P239: Implanting a wide-bore stent into the ductus venosus of fetal sheep distinctly increases placental blood flow rate

2003 ◽  
Vol 22 (S1) ◽  
pp. 134-134
Author(s):  
M. Tchirikov ◽  
H. J. Schr�der
1978 ◽  
Vol 39 (2) ◽  
pp. 347-356 ◽  
Author(s):  
H. W. Symonds ◽  
R. H. Bubar ◽  
W. CRACKEL ◽  
A. R. Twardock

1. Placental blood flow rate and calcium transfer rate were measured at 61 d of pregnancy in guinea-pigs carrying between one and eight foetuses.2. Placental blood flow rate was significantly correlated with foetal weight. Ca transfer rate was related to placental size. Irrespective of litter size the mean amount of Ca transferred across a placenta was between 0.22 and 0.34 mg/h per g placental tissue.3. It was concluded that there was a limit to the rate of transfer which was produced by a combination of limitations in placental blood flow rate, maternal plasma Ca concentration and placental tissue transfer capacity.


1997 ◽  
Vol 272 (5) ◽  
pp. E817-E823 ◽  
Author(s):  
R. Gagnon ◽  
J. Murotsuki ◽  
J. R. Challis ◽  
L. Fraher ◽  
B. S. Richardson

The purpose of this study was to determine the endocrine and circulatory responses of the ovine fetus, near term, to sustained hypoxemic stress superimposed on chronic hypoxemia. Fetal sheep were chronically embolized (n = 7) for 10 days between 0.84 and 0.91 of gestation via the descending aorta until arterial oxygen content was decreased by approximately 30%. Control animals (n = 8) received saline only. On experimental day 10, both groups were embolized over a 6-h period until fetal arterial pH decreased to approximately 7.00. Regional distribution of lower body blood flows was measured on day 10, before and at the end of acute embolization. On day 10, the chronically embolized group had lower arterial oxygen content (P < 0.05), Po2 (P < 0.01), and placental blood flow (P < 0.05) than controls and higher prostaglandin E2 (PGE2) and norepinephrine plasma concentrations (both P < 0.05). In response to a superimposed sustained hypoxemic stress, there was a twofold greater increase in PGE2 in the chronically embolized group than in the control group (P < 0.05). However, the increase in fetal plasma cortisol in response to superimposed hypoxemic stress was similar in both groups, despite significantly lower adrenocorticotropic hormone and adrenal cortex blood flow responses in the chronically hypoxemic group (both P < 0.05). We conclude that PGE2 response to a sustained superimposed reduction in placental blood flow, leading to metabolic acidosis, is enhanced under conditions of chronic hypoxemia and may play an important role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.


1991 ◽  
Vol 260 (4) ◽  
pp. H1205-H1213 ◽  
Author(s):  
R. P. Paulick ◽  
R. L. Meyers ◽  
C. D. Rudolph ◽  
A. M. Rudolph

Acute fetal hypoxemia increases the vascular resistance of the umbilical veins as well as that of the liver. Because, at least in the human, the umbilical-placental circulation has no autonomic innervation, circulating hormones could well be responsible for this increase in umbilical-placental outflow resistance. In chronically instrumented fetal sheep, norepinephrine, epinephrine, vasopressin, and angiotensin II were infused in sequentially increasing doses into the descending aorta and vascular resistance to umbilical-placental blood flow was measured. Norepinephrine and epinephrine increased the vascular resistance of the umbilical veins in a dose-dependent manner. Both catecholamines also increased the vascular resistance of the liver, resulting in an increase in ductus venosus blood flow. In contrast, vasopressin and angiotensin II had no effect on umbilical-placental outflow resistance. Thus catecholamines may be responsible for the increase in the vascular resistance of the umbilical veins and liver in response to acute fetal hypoxemia.


1989 ◽  
Vol 256 (3) ◽  
pp. H613-H620 ◽  
Author(s):  
H. S. Iwamoto ◽  
T. Kaufman ◽  
L. C. Keil ◽  
A. M. Rudolph

A majority of previous studies of fetal responses to acute hypoxemia has focused on the response of the sheep fetus greater than 120 days of gestation when many regulatory systems have been established. To assess the response of younger, less well-developed fetuses, we exposed two groups of fetal sheep (I, 84-91 days; II, 97-99 days gestational age) to acute hypoxemia by giving the ewe a gas mixture containing 9% O2 to breathe. We decreased descending aortic PO2 in both groups of fetuses [I, 24 +/- 6 to 14 +/- 3 (SD) Torr; II, 23 +/- 3 to 12 +/- 4 Torr] by a degree similar to that achieved in previous studies of fetuses greater than 120 days of gestation. Mean arterial blood pressure (I, 31 +/- 6; II, 40 +/- 3 Torr) did not change significantly from control values, and heart rate (I, 224 +/- 27; II, 203 +/- 16 beats/min) increased significantly in group II fetuses with hypoxemia. In group I and II fetuses, as in older fetuses, cerebral, myocardial, and adrenal blood flows, measured by the microsphere technique, increased, and pulmonary blood flow decreased. These responses mature early and are likely local vascular responses to decreases in oxygen content. Combined ventricular output and umbilical-placental blood flow decreased significantly in both groups. Unlike the response of the fetus greater than 120 days, acute hypoxemia did not decrease blood flow to the musculoskeletal and cutaneous circulations (group I only), gastrointestinal, or renal circulations.(ABSTRACT TRUNCATED AT 250 WORDS)


1980 ◽  
Vol 48 (5) ◽  
pp. 776-780 ◽  
Author(s):  
M. K. Stock ◽  
E. H. Lanphier ◽  
D. F. Anderson ◽  
L. C. Anderson ◽  
T. M. Phernetton ◽  
...  

The effect of simulated standard no-decompression dives to 60 and 100 ft of seawater was tested in 12 near term sheep carrying 16 fetuses. In the immediate postdive period there were no significant changes in fetal blood pressure or fetal placental or renal blood flow, but the maternal blood pressure was elevated and the maternal placental blood flow was depressed. Six surgically prepared fetuses were dived to 100 ft. Five died within 20 min of ascent and the sixth suffered severe cardiac arrhythmia and hypotension. At autopsy all fetuses were observed to have massive bubbling in the arterial system and heart. Five fetuses were dived to 100 ft without surgery. Two were alive 3 h later and no bubbles were present at autopsy, and three were born alive at term. With the 60-ft dives, three fetuses were subjected to surgery and all suffered massive bubbling. Two fetuses were dived to 60 ft without surgery; one was alive after 3 h and the other was born alive at term. We conclude that surgery and monitoring result in the formation of postdive gas bubbles that would not otherwise appear.


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