Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus

Giussani, Dino A.; Riquelme, Raquel; Moraga, Fernando A.; Mcgarrigle, H. H. G.; Gaete, C; Sanhueza, Emilia M.; Hanson, MA; Llanos, Aníbal J.

doi:10.1152/ajpregu.1996.271.1.r73

Cited by 40 publications

(62 citation statements)

References 17 publications

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“…This suggests that there is a development in the compensatory ability of the chick embryo to provide oxygen delivery to these vital organs under hypoxic conditions. The redistribution of the CO in response to hypoxia, favouring the heart and brain at the expense of intestine, liver and carcass is similar to that found in mammalian fetuses of the sheep (Jensen et al 1991;Peeters et al 1979), rhesus monkey (Jackson, Piasecki & Novy, 1987) and llama (Giussani et al 1996). Since the chick embryo is independent of the mother, the similarity in response to hypoxia suggests that in the mammalian fetus such responses may occur independently of maternal or placental factors.…”

Section: Discussion Response To Hypoxiasupporting

confidence: 72%

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Mulder

Golde

Prinzen

et al. 1998

The Journal of Physiology

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The fetus develops cardiovascular adaptations to protect vital organs in situations such as hypoxia and asphyxia. These include bradycardia, increased systemic blood pressure and redistribution of the cardiac output. The extent to which they involve maternal or placenta influences is not known. The objective of the present work was to study the cardiac output distribution in response to hypoxia in the chick embryo, which is independent of the mother. Fertilized eggs were studied at three incubation times (10‐13 days, 14‐16 days and 17‐19 days of a normal incubation time of 21 days). Eggs were placed in a Plexiglass box in which the oxygen concentration could be changed. Eggs were opened at the air cell and a chorioallantoic vein was catheterized. Cardiac output distribution was measured with 15 μm fluorescent microspheres injected during normoxia, during the last minute of a 5 min period of hypoxia and after 5 min of subsequent reoxygenation. Hypoxia caused a redistribution of the cardiac output in favour of heart (+17 to +160 % of baseline) and brain (+21 to +57 % of baseline) at the expense of liver (‐3 to ‐65 % of baseline), yolk‐sac (‐46 to ‐77 % of baseline) and carcass (‐6 to ‐33 % of baseline). The magnitude of the changes in cardiac output distribution to the heart, brain, liver and carcass in response to hypoxia increased with advancing incubation time. The data demonstrate the development of a protective redistribution of the cardiac output in response to hypoxia in the chick embryo from day 10 of incubation.

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Section: Discussion Response To Hypoxiasupporting

confidence: 72%

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Mulder

Golde

Prinzen

et al. 1998

The Journal of Physiology

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“…The generic fetal response to acute hypoxia includes hypertension (17,19,20), bradycardia (19), and elevated catecholamine (17,20) and lactate levels (6,15,36). In chicken embryos, however, acute hypoxia elicits hypotension (12).…”

Section: Discussionmentioning

confidence: 99%

Hypotension in the chronically hypoxic chicken embryo is related to the β-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia

Lindgren

Crossley

Villamor

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Lindgren I, Crossley II D, Villamor E, Altimiras J. Hypotension in the chronically hypoxic chicken embryo is related to the ␤-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia. Am J Physiol Regul Integr Comp Physiol 301: R1161-R1168, 2011. First published July 27, 2011; doi:10.1152/ajpregu.00458.2010.-Prolonged fetal hypoxia leads to growth restriction and can cause detrimental prenatal and postnatal alterations. The embryonic chicken is a valuable model to study the effects of prenatal hypoxia, but little is known about its long-term effects on cardiovascular regulation. We hypothesized that chicken embryos incubated under chronic hypoxia would be hypotensive due to bradycardia and ␤AR-mediated relaxation of the systemic and/or the chorioallantoic (CA) arteries. We investigated heart rate, blood pressure, and plasma catecholamine levels in 19-day chicken embryos (total incubation 21 days) incubated from day 0 in normoxia or hypoxia (14 -15% O2). Additionally, we studied ␣-adrenoceptor (␣AR)-mediated contraction, relaxation to the ␤-adrenoceptor (␤AR) agonist isoproterenol, and relaxation to the adenylate cyclase activator forskolin in systemic (femoral) and CA arteries (by wire myography). Arterial pressure showed a trend toward hypotension in embryos incubated under chronic hypoxic conditions compared with the controls (mean arterial pressure 3.19 Ϯ 0.18 vs. 2.59 Ϯ 0.13 kPa, normoxia vs. hypoxia, respectively. P ϭ 0.056), without an accompanied bradycardia and elevation in plasma norepinephrine and lactate levels. All vessels relaxed in response to ␤AR stimulation with isoproterenol, but the CA arteries completely lacked an ␣AR response. Furthermore, hypoxia increased the sensitivity of femoral arteries (but not CA arteries) to isoproterenol. Hypoxia also increased the responsiveness of femoral arteries to forskolin. In conclusion, we suggest that hypotension in chronic hypoxic chicken embryos is the consequence of elevated levels of circulating catecholamines acting in vascular beds with exclusive (CA arteries) or exacerbated (femoral arteries) ␤AR-mediated relaxation, and not a consequence of bradycardia. prenatal hypoxia; hypoxic hypotension; chorioallantoic membrane; ␤-adrenoceptors; ␣-adrenoceptors

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“…For fetal cardiovascular variables, absolute values and absolute changes from mean normoxic baseline during the acute hypoxemia protocol were first analyzed by the summary measures method (44). This well-documented process focuses on the number of comparisons, simplifies the data analysis, and helps prevent statistical invalidity when multiple measurements are made on the same individuals (25,26,44). Functional chemoreflex analysis was performed to assess the effects of advancing gestation on fetal cardiac and vasomotor chemoreflex responses.…”

Section: Data and Statistical Analysesmentioning

confidence: 99%

Development of the ovine fetal cardiovascular defense to hypoxemia towards full term

Fletcher¹,

Gardner²,

Edwards³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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. Development of the ovine fetal cardiovascular defense to hypoxemia towards full term. Am J Physiol Heart Circ Physiol 291: H3023-H3034, 2006. First published July 21, 2006 doi:10.1152/ajpheart.00504.2006.-We tested the hypothesis that fetal cardiovascular responses to hypoxemia change close to full term in relation to the prepartum increase in fetal basal cortisol and investigated, in vivo, the neural and endocrine mechanisms underlying these changes. Fetal heart rate and peripheral hemodynamic responses to 1 h of hypoxemia were studied in 25 chronically instrumented sheep within three narrow gestational age ranges: 125-130 (n ϭ 13), 135-140 (n ϭ 6), and Ͼ140 (n ϭ 6) days (full term ϳ145 days). Chemoreflex function and plasma concentrations of vasoconstrictor hormones were measured. Reductions in fetal arterial PO2 during hypoxemia were similar at all ages. At 125-130 days, hypoxemia elicited transient bradycardia, femoral vasoconstriction, and increases in plasma concentrations of catecholamines, neuropeptide Y (NPY), AVP, ACTH, and cortisol. Close to full term, in association with the prepartum increase in fetal basal cortisol, there was a developmental increase in the magnitude and persistence of fetal bradycardia and in the magnitude of the femoral constrictor response to hypoxemia. The mechanisms mediating these changes close to full term included increases in the gain of chemoreflex function and in the magnitudes of the fetal NPY and AVP responses to hypoxemia. Data combined irrespective of gestational age revealed significant correlations between fetal basal cortisol and fetal bradycardia, femoral resistance, chemoreflex function, and plasma AVP concentrations. The data show that the fetal cardiovascular defense to hypoxemia changes in pattern and magnitude just before full term because of alterations in the gain of the neural and endocrine mechanisms mediating them, in parallel with the prepartum increase in fetal basal cortisol.fetus; prepartum cortisol surge; glucocorticoid IN ALL MAMMALIAN SPECIES studied to date, fetal basal cortisol concentration increases immediately before full term (23). In the ovine fetus, this increase in plasma cortisol begins in the last 15 days of gestation, at ϳ130 days (full term ϳ145 days) (3, 43), and increases most dramatically within the last 5 days before delivery, between 140 and 145 days. The prepartum cortisol surge is known to be an important factor in the developmental maturation of fetal tissues and physiological systems in preparation for the transition to neonatal life (23). For example, the prepartum maturation of basal cardiovascular function in the fetus is influenced by cortisol. The developmental increase in ovine fetal mean arterial blood pressure (FBP) and fall in fetal heart rate (FHR) are prevented by fetal adrenalectomy and restored to normal by cortisol replacement (63). Similarly, the prepartum cortisol surge has been associated with developmental changes in the basal activity of many fetal endocrine vasoconstrictor mechanisms, such as the norad...

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Chemoreflex and endocrine components of cardiovascular responses to acute hypoxemia in the llama fetus

Cited by 40 publications

References 17 publications

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Hypotension in the chronically hypoxic chicken embryo is related to the β-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia

Development of the ovine fetal cardiovascular defense to hypoxemia towards full term

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