Respiration and the Respiratory System

Harned, Herbert S.

doi:10.1007/978-1-4684-2316-7_6

Cited by 6 publications

(6 citation statements)

References 185 publications

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“…Most of the CCE that enters the circulation diffuses into the erythrocytes, where its conversion to carbonic acid (H2CO3) is facilitated by the enzyme carbonic anhydrase [12]. It is known that this enzyme is only present in low concentration in fetal blood, and there may be insufficient time dur ing the passage of fetal blood through the pla cental circuit to convert H2CO3 back into CCE [14], It seems unlikely, therefore, that raising the PaCCE gradient across the placenta even more, by lowering the maternal PaCCE artifi cially, may succeed in clearing fetal carbon dioxide excess. In addition, this maneuver may cause uterine vasoconstriction, thereby reducing umbilical blood flow, and may shift the maternal oxyhemoglobin dissociation curve to the left, decreasing the amount of oxygen available to the fetus [11,12,15],…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that the fetus' ability to maintain a stable acid-base status is limited, and that correction of metabolic acidosis occurs only slowly [12,13], The same apparently holds true for 'respi ratory' acidosis. It is not entirely clear why CO2, which diffuses rapidly across the placen ta in physiologic conditions [11,12], both in human and in sheep [14], would fail to do so when the fetal-maternal gradient rises to ex treme levels. Most of the CCE that enters the circulation diffuses into the erythrocytes, where its conversion to carbonic acid (H2CO3) is facilitated by the enzyme carbonic anhydrase [12].…”

Section: Discussionmentioning

confidence: 99%

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Carbon Dioxide Pneumoamnios Causes Acidosis in Fetal Lamb

Luks

Deprest

Marcus³

et al. 1994

Fetal Diagn Ther

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Recently developed techniques of video-endoscopic surgery may offer new hope for the future of fetal surgery. To allow this approach, the amniotic cavity has to be temporarily enlarged, either by carbon dioxide (CO₂) insufflation or by amnioinfusion. In 6 anesthetized ewes, CO₂ insufflation of the amniotic cavity produced severe fetal hypercapnia (from 57.6 ± 1.6 to 87.0 ± 7.0 torr) and acidosis (from 7.22 ± 0.03 to 7.11 ± 0.08) despite normal maternal CO₂ pressure and pH. CO₂ pneumoamnios does not therefore appear to be an ideal working medium. Fetal endoscopic surgery through amnioinfusion of physiologic fluid may be a safer alternative.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Carbon Dioxide Pneumoamnios Causes Acidosis in Fetal Lamb

Luks

Deprest

Marcus³

et al. 1994

Fetal Diagn Ther

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“…The value of the 'energy equivalent' is about 5 cal (ml 02)-1 STPD (21 J (ml O2)-1 or 468 J (mmol 02) 1). Fetal oxygen consumption has frequently been measured and ranges from about 4 to 12 ml min-1 kg-1 (Harned, 1978;Power, Schroder & Gilbert, 1984;, and about 8 ml min-1 kg-' may be regarded as average. Fetal heat production thus varies from 1.2 to 3 5 W kg-' with 2 8 W kg-' as estimated mean.…”

Section: Fetal Heat Productionmentioning

confidence: 99%

“…Placental oxygen consumption ranges from 6-7 to more than 14 ml 02min-m kg-'. Accepting 8 ml min-' as a representative value (Harned, 1978;, it therefore generates about 1-5 W in sheep (placental weight is 0-5 kg). The contribution of the placental heat production to the fetal-maternal temperature difference has been estimated to be 0-07°C (Schr6der, Gilbert & Power, 1988).…”

Section: Placental Heat Exchangementioning

confidence: 99%

Engine and radiator: fetal and placental interactions for heat dissipation

Schröder¹,

Power²

1997

Experimental Physiology

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SUMMARYThe 'engine' of fetal metabolism generates heat (3-4 W kg-' in fetal sheep) which has to be dissipated to the maternal organism. Fetal heat may move through the amniotic/allantoic fluids to the uterine wall (conductive pathway; total conductance, 1-1 W 0C-' kg-') and with the umbilical arterial blood flow (convective pathway) to the placenta. Because resistance to heat flow is larger than zero fetal temperature exceeds maternal temperature by about 0 5°C (0.3-1°C). Probably 85 % of fetal heat is lost to the maternal organism through the placenta, which thus serves as the main 'radiator'. Placental heat conductivity appears to be extremely high and this may lead to impaired heat exchange (guinea-pig placenta). A computer simulation demonstrates that fetal temperature is essentially clamped to maternal temperature, and that fetal thermoregulatory efforts to gain thermal independence would be futile. Indeed, when the late gestational fetus in uter^o is challenged by cold stress, direct and indirect indicators of (non-shivering) thermogenesis (oxygen consumption, increase of plasma glycerol and free fatty acid levels) change only moderately. In prematurely delivered lambs, however, cold stress provokes summit metabolism and maximum heat production. Only when birth is imitated in utero (by cord clamping, external artificial lung ventilation and cooling) do thermogenic efforts approach levels typical of extra-uterine life. This suggests the presence of inhibitors of thermogenesis of placental origin, e.g. prostaglandins and adenosine. When the synthesis of prostaglandins is blocked by pretreatment with indomethacin, sheep fetuses react to intra-uterine cooling with vigorous thermogenic responses, which can be subdued by infusion of prostaglandin E2 (PGE2). Since the sheep placenta is known to produce sufficient amounts of PGE2, it seems that the placenta controls fetal thermogenic responses to some extent. This transforms the fetus into an ectothermic organism, and yet allows the newborn the full exploitation of thermoregulatory responses typical of endothermic animals.

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“…cold stimulation, release of immersion, acidic and hypercarbic stimulation of peripheral and central chemo-sensing mechanisms (for review see ref. 15). Other stimuli, such as the perception of tactile and painful stimuli, sound and gravity may contribute to an increased muscular activity and thus to a high metabolic rate.…”

Section: Discussionmentioning

confidence: 99%

THE INFLUENCE OF DIFFERENT ENVIRONMENTAL TEMPERATURES ON PULMONARY GAS EXCHANGE and BLOOD GAS CHANGES AFTER BIRTH

Tunell

1975

Acta Paediatrica

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Tunell, R. (Department of Paediatrics, Karolinska Sjukhuset, Stockholm, Sweden). The influence of different environmental temperatures on pulmonary gas exchange and blood gas changes after birth. Acta Paediatr Scand, 64: 57, 1975.-The oxygen uptake (VOJ and respiratory exchange ratio (R) was determined during the first 20 min and at one and at 2 hours after birth in 16 healthy full-term newborn infants studied in different environmental temperatures. Arterial blood gases and acid-base balance were determined on repeated blood samples from the abdominal aorta. The infants were grouped in a "warm" group (n=lO) where efforts were made to avoid cooling after birth, and a "cold" group (n=6) where a decrease in rectal temperature to a mean value of 354°C a t 2 hours occurred. Irrespective of environmental temperature, VO, was approximately 10 ml/kg min during the first 8 min after birth, thereafter decreasing to about 6-7 ml/kg min. During the first 8 min the main increase in Pa,, occurred and about 2 ml/kg min of the VOs was accounted for by changes in oxygen stores after birth. At 16-20 min and at 60 min after birth a negative relationship was found between V,, and Pa%. During the period 8-120 min after birth a close relationship was found between VO, and the degree of muscular activity. Within &16 min after birth, R values above 1.0 were regularly found simultaneously with the main decrease in Paco2. In infants kept "cold" a tendency to hyperventilate was found, probably elicited by cold stimuli. The rapid drop in deep body temperature regularly seen after birth could thus not be explained by a limited ability to increase pulmonary gas exchange. A high degree of evaporative heat loss, a relatively low "basal" metabolic rate and a limited response in "non-shivering thermogenesis" seem to be the main reasons for the heat loss after birth.

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Respiration and the Respiratory System

Cited by 6 publications

References 185 publications

Carbon Dioxide Pneumoamnios Causes Acidosis in Fetal Lamb

Carbon Dioxide Pneumoamnios Causes Acidosis in Fetal Lamb

Engine and radiator: fetal and placental interactions for heat dissipation

THE INFLUENCE OF DIFFERENT ENVIRONMENTAL TEMPERATURES ON PULMONARY GAS EXCHANGE and BLOOD GAS CHANGES AFTER BIRTH

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