Prolonged reductions in placental blood flow and cerebral oxygen delivery in preterm fetal sheep exposed to endotoxin: possible factors in white matter injury after acute infection

2003 ◽  
Vol 10 (5) ◽  
pp. 283-290 ◽  
Author(s):  
P Dalitz
Keyword(s):  
Blood Flow ◽  
White Matter ◽  
Oxygen Delivery ◽  
Acute Infection ◽  
White Matter Injury ◽  
Cerebral Oxygen ◽  
Fetal Sheep ◽  
Placental Blood ◽  
Placental Blood Flow

Fetal sheep endocrine responses to sustained hypoxemic stress after chronic fetal placental embolization

1997 ◽  
Vol 272 (5) ◽  
pp. E817-E823 ◽  
Author(s):  
R. Gagnon ◽  
J. Murotsuki ◽  
J. R. Challis ◽  
L. Fraher ◽  
B. S. Richardson
Keyword(s):  
Blood Flow ◽  
Oxygen Content ◽  
Regional Distribution ◽  
Arterial Oxygen ◽  
Control Group ◽  
Fetal Sheep ◽  
Arterial Oxygen Content ◽  
Placental Blood ◽  
Chronic Hypoxemia ◽  
Placental Blood Flow

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.

Relation between cerebral oxygen delivery and neuronal cell damage in fetal sheep near term

1996 ◽  
Vol 8 (3) ◽  
pp. 317 ◽  
Author(s):  
R Berger ◽  
T Lehmann ◽  
J Karcher ◽  
W Schachenmayr ◽  
A Jensen
Keyword(s):  
Blood Flow ◽  
Brain Damage ◽  
Oxygen Delivery ◽  
Cell Damage ◽  
Fetal Brain ◽  
Neuronal Cell ◽  
Arterial Blood Flow ◽  
Cerebral Oxygen ◽  
Fetal Sheep ◽  
Arterial Blood

Asphyxia is one of the major causes for fetal brain damage. Although the quality of life of the so affected children is mostly very limited, the pathogenesis of hypoxic fetal brain damage is poorly understood. Particularly, there is a lack of studies, in which cerebral oxygen delivery is directly correlated to the extent of neuronal cell damage in the same brain specimens. Therefore, we measured cerebral oxygen delivery before (- 1 h), during (+3 min & +27 min) and after (+10 min, +4 h, +72 h) 30 min of ischaemia in 5 chronically catheterized normoxemic fetal sheep at 129 +/- 1 days gestation (term is at 147 days) using the microsphere method. In contrast to previous studies (Williams et al. 1990), we arrested carotid arterial blood flow above the lingual artery for 30 min during surgery. Seventy-two hours later the fetal brains were fixed in vivo under barbiturate anaesthesia of both the fetus and the ewe. After cerebral blood flow analysis neuronal cell damage was assessed with light microscopy in 43 specimens of the fetal brain after cresyl violet/fuchsin staining using a scoring system. After arrest of carotid arterial blood flow cerebral blood flow was reduced by 80%. Neuronal cell damage was focussed on the cerebral cortex. Almost no damage could be detected in deeper parts of the brain. In the cerebrum there was threshold oxygen delivery of 3 ml O2/100 g tissue/min, below which neuronal damage occurred. However, there was no correlation between cerebral oxygen delivery and neuronal cell damage in specimens of the cerebrum, in which oxygen delivery was less than 3 ml O2/100 g tissue/min, suggesting selective vulnerability. Therefore, in addition to the reduction in cerebral oxygen delivery, other variables, e.g. neurotransmitter release, receptor pattern or oxygen radicals, may be involved in the development of brain damage.

Responses to acute hypoxemia in fetal sheep at 0.6-0.7 gestation

1989 ◽  
Vol 256 (3) ◽  
pp. H613-H620 ◽  
Author(s):  
H. S. Iwamoto ◽  
T. Kaufman ◽  
L. C. Keil ◽  
A. M. Rudolph
Keyword(s):  
Blood Flow ◽  
Fetal Sheep ◽  
Blood Flows ◽  
Arterial Blood ◽  
Regulatory Systems ◽  
Group I ◽  
Placental Blood ◽  
Placental Blood Flow ◽  
Sheep Fetus ◽  
I 31

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)

Responses of fetal sheep to simulated no-decompression dives

1980 ◽  
Vol 48 (5) ◽  
pp. 776-780 ◽  
Author(s):  
M. K. Stock ◽  
E. H. Lanphier ◽  
D. F. Anderson ◽  
L. C. Anderson ◽  
T. M. Phernetton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Maternal Blood ◽  
Arterial System ◽  
Fetal Sheep ◽  
Monitoring Result ◽  
Placental Blood ◽  
Near Term ◽  
Placental Blood Flow ◽  
Maternal Blood Pressure

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.

Maturational Effects of Lipopolysaccharide on White-Matter Injury in Fetal Sheep

2005 ◽  
Vol 20 (12) ◽  
pp. 960-964 ◽  
Author(s):  
Pernilla Svedin ◽  
Ingmar Kjellmer ◽  
Anna-Karin Welin ◽  
Sofia Blad ◽  
Carina Mallard
Keyword(s):  
White Matter ◽  
White Matter Injury ◽  
Fetal Sheep
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