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)

Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

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.

Regional adrenal blood flow responses to adrenocorticotropic hormone after chronic embolization of the fetal placental circulation in sheep

1996 ◽  
Vol 148 (3) ◽  
pp. 517-522 ◽  
Author(s):  
A M Carter ◽  
J R G Challis ◽  
P Svendsen
Keyword(s):  
Blood Flow ◽  
Adrenal Cortex ◽  
Adrenocorticotropic Hormone ◽  
Maternal Blood ◽  
Arterial Oxygen ◽  
Fetal Sheep ◽  
Cortical Blood Flow ◽  
Arterial Oxygen Content ◽  
Blood Flows ◽  
Placental Blood

Abstract To ascertain whether repeated hypoxic stress would alter the response of the adrenal cortex to adrenocorticotropic hormone (ACTH), by premature activation of the hypothalamic–pituitary–adrenal axis, we studied fetal sheep subjected to daily reduction of arterial oxygen content by embolization of the fetal placental circulation with 15 μm microspheres for 8 days from about day 124 of gestation (term ∼147 days) and sham-embolized controls. Starting before the final embolization (or shamembolization) on day 8, and continuing for 24 h, the fetus was given an intravenous infusion of ACTH1–24 (0·5 μg/h) or vehicle. Fetal and maternal blood samples were taken for determination of immunoreactive cortisol, and regional adrenal and fetal placental blood flows were measured by the microsphere technique at three time points: 1 h before infusion, 3 h after the start of the infusion (1 h after embolization), and after 24 h of infusion. Prior to infusion of ACTH or vehicle, fetal placental blood flow was lower in microsphere-embolized fetuses than in sham-embolized controls (199 ± 15 vs 292 ± 25 ml/min per 100 g tissue; mean ± s.e.; P<0·01). However, plasma cortisol and adrenal cortical blood flow did not differ between embolized fetuses and controls. Adrenal vascular responses to the 24-h infusion of ACTH were similar in embolized and shamembolized fetuses. Adrenal cortical blood flow increased 3-fold (P<0·05) due to decreased vascular resistance (P<0·01), with no change in adrenal medullary blood flow. Thus, while daily embolization of the fetal placental circulation caused a sustained decrease in cotyledonary blood flow, no evidence of altered responsiveness of the adrenal cortex to ACTH was found in these experiments. Journal of Endocrinology (1996) 148, 517–522

Regulation of fetal placental blood flow in the lamb

1984 ◽  
Vol 247 (3) ◽  
pp. R567-R574 ◽  
Author(s):  
D. F. Anderson ◽  
J. J. Faber
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Fetal Growth ◽  
Control Value ◽  
Flow Restriction ◽  
Arterial Blood ◽  
Placental Blood ◽  
Carotid Arterial ◽  
Placental Blood Flow

Inflatable occluders were placed on the distal aorta of 11 fetal lambs. After 1 wk of control measurements, fetal placental blood flow was reduced to about two-thirds of its control value for an average period of 2 wk. No allowance was made for fetal growth. During the period of flow restriction, fetal growth was 2%/day. Femoral arterial blood pressure was reduced from a control value of 41 to 27 mmHg (P less than 0.001). There was an insignificant increase in carotid arterial blood pressure from 48 to 50 mmHg. Placental resistance to flow did not decrease more than could be accounted for by the increase in gestational age in the course of the experiment. It is concluded that fetal placental blood flow is not under feedback control, since neither of the determinants of flow (i.e., driving pressure and resistance) responded to its chronic reduction.

Regional adrenal blood flow responses to adrenocorticotropic hormone in fetal sheep

1993 ◽  
Vol 264 (2) ◽  
pp. E264-E269 ◽  
Author(s):  
A. M. Carter ◽  
B. S. Richardson ◽  
J. Homan ◽  
M. Towstoless ◽  
J. R. Challis
Keyword(s):  
Blood Flow ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Isotonic Saline ◽  
Fetal Sheep ◽  
Cortical Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Regional Blood Flows ◽  
Acth Concentration

To determine whether adrenocorticotropic hormone (ACTH) at plasma concentrations measured during mild hypoxemia and at term affects adrenal blood flow, we measured regional blood flows in five unanesthetized normoxemic fetuses (125–130 days gestation) during a 24-h intravenous infusion of ACTH-(1–24) in isotonic saline solution. Another five fetuses received an infusion of vehicle. Blood flows were determined before the infusion, at 2 and 24 h from its onset, and 24 h afterward using radionuclide-labeled microspheres. Blood flow to the adrenal medulla was fivefold greater than that to the adrenal cortex. Adrenal blood flow rose 99% at 24 h of the ACTH infusion. There was a large increase in adrenal cortical blood flow of 272% at this time but medullary blood flow did not change significantly during ACTH infusion. The rise in cortical blood flow was attributable to decreased vascular resistance. No significant alterations occurred in fetal arterial blood pressure and heart rate, or in blood flow to other lower body organs of the fetus or to the placental cotyledons. These findings are consistent with the hypothesis that the increase in adrenal blood flow observed during fetal hypoxia is associated with changes in plasma ACTH concentration. They are also indicative of selective regulation of cortical and medullary blood flows in the sheep fetus at this stage of gestation.

NO supports right ventricular flow dominance and whole body O2 utilization in midgestation fetal lambs

2001 ◽  
Vol 280 (4) ◽  
pp. R1016-R1022 ◽  
Author(s):  
Joseph J. Smolich
Keyword(s):  
Blood Flow ◽  
Flow Distribution ◽  
The Body ◽  
Whole Body ◽  
Blood Flow Distribution ◽  
Blood Flows ◽  
Blood Flow Ratio ◽  
Placental Blood ◽  
Flow Changes ◽  
Placental Blood Flow

It is unknown if nitric oxide (NO) modulates the relative levels of left (LV) and right (RV) ventricular output, fetal O2 consumption, or blood flow distribution between the body and placenta at midgestation. To address these questions, six fetal lambs were instrumented at 89–96 days gestation (term 147 days), and blood flows were measured with radioactive microspheres 3–4 days later at baseline and after inhibition of NO synthesis with 10 mg/kg (l-NNA10) and 25 mg/kg (l-NNA25) N ω-nitro-l-arginine. LV output fell by 74 ± 15 ml · min−1 · kg−1 atl-NNA10 ( P < 0.005), whereas RV output decreased by 90 ± 18 ml · min−1 · kg−1 atl-NNA10 ( P < 0.02) and by a further 80 ± 22 ml · min−1 · kg−1 atl-NNA25 ( P < 0.05). As a result, RV output exceeded LV output at baseline ( P = 0.03) and l-NNA10 ( P < 0.02) but not at l-NNA25. Fetal body blood flow fell by 95 ± 25 ml · min−1 · kg−1 atl-NNA10 ( P < 0.01), but because placental blood flow decreased by 70 ± 22 ml · min−1 · kg−1 atl-NNA10 ( P < 0.01) and a further 71 ± 21 ml · min−1 · kg−1 atl-NNA25 ( P < 0.01), the fetal body-to-placental blood flow ratio was near unity at baseline andl-NNA10 but rose to 1.5 ± 0.3 atl-NNA25 ( P < 0.05). In association with these flow changes, fetal O2 consumption declined by 1.4 ± 0.3 ml · min−1 · kg−1 atl-NNA10 ( P < 0.05) and by a further 1.5 ± 0.6 ml · min−1 · kg−1 atl-NNA25 ( P < 0.02). These findings suggest that, in midgestation fetal lambs, NO supports an RV flow dominance, whole body O2 utilization, and the maintenance of a near-equal fetoplacental blood flow distribution.

Fever and regional blood flows in wethers and parturient ewes

1988 ◽  
Vol 65 (1) ◽  
pp. 165-172 ◽  
Author(s):  
C. M. Blatteis ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
T. A. Mashburn
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Full Term ◽  
Blood Flows ◽  
Pregnant Sheep ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Placental Blood Flow

To determine whether the reported absence of fever in full-term-pregnant ewes might be associated with shifts of regional blood flows from thermogenic tissues to placenta during this critical period, fevers were induced twice by injections of Escherichia coli lipopolysaccharide (LPS, 0.25 microgram/kg iv) into each of six Merino ewes from 8 to 1 days prepartum, and their regional blood flow distribution was measured with radioactive, 15-microns-diam microspheres before and during the rise in fever (when their rectal temperature had risen approximately 0.4 degree C). Unexpectedly, fever always developed, rising to heights not significantly different at any time before parturition [4-8 days prepartum = 0.81 +/- 0.23 degree C (SE); 1-3 days prepartum = 0.75 +/- 0.17 degree C) and similar to those in three wethers treated similarly (0.90 +/- 0.10 degree C). Generally, during rising fever, blood flow in the ewes shifted away from heat loss tissues (e.g., skin, nose) to heat production tissues (e.g., shivering muscle, fat) and cardiac output increased; blood flow through redistribution organs (e.g., splanchnic bed) decreased. The reverse occurred during defervescence. Utero-placental blood flow remained high in the febrile ewes. These regional blood flow distributions during febrigenesis and lysis are essentially the same as those during exposures to ambient cold and heat, respectively. Some differences in the responses of cardiac output and its redistribution, however, were apparent between wethers and pregnant ewes. We conclude that 1) the previously reported "absence of fever in the full-term-pregnant sheep" should not be regarded as a general phenomenon and 2) full-term-pregnant sheep support fever production without sacrificing placental blood flow.

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