After birth it is desirable that these relationships be·reversed. When the blood is oxygenated in the lungs it fmds a greater oxygen tension prevailing there than in the placenta and the avidity of the fetal hemoglobin is no longer needed. 0n the other hand an· active tissue metabolism calls for more eilicient transfer of oxygen in the other direction at the peripheral capillaries. It; would seem that there is an anticipation of this need some time before it becomes acute in the goat, for the fetal oxygen dissociation curve shifts gradually to the right and assumes a less inllected form during late gestation. The fctus is thus prepared in late fetal life for conditions it will meet after birth. In some newborn human infants the shift has not gone as far to the right as that of the newbom goat, and one may say that they correspond to goat fetuses about a month before birth.« carbon dioxide dissociation curves of fetal blood have been constructed in the goat, ox and man.7-I1-I9-24-27-2S The results of Eastman and his colleagues show that the fetal blood takes up carbon dioxide less readily and gives it up with greater ease than the nowpregnant adult blood at any given partial pressure of the gasU However, the diiference between mother and fetus in this respect is not marked. At about six weeks before term in the goat the fetal carbon dioxide dissociation curve lies on the left of the maternal curve.27 By full term it has shifted well to the rights« The carbon dioxide dissociation curve of the pregnant cow was found to be displaced slightly to the right of that of the eightmonth fetus.U The human carbon dioxide dissociation curves at birth are illustrated in Fig. 28. 16
Fig. 28. Carbon dioxides dissociation curves of the blood of the human fetus at birth, its mother and notppregnant human adult. (Eastman, et al.: Johns Hopkins I-Iosp. Bull., Vol. 53, 1933.)
Calculations of the blood pH have been made from the carbon dioxide dissociation curves of goat’s blood. Direct measurements in the blood of goats (glass electrode) coincide with the calculated pH va1ues.8 The fetal blogdis lesssallcaline than that of the normal non-pregnant goat, falling within the range of pH 7.27!-7.38, although it is more allcaline than that of the mother six weelcs before the end of gestation. The lowered pH (decreased alkalinity) of the maternal blood·is adequate to explain the shift to the right of the maternal oxygen dissociation curve. In normal human newborns the average pI-I of the umbilical artery blood has been found to be 7.32 and that of the umbilical vein blood, 7.35. The latter is about the pH of the mother’s cubital vein blood, which is less allcaline than blood of normal nonpregnant individuals.29
A deficiency of carbonic anhydrase in fetal blood may explain the higher allcali reserve of the fetal blood plasma in goats six weeks before term.30 The gradual shift to the right of the fetal dissociation curve for carbon dioxide during the latter part of gestation in the goat may indicate a gradual depletion of the allcali reserve.
Oxygen and Carbon Dioxide Contents of Fetal Blood
It is essential to learn how much oxygen the fetal blood actually contains as it leaves the placenta, at various places in the fetal circulation and when it returns again to the placenta. In the first place, how does the blood of the umbilical vein compare with that of the umbilical artery? A number of studies have been made in human fetuses at the moment of birth. Results fluctuate widely but this can be minimized to some extent by discarding cases of asphyxia at birth. One must bear in mind the technical diköcuL ties encountered in obtaining fetal blood under physio1ogic conditions. There can be no doubt that maximum values for oxygen are more representative of the true condition than are averages which contain values obtained under partial anoxemia. Table 13 summarizes the more recent and reliable data from human infants obtained at the moment of birth.12-I5-25-31 In addition EastmanIs found 6.3 volumes per cent oxygen in the umbilical artery and 13.3 volumes per cent in the vein at one Caesarean section. 0thers who have drawn blood at Caesarean sections have obtained very low values for oxygen.
In half of Noguchi's experiments the infants had talcen their first breath before blood samples could be drawn, but it was demonstrated that this did not signiiicantly alter the analyses. Haselhorst and stromberger obtained similar results. Noguchi found no dilference betwesen 16 male and 14 female fetuses in the oxygen capacity of the blood.
Uppxn Latr-re am) Avaov Var-uns rot: Oxrogn am) cannot«- Dxoxrvs IN Btoov or« Eurem· Its-Danks U« Mosis-Nr or« Bank:
Umbilieal artery Umbilieal vein
No. I ti t f «« S« «« »He, vor A, o, m. A, co- m. A, o, v0I. A, cohigh ave. high ave. high we. high ave.
Haselhorst « s and Strom- l bot-get. . . . . 22 . . . . . . . . . . . . . . . . . . . . 14.88 I0.I4 47.88 40.71 28 8.02 840 52.85 46.21 . . . . . . . . . . - . . . . . · . . . ..
Biclone . . . . . . 9 15.60 12.95 62.26 50.06 17.57 I4.94 46.67 , 41.21
Eastman.... 15 5.90 8.30 . . . . . . . . .. I8.20 l0.50 . . . . . . . . ..
Nosuchi..... 80 10.00 4.40· 58.70 4420 I5.90 11.00 47.70 38.00
The percentage saturation of umbilical blood has been determined by the investigators cited above and the values are recorded in Table 14. We wish to stress the point that these are averages and not upper limits. If we accept the figure 21 volumes per cent as the average oxygen capacity of human fetal blood at full te«rm normal birth, and limit consideration to the highest values for oxygen content (Table 13) , the umbilical vein blood appears to be between 63 and 84 per cent saturated at birth depending upon whose data are used. This assumption is not entirely valid because individual variation is to be expected in the amount of hemoglobin and oxygen capacity, but it may more nearly express the true condition of the fetal blood than do the mean figures in Table 14. Eastman found no rnore than 63 per cent saturation with oxygen in the umbilical veinss but it is apparent that a much higher saturation was encountered by Bidone. 31
Table 14 Avnnaon Print-ausknei- Oxogen saturation or« Humm- Fnsrat Bnoov Ast« Bank: Umb. vem l Froh. artery A) sat 70 set. Heselhort and stromberger . . . . . . . . . . . . .. 45 . 6 15 . s
Eastman . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50.5 15.8
Bastman (caesarean) . . . . . . . . » . . . . . . . . 034 l s0.2
Noguchi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 .7 21 .7
Bidone (estimation) . . . . . . . . . . . . . . . . . . . . 7813 63-8
The data available in lower animalzs are similar to those obtained in man. Great variation in the content of oxygen and carbon dioxide in the umbilical vessels has been reported in the goat, sheep, ox, dog and cat, 6, 7, 9, 11, 32-34 but if we admit only the highest values and consider that technical limitations may have reduced other values we are left with quite a different conception of respiratory conditions than we get from the average values. It would seem that the fetus does not thrive on venous blood.
The greatest number of analyses have been made by Barcroft and his col1eagues who found that the superior limits of saturation with oxygen in the umbilical vein blood of fetal goats vary between 6o per cent and 87 per cent from the tenth to the nineteenth weelcs of gestation, fa1ling off to about 45 per cent in the last two weelcsk similarly in the sheep, blood going to the fetus (umbilica1 vein) was found to be as much as 86 per cent saturated before the 137th day; after that lower values were the rules« One of the most important observations on oxygen content of the blood of sheep fetuses 75 to 140 days gestation was made recent1y by Barcroft and Mason,35 who devised a technique for obtaining blood from the umbilical vein or artery without delivering the fetus from the uterus and with a minimum of manipulation.
- In the final paper (Barcroft, J., J. A. Kennedy & M. F. Mason, 1940, J. Physiol» 97: 347) it was reported that the highest values were found between the 75th and Iooth days ok gestation and that they dropped considembly in the final week (a physiologic anoxemia).
When this was done and the tendency toward placental separation avoided the blood going to the fetuses was found to be more than 90 per cent saturated with oxygen in half (five) their experiments and not less than 7o per cent saturated in the others. These results are shown in Table 15.
Tun-n 15 Piave-Durham Oxford-N Hektorn-icon« or« Ums-text« Am) Ums-Zum Bhoov m srmv sitt-Et
9073 or As— 79- SO- l IV— 49 · over 8075 7098 6073 5095 4073 No. ok easesk Utah. vein . . . . . . - 5 s 2 . . l . . . . No. of case-s: Urnb. arterzc . . . . . . . . . 3 6 I No. ok case-s: Ufer. venule · l (Ple.cental vein) . . . . . . . . . . . . . . . 8 I 2
1t is evident that the oxygen content of the umbilical vein during life in utero is not as low as most studies lead one to be— lieve. The better the teczhnical procedures, the higher the values obtained. ·0ther investigators have encountered 85 to go per cent saturation in the umbilical vein blood occasionally. BidonesI re— ported 17.6 volumes per cent oxygen (approximately 84 per cent saturated) in one human fetus before respiration started at birth. Roos and Romijn 11 found that the umbilical vein blood of the fetal calf of 7.5 to 8.5 months was saturated to a rather high degree, 90 per cent in one experiment.
Granting during fetal life that the blood coming from the placenta to the fetus by way of the umbilical vein is as much as 90 per cent saturated with oxygen does not entitle us to conclude that the fetal tissues are bathed continuous1y in blood so rich in this gas. The umbilical vein blood is diluted by reduced blood from the lower parts of the fetal body when it enters the fetal inferior vena cava. The degree of dilution is an unlcnown and perhaps not a constant factor. The inferior vena caval blood enters the right atrium of the heart and most of it passes into the left atrium by way of the foramen ovale, where it may be diluted a second time by blood returning from the fetal lungs (see Fig. 17, p. 43). This pulmonary blood is reduced because, even if little oxygen is removed by the tissues of the fetal lungs, much of the blood has already traversed the heart and upper parts of the body before passing to the lungs. The blood which is sent through the ascending aorta and the great vessels which spring from the aortic arch, i.e., the blood which goes to the heart and brain, cannot be as saturated constantly with oxygen as that which enters the liver and inferior «vena cava from the umbilical vein and ductus venosus.
Barcroft, Icramer and MillilcanW have attempted to determine the degree of oxygen saturation in the carotid artery blood of sheep fetuses near the end of the gestation period. They used an ingenious mechanism consisting of a photoelectric cell and micro-lamp between which the carotid artery was placed. The blood acted as a red älter, oxyhemoglobin transmitting more light in the red end of the spectrum than reduced hemoglobin. Variations in the current from the photoelectric cell deflected a galvan— ometer mirror, and a beam of light from the mirror was used to record continuous1y on moving photographic paper. Respirations were recorded simultaneously. The mechanism was calibrated by analyses made with the Van slyke manometric apparatus. Two records are reproduced in Figs. 29 and 30 and their interpretation in Fig. 31. It will be seen that complete saturation of the fetal blood was eikected more readily when the 1ambs breathed oxygen than when they breathed air. In other experiments it was found that several hours were required for a complete saturation of the newborn blood without the aid of oxygen. The carotid artery blood of sheep fetuses studied at Caesarean Section was found initially to be between 32 and 70 per cent saturated with oxygen. How much higher than this the saturation is in the normal undisturbed fetus in utero we do not know.
- It has been demonstrated recently that the carotid arterial blood is as much as 88 per cent saturated with oxygen in the sheep fetus prior to the last weelc of gestation (Barcrokt, J D. H. Barron, A. T. Cowie 8c P. H. Forsham, 194o, J. Physiol 972 gas)
Figs. 29, 30. Two Photographie records ok the changes in the oxygen saturation of the carotid blood during the initiation of respiration at birth in the sheep fetus. The sensitivity of the apparatus diifered in the two experiments For interpretation, see Fig. 31. (Barcrokt, et al.: Dur. Physiol» Vol. 94, 1939.)
It has been very difficult to obtain satisfactory data on the blood gas contents of fetal blood because of technical difficulties No one can doubt that operative procedures in exposing and opening the Uterus bring about changes in the respiratory relationships in the placenta. Any series of experiments will give some results below 25 per cent saturation witsh oxygen in umbilical vein blood, but one is justiiied in concluding that these values are not physiologic. The blood can actually be observed to darken before a sample can be drawn for analysis
Fig. 31. Interpretation of Fig. 29 and G) ok Fig. so, showing percentage saturation ok the lamb’s bloock in the carotid artery at birth. Umbilical cord tied at ↑ ; lamb breathing oxygen at o—o. (Barcroft. et a1.: Jour. Physiol» Vol. 94 1939.)
At the end of fetal life there is some evidence that the oxygen carried by the umbilical vein blood is normally more reduced in goats and in cats than it was earlier.9- 38 This constitutes a physiologic anoxemia. A kactor which may play a part in regulating the amount of oxygen available to the fetus in the latter part of gestation in the cat, and which has been generally overloolcecL is the motor activity of the Uterus itself.
Prelabor contractions of the uterus are of physiologic occurrence. It has usually been assumed that should they become severe they would block the fetal circulation through the placenta and lead to anoxemia in the fetus. clarlc’s37 studies of blood pressure reilexes in cat fetusespointed in this direction. In our laboratory we have observed that the contractions, providing they are not severe, are accompanied by improvement in color of the umbilical veins and that relaxation of the uterus results in darkening of. the blood. Furthermore, analyses of the blood leaving the pIacenta on the maternal side, drawn from placental tributaries of the uterine vein, showed iluctuation in oxygen content, less oxygen being present during and just following a uterine contraction than in the interval of the relaxation. These values are the reciprocaIs of those observed on the fetal side of the placenta (umbilical vein) . Blood was drawn from the placental tributaries without interfering at all with the fetuses and with little manipu1ation of the uterus. The pregnant animals were not anesthesized but had been decerebrated some time before. It is apparent that one can not spealc of the conditions of fetal respiration, at least during the last few days of pregnancy, as though they were constant. They Auctuate normally from moment to moment; and whereas 95 per cent saturation with oxygen may be attained at times, it is doubts ful if the average amount available to the fetus during the latter part of fetal life can be as great as it was earlier. The physiologic anoxemia of the fetus in late gestation will be given consideration in succeeding chapters. 0ther mechanisms have been suggested whereby dilation and contraction of uterine vessels play a part in regulating blood Aow through the placentaks
Asphyxia at Birth
Much has been written concerning the conditions under which the fetus at birth fails to begin breathing. Asphyxia is the cause of death in an alarming number of cases, especially so as the demands for obstetricaI anesthesia become more urgent. In recent years much light has been cast upon this subject by studies in the blood gases at birth. some investigators have held to the old conception of asphyxia as an accumulation of carbon dioxide and have supposed that this was the case in the blood of newborns which failed to breathe. 39 In view of Henderson’s 40 conception of asphyxia as a decrease in carbon dioxide as well as in oxygen one should expect that in the asphyiciated ketus, as well as in adults subjected to asphyxial conditions, the blood carbonates would shift to the tissues and hemoglobin, and the blood would contain less carbon dioxide.
Eastman 4l,42 appears to be the iirst investigator to demonstrate the truth of Henderson’s theory in asphyxia neonatorum. He found that there is a reduction in oxygen content of umbilical vein blood to very low levels (sometimes less than one volume per cent) , that the carbon dioxide is lilcewise lowered and that the pH of the blood may fall below 7.oo in fatal cases. Noguchirks 29 determined that there was some shift of plasma fluid in the fetus, probably to the fetal tissues but not across the placenta, that the oxygen was greatly lowered and that the carbon dioxide shifted to the cells from the plasma but was not greatly lowered in total amount. He also found a marked lowering of the pH of the blood and concluded that asphyxia neonatorum is «a state of uncompensated allcali delicit in consequence of oxygen want. Cat fetuses depressed at experimental Caesarean section resemble human infants in asphyxia neonatorum. The oxygen content of their blood drops severely, and so does the carbon dioxide content.
i. Dator-oft, J» W. Herlcel 8c R. M. I-Iill. i933. Physiol» 77: i94.
2. Barcrofy J» L. B. Flexneiy W. I-Ierlcel, E. F. Mccarthy sc T. Mochi-Lin. i934. 1bid» Sz- Fig.
3. Mossmath H. W. i926.» Am. J. Anat» 37: 433.
4. Bancoft, J. 8c J. A. Kennedyc i939. J. Physiol» 95: i73.
5. Bancoft, J J. A. Kennedy Z: M. F. Masotr iggg Ibid» 95: Läg. S. Gohnstein, J. sc N. Zuntz i884. Pflüger-T Arch» 34: i73.
7. Huggett A. sc. G. i927. J. Physiol» se: 373.
8. Bann-oft, J» R. H. E. Elliott, L. B. Flexney F. G. I-Iall, W. Herlceh E. F. Mccarthyz T. Mcclurkin s: M. Talaat. i934. Ibid» As: i92.
9. Baker-oft. J. i935. Proc. Roy. soc» Lond. B, ii8: 242.
10. Barcrofh J» K. Kramer s: G. A. Millilcan. i939. J. Physiol» 94: 57i.
11. Roos, J. sc G. Romijix i938. Ibid» ge: 249.
12. I-Iaselhorst, G. 8cK. strombeisgen i93o. Ztscliin Geburtsh. Gynäk» 98: 49.
13. Haselliorsh G. se K. strombeigen i93i. Ibid., ioo: 48; i932. Ibid» io2: i6.
14. Haselhorst, G. i93i. Arch. Gynälc» i44: 558.
15. Eastmam N. J. i930. Johns Hopkins Hosp. Bull» 47: 22 i.
16. Eastman, N. J» E. M. K. Geiling s: A. M. DeLawdeia i933. Ibid» 53: 246. ooeo Tkscp 023
. Noguchi, M. 1937. Jap. Obst. Gyn» so: s18.
Bat-Gott, J. 19s5. The Respiratory Function ok the Blood, cambriclge Univ. Press.
. steele, A. G. s: W. F. Winclle. 1g38. J. Physiol» 94: 5s5.
Haurowitz F. 1935. Hoppesey Ztschn physiol. chekn» s3s: 1s5. Hill, R. 1935. cited by J. Barcrokh Pkoe. Roy. soc» LoncL B, us: s4s. christotkeisem A. K. 1934. compr. read. soc. Biol» u7: 641.
. Anselmino, K. J. s: F. Hoffmann. 193o. Arch. Gynä1c» 143, 477.
Leibson, R. G., I. I. Lilchnitzlcy sc M. G. sank. 1g36. J. Physiol» 87: 97. NoguchL M. 1937. Jap. J. Obst. Gyn» so: 358.
Bat-most, J. 1938. The Brain and Its Environmenh Yale Univ. Press,
New I-Iaven. . Mccarthy, E. F. 1933. J. Physiol» so: so6. Iceys, A. B. 1934. Ibicl» so: 491.
. Noguchi. M. 1937. Jap. J. Obst. Gyn» so: s48.
Roughtoty F. J. W. 1935. Physiol. Ren, is: s41. Bidone, M. igzh Ann. ostet. since» 53: 197. Kellogg, H. B. 193o. Am. J. Physiol» 91: 637.
. Bat-Gott, 1936. Physiol. Reif» is: 1o3.
. steele, A. G. sc: W. F. Windle. 193g. Physiol» 94: Ist. . Baker-oft, J. s: M. F. Mason. 1938. Ibicl» 93: ssP.
. Winde, W. F. B: A. G. steele.
1938. Proe. soc. Exp. Biol. sc Med» Zg: s46.
. Oliv-le, G. A. . 1934. J. Physiol» 83: ss9. . schnitt, W. 19s5. Deut. mecl. Wehnsehr» 51(1): 189.
Kam, I-I. F. s: J. Kreiselmatx 193o. Am. J. Obst. Gyn., so: 8s6.·
. Henderson, Y. 19s8. J.A.M.A» go: 583. . Eastmam N. J. 193s. Johns Hoplcins I-Iosp. Bull., so: 39. . Eastmath N. sc c. M. McLane.
1931. 1bid 48: s61.
Cite this page: Hill, M.A. (2019, August 24) Embryology Book - Physiology of the Fetus 5. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Book_-_Physiology_of_the_Fetus_5
- © Dr Mark Hill 2019, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G