Nitric Oxide and Fetal Organ Blood Flow During Normoxia and Hypoxemia in Endotoxin-Treated Fetal Sheep

2005 ◽  
Vol 105 (1) ◽  
pp. 145-155 ◽  
Author(s):  
Audrey B. C. Coumans ◽  
Yves Garnier ◽  
Sirma Supçun ◽  
Arne Jensen ◽  
Richard Berger ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Organ Blood Flow ◽  
Fetal Sheep ◽  
Fetal Organ

scholarly journals Mechanisms of calcitonin gene-related peptide-induced increases of pulmonary blood flow in fetal sheep

2000 ◽  
Vol 279 (4) ◽  
pp. H1654-H1660 ◽  
Author(s):  
Yasushi Takahashi ◽  
Maartje De Vroomen ◽  
Christine Roman ◽  
Michael A. Heymann
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arteries ◽  
Calcitonin Gene Related Peptide ◽  
Fetal Sheep ◽  
Nitric Oxide Synthase Inhibitor ◽  
Flow Transducer ◽  
Related Peptide ◽  
Calcitonin Gene

Fetal pulmonary blood flow is regulated by various vasoactive substances. One, calcitonin gene-related peptide (CGRP), increases pulmonary blood flow. We examined four key physiological mechanisms underlying this response using the blocker drugs CGRP receptor blocker (CGRP8–37), nitric oxide synthase inhibitor [ N ω-nitro-l-arginine (l-NNA)], adenosine triphosphate-dependent potassium (KATP) channel blocker (glibenclamide), and cyclooxygenase inhibitor (indomethacin) in 17 near-term fetal sheep. Catheters were placed in the left (LPA) and main pulmonary arteries, and an ultrasonic flow transducer was placed around the LPA to measure flow continuously. CGRP was injected directly into the LPA (mean 1.02 μg/kg) before and after blockade, and responses to CGRP were statistically compared. Before blockade, CGRP increased LPA blood flow from 23 ± 25 to 145 ± 77 ml/min (means ± SD), and these increases were significantly attenuated by CGRP8–37( n = 6; 91% inhibition), l-NNA ( n = 6; 86% inhibition), and glibenclamide ( n = 6; 69% inhibition). No significant changes were found with indomethacin ( n = 6; 4% inhibition). Thus, in the fetal pulmonary circulation, CGRP increases pulmonary blood flow not only through its specific receptor but also, in part, through nitric oxide release and KATP channel activation.

Control of organ blood flow in fetal sheep during normoxia and hypoxia

1989 ◽  
Vol 257 (4) ◽  
pp. H1132-H1139 ◽  
Author(s):  
A. H. Jansen ◽  
J. Belik ◽  
S. Ioffe ◽  
V. Chernick
Keyword(s):  
Blood Flow ◽  
Rem Sleep ◽  
Skeletal Muscles ◽  
Nrem Sleep ◽  
Adaptation To Hypoxia ◽  
Organ Blood Flow ◽  
Fetal Sheep ◽  
Blood Flows ◽  
Carotid Bodies ◽  
Fetal Breathing

The role of peripheral chemoreceptors in the circulatory adaptation to hypoxia and the effects of rapid-eye-movement (REM) and non-REM (NREM) sleep and breathing activity on organ blood flow were assessed in fetal sheep. Blood flow was measured with isotope-labeled microspheres on intact, vagotomized (VX), and sinoaortic-denervated (SAD) fetuses. Denervation did not change the biventricular cardiac output (Biv. CO) or organ blood flows during normoxia. In intact fetuses the blood flow was increased during hypoxemia in brain, adrenals, and heart but not in kidneys, skeletal muscles, or placenta. The increase in organ blood flow during hypoxemia was reduced in the VX group and even more in SAD fetuses, but in the latter group, blood flow was still increased in mid-brain, medulla, pons, skeletal muscles, and heart. Sleep states per se did not significantly affect the blood flow to any organs tested. However, the Biv. CO and blood flow to all organs except kidneys and adrenals was increased during fetal breathing in REM sleep. We conclude that 1) during moderate hypoxemia both aortic and carotid bodies plus an additional mechanism are involved in redistributing fetal blood flow, and 2) changes in organ perfusion during REM sleep are due to concomitant fetal breathing.

INCREASED ORGAN BLOOD FLOW IN SEPSIS AND ITS REVERSAL WITH THE NITRIC OXIDE SYNTHASE INHIBITOR L-NAME

1993 ◽  
Vol 21 (Supplement) ◽  
pp. S280 ◽  
Author(s):  
Jörg Meyer ◽  
Joseph Stothert ◽  
Valerie Pollard ◽  
Frank Hinder ◽  
David Hemdon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Organ Blood Flow ◽  
Nitric Oxide Synthase Inhibitor ◽  
Synthase Inhibitor ◽  
Oxide Synthase

Organ blood flow in response to infusion of arginine vasopressin in premature fetal sheep

2020 ◽  
Vol 62 (6) ◽  
pp. 688-693
Author(s):  
Shimpei Watanabe ◽  
Tadashi Matsuda ◽  
Takushi Hanita ◽  
Hideyuki Ikeda ◽  
Shouta Koshinami ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arginine Vasopressin ◽  
Organ Blood Flow ◽  
Fetal Sheep

Fetal cerebral and peripheral circulatory responses to hypoxia after nitric oxide synthase inhibition

2001 ◽  
Vol 281 (2) ◽  
pp. R381-R390 ◽  
Author(s):  
Andrew P. Harris ◽  
Sabah Helou ◽  
Christine A. Gleason ◽  
Richard J. Traystman ◽  
Raymond C. Koehler
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Treated Group ◽  
Arterial Oxygen ◽  
Control Group ◽  
Fetal Sheep ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
Nos Inhibitor ◽  
Oxide Synthase

The increase in cerebral blood flow (CBF) during hypoxia in fetal sheep at 0.6 gestation is less than the increase at 0.9 gestation when normalized for differences in baseline CBF and oxygen consumption. Nitric oxide (NO) synthase (NOS) catalytic activity increases threefold during this period of development. We tested the hypothesis that administration of the NOS inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) decreases the CBF response to systemic hypoxia selectively at 0.9 gestation. We also tested whether any peripheral vasoconstriction during hypoxia is potentiated byl-NAME at 0.9 gestation. Administration ofl-NAME increased arterial blood pressure and decreased microsphere-determined CBF during normoxia in fetal sheep at both 0.6 and 0.9 gestation. With subsequent reduction of arterial oxygen content by ∼50%, the percent increase in forebrain CBF in a control group (57 ± 11%; ± SE) and l-NAME-treated group (51 ± 6%) was similar at 0.6 gestation. Likewise, at 0.9 gestation, the increase in CBF was similar in control (90 ± 25%) andl-NAME (80 ± 28%) groups. At 0.9 gestation,l-NAME treatment attenuated the increase in coronary blood flow and increased gastrointestinal vascular resistance during hypoxia. We conclude that NO exerts a basal vasodilatory influence in brain as early as 0.6 gestation in fetal sheep but is not an important mechanism for hypoxic vasodilation in brain at either 0.6 or 0.9 gestation. Thus the developmental increase in NOS catalytic capacity does not appear to be responsible for developmental increases in the CBF response to hypoxia during this period. In contrast, NO modulates the vascular response to hypoxia in heart and gastrointestinal tract.

Hemodynamics and organ blood flow in fetal sheep subjected to chronic anemia

1991 ◽  
Vol 261 (6) ◽  
pp. R1542-R1548 ◽  
Author(s):  
L. E. Davis ◽  
A. R. Hohimer
Keyword(s):  
Blood Flow ◽  
Hydrostatic Pressure ◽  
Venous Pressure ◽  
Arterial Oxygen ◽  
Organ Blood Flow ◽  
Fetal Sheep ◽  
Chronic Anemia ◽  
Arterial Oxygen Content ◽  
Extravascular Fluid ◽  
Arterial Ph

To investigate cardiovascular adaptation to chronic anemia we studied eight ovine fetuses made anemic by serial isovolemic hemorrhage and seven nonanemic controls. After 1 wk carotid arterial oxygen content was reduced to 1.6 +/- 0.2 ml/dl and hematocrit to 13.3 +/- 1.6% in anemic fetuses compared with 6.9 +/- 1.2 ml/dl and 32.4 +/- 3.9% in controls. Cardiac output was higher in the anemic group (753 +/- 102 vs. 490 +/- 66 ml.min-1.kg fetus-1) as stroke volume and heart rate both increased. Blood flow to the carcass, skin, kidneys, intestines, brain, and heart was increased. Vascular resistance fell in all tissues except the placenta. Central venous pressure, arterial pH, plasma total protein, and blood volume were not different although extravascular fluid accumulated in six of the anemic fetuses. The estimated capillary hydrostatic pressure was greater in anemic (7.6 +/- 1.8 mmHg) than control fetuses (5.0 +/- 1.5 mmHg) and the ratio of precapillary to postcapillary resistance was less. We conclude that reduction in the ratio of precapillary to postcapillary resistance in chronic fetal anemia increases blood flow, oxygen delivery, and capillary hydrostatic pressure.

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