scholarly journals Is fetal cerebral vascular resistance affected by the presence of nuchal cord(s) in the third trimester of pregnancy?

2005 ◽  
Vol 25 (5) ◽  
pp. 454-458 ◽  
Author(s):  
D. M. Sherer ◽  
M. Sokolovski ◽  
M. Dalloul ◽  
F. Khoury-Collado ◽  
O. Abulafia
Keyword(s):  
Vascular Resistance ◽  
Third Trimester ◽  
The Third ◽  
Nuchal Cord ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

FETAL CEREBRAL VASCULAR RESISTANCE

The Lancet ◽  
1987 ◽  
Vol 330 (8555) ◽  
pp. 392-393 ◽  
Author(s):  
P. Kirkinen ◽  
R. Müller ◽  
H. Baumann ◽  
D. Mieth ◽  
G. Duc ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Pulmonary endothelial nitric oxide production is developmentally regulated in the fetus and newborn

1993 ◽  
Vol 265 (4) ◽  
pp. H1056-H1063 ◽  
Author(s):  
P. W. Shaul ◽  
M. A. Farrar ◽  
R. R. Magness
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Pulmonary Arteries ◽  
Late Gestation ◽  
No Production ◽  
Third Trimester ◽  
Developmentally Regulated ◽  
The Third ◽  
Endothelial Nitric Oxide

To define the role of endothelial nitric oxide (NO) in developmental changes in pulmonary vascular resistance and oxygen responsiveness, we determined the ontogeny of endothelial NO production and of oxygen modulation of that process in pulmonary arteries from fetal and newborn lambs. NO production was assessed by measuring endothelium-dependent arterial guanosine 3',5'-cyclic monophosphate synthesis. Basal NO rose two-fold from late gestation to 1 wk of age and another 1.6-fold from 1 to 4 wk. Acetylcholine-stimulated NO also increased 1.6-fold from 1 to 4 wk. The maturational rise in NO was evident at high Po2 in vitro, and it was not modified by L-arginine. This suggests that the developmental increase may alternatively involve enhanced calcium-calmodulin-mediated mechanisms, increased expression of NO synthase, or greater availability of required cofactor(s). With an acute decline in Po2 in vitro from 680 to 150 or 40 mmHg, there was 50-88% attenuation of basal and acetylcholine-stimulated NO late in the third trimester and in the newborn but not early in the third trimester. Parallel studies of mesenteric endothelium revealed postnatal increases in basal and stimulated NO but no decline in NO at lower Po2. Ontogenic changes in endothelial NO production and in oxygen modulation of that process may be involved in the maturational decrease in vascular resistance and the development of oxygen responsiveness in the pulmonary circulation.

Cerebral Vascular Resistance in Experimental Renal and DCA Hypertension

1971 ◽  
Vol 6 (1-6) ◽  
pp. 39-42 ◽  
Author(s):  
H. Flohr ◽  
H.W. Dahners ◽  
H. Conradi ◽  
D. Redel ◽  
W. Breull ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

Vasopressin and prostanoid mechanisms in control of cerebral blood flow in hypotensive newborn pigs

1990 ◽  
Vol 258 (2) ◽  
pp. H408-H413 ◽  
Author(s):  
W. M. Armstead ◽  
C. W. Leffler ◽  
D. W. Busija ◽  
R. Mirro
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Cerebral Metabolic Rate ◽  
Cerebral Vasoconstriction ◽  
Newborn Pigs ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

scholarly journals Interrelationships Among Regional Cerebral Blood Flow, Mean Transit Time, Vascular Volume and Cerebral Vascular Resistance

Stroke ◽  
1974 ◽  
Vol 5 (6) ◽  
pp. 719-724 ◽  
Author(s):  
YOSHIHIRO KURIYAMA ◽  
TAKASHI AOYAMA ◽  
KUNIHIKO TADA ◽  
SHOTARO YONEDA ◽  
TADAATSU NUKADA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Vascular Resistance ◽  
Transit Time ◽  
Regional Cerebral Blood Flow ◽  
Mean Transit Time ◽  
Regional Cerebral Blood ◽  
Vascular Volume ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular

scholarly journals Transient changes in cerebral vascular resistance during the Valsalva maneuver in man.

Stroke ◽  
1984 ◽  
Vol 15 (1) ◽  
pp. 76-79 ◽  
Author(s):  
J C Greenfield ◽  
J C Rembert ◽  
G T Tindall
Keyword(s):  
Vascular Resistance ◽  
Valsalva Maneuver ◽  
Cerebral Vascular Resistance ◽  
Cerebral Vascular
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