Blood flow to fetal organs as a function of arterial oxygen content

Peeters, Louis L.H.; Sheldon, Roger E.; Jones, Mathew; Makowski, Edgar L.; Meschia, Giacomo

doi:10.1016/s0002-9378(16)32989-1

Cited by 481 publications

(248 citation statements)

References 23 publications

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“…This suggests that there is a development in the compensatory ability of the chick embryo to provide oxygen delivery to these vital organs under hypoxic conditions. The redistribution of the CO in response to hypoxia, favouring the heart and brain at the expense of intestine, liver and carcass is similar to that found in mammalian fetuses of the sheep (Jensen et al 1991;Peeters et al 1979), rhesus monkey (Jackson, Piasecki & Novy, 1987) and llama (Giussani et al 1996). Since the chick embryo is independent of the mother, the similarity in response to hypoxia suggests that in the mammalian fetus such responses may occur independently of maternal or placental factors.…”

Section: Discussion Response To Hypoxiasupporting

confidence: 71%

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Mulder

Golde

Prinzen

et al. 1998

The Journal of Physiology

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The fetus develops cardiovascular adaptations to protect vital organs in situations such as hypoxia and asphyxia. These include bradycardia, increased systemic blood pressure and redistribution of the cardiac output. The extent to which they involve maternal or placenta influences is not known. The objective of the present work was to study the cardiac output distribution in response to hypoxia in the chick embryo, which is independent of the mother. Fertilized eggs were studied at three incubation times (10‐13 days, 14‐16 days and 17‐19 days of a normal incubation time of 21 days). Eggs were placed in a Plexiglass box in which the oxygen concentration could be changed. Eggs were opened at the air cell and a chorioallantoic vein was catheterized. Cardiac output distribution was measured with 15 μm fluorescent microspheres injected during normoxia, during the last minute of a 5 min period of hypoxia and after 5 min of subsequent reoxygenation. Hypoxia caused a redistribution of the cardiac output in favour of heart (+17 to +160 % of baseline) and brain (+21 to +57 % of baseline) at the expense of liver (‐3 to ‐65 % of baseline), yolk‐sac (‐46 to ‐77 % of baseline) and carcass (‐6 to ‐33 % of baseline). The magnitude of the changes in cardiac output distribution to the heart, brain, liver and carcass in response to hypoxia increased with advancing incubation time. The data demonstrate the development of a protective redistribution of the cardiac output in response to hypoxia in the chick embryo from day 10 of incubation.

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Section: Discussion Response To Hypoxiasupporting

confidence: 71%

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Mulder

Golde

Prinzen

et al. 1998

The Journal of Physiology

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“…To date, 02 balance studies in animals and man have focused on normal, physiologic relationships,'-5 the acute pathophysiology of disease states,2' S1 or laboratory manipulations. [12][13][14][15][16][17][18][19][20] From the University of New Mexico School of Medicine, Departments of Pediatrics and Physiology, Albuquerque.…”

mentioning

confidence: 99%

Systemic oxygen transport in patients with congenital heart disease.

Berman¹,

Wood²,

Yabek³

et al. 1987

Circulation

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“…The renal blood flow is estimated as 2-3% of the cardiac output under physiological conditions because of the very high pulsatility index (i.e., a very high resistance) in the human fetal renal artery. During hypoxemia, the renal blood flow fell by 25-50% as compared to the baseline values, but the exact mechanism of this reduction has not been elucidated [17]. This would imply that, instead of a local vasoconstriction of the renal vasculature, the fetal renal blood flow may be maintained by a combination of mechanisms including an increase in arterial pressure and the intrarenal action of various metabolites, which ultimately induce a similar hemodynamic change [18].…”

Section: Discussionmentioning

confidence: 99%

“…We investigated intrauterine hypoxia using indirect ultrasonographic signs: renal hyperechogenicity, and decreased flow parameters in the umbilical artery and the renal artery [5,17,20]. The screened pregnancies were those with chronic hypoxia, caused by pregnancy-associated hypertension and/or proteinuria and intrauterine growth retardation.…”

Section: Discussionmentioning

confidence: 99%

Fetal renal artery flow and renal echogenicity in the chronically hypoxic state

Surányi¹,

Streitman²,

Pál

et al. 2000

Pediatr Nephrol

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The object of this study was to investigate the fetal renal arterial blood flow in normal and hyperecho-genic kidneys during the third trimester of gestation. The pregnancies screened were all chronically hypoxic. Depending on the etiology of the intrauterine chronic hypoxia, the cases were divided into two study groups. Group I comprised 120 pregnant women with pregnancy-associated hypertension and/or proteinuria. Group II consisted of 87 pregnancies with intrauterine growth retardation. Both study groups included pregnant women from the third trimester. Hyperechogenic renal medullae were detected in 15 out of 120 cases with pregnancyassociated hypertension and/or proteinuria, and in 22 fetuses of the 87 pregnancies involving intrauterine growth retardation. Fetal renal hyperechogenicity appears to be an indicator of fetal arterial circulatory depression, correlated with pathological changes in the resistance index for the fetal renal arteries. The fetal renal arterial blood flow resistance index was significantly lower in hyperechogenic cases. This may also be an in utero indication of subsequent intrauterine and neonatal complications, such as cesarean section because of fetal distress (43%), treatment in a neonatal intensive care unit (51%) or increased perinatal mortality (5.4%, as compared with 0.8-1.0% in the normal population). Detailed ultrasound and Doppler examinations of renal parenchyma and arteries appear to be useful methods in the prenatal diagnosis of reduced renal perfusion and of intrauterine hypoxia to detect possible pathological fetal conditions in utero.

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Blood flow to fetal organs as a function of arterial oxygen content

Cited by 481 publications

References 23 publications

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Systemic oxygen transport in patients with congenital heart disease.

Fetal renal artery flow and renal echogenicity in the chronically hypoxic state

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