The Chicken Embryo in Developmental Physiology of the Cardiovascular System: A Traditional Model with New Possibilities

Ruijtenbeek, K.; Mey, Jo G. R. De; Blanco, Carlos E.

doi:10.1152/ajpregu.00107.2002

Cited by 33 publications

(37 citation statements)

References 36 publications

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“…Chicken embryos have a mammalian-like circulation, with an extraembryonic circuit involved in the gas exchange (the chorioallantois), analogous to the placenta, and they maintain bilaterally developed DA (3). During the past few years, our group has analyzed developmental changes in reactivity of chicken embryo systemic and pulmonary arteries (26,38,51,52). In the present study, we hypothesized that the responsiveness of the chicken embryo DA to O 2 and other vasoconstrictors is developmentally regulated.…”

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confidence: 97%

Ontogeny of chicken ductus arteriosus response to oxygen and vasoconstrictors

Ågren¹,

Cogolludo²,

Kessels³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

108

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The present study aimed to characterize the contractile reactivity of the chicken ductus arteriosus (DA) from the last stage of prenatal development and throughout the perinatal period. Isolated DA rings from 15-day, noninternally-pipped 19-day, and externally-pipped 21-day embryos were studied using myograph techniques. On embryonic day 15, the chicken DA did not respond to O 2 (0 to 21%), norepinephrine (NE), or phenylephrine (Phe) but contracted in response to high-K ϩ solution, the inhibitor of voltage-gated channels 4-aminopyridine, U-46619, and endothelin (ET)-1. These responses increased with advancing incubation age. Contractile responses to O 2, NE, and Phe were present in the 19-and 21-day embryo. Oxygen-induced contraction was restricted to the pulmonary side of the DA and was augmented by the nitric oxide synthase inhibitor N -nitro-L-arginine methyl ester and the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and reduced by the peptidic ET A and ETB-receptor antagonist PD-142,893. Transmural electrical stimulation of nerves, the nonselective cyclooxygenase (COX) inhibitor indomethacin, the COX-1 inhibitor valeryl salicylate, the COX-2 inhibitor nimesulide, the inhibitor of ATP-sensitive K ϩ channels glibenclamide, and the inhibitor of Ca 2ϩ -activated K ϩ channels tetraethylammonium did not cause contraction of the DA rings at any age. We conclude that transition to ex ovo life is accompanied by dramatic changes in chicken DA reactivity. At 0.7 incubation, excitation-contraction and pharmacomechanical coupling for several contractile agonists are already present, whereas the constrictor effects of O 2 and cathecolamines appear later in development and are located in the pulmonary side of the DA. ductus arteriosus; chicken embryo; potassium channels; oxygen sensing; cathecolamines.THE DUCTUS ARTERIOSUS (DA) is a vessel that connects the pulmonary artery to the aorta and provides, during the fetal life, a pulmonary-to-systemic diversion that shunts more than half of the right ventricle output away from the nonventilated lungs into the systemic circulation (43, 47). The main factors maintaining patency of the DA in utero are low O 2 tension, high levels of circulating PGE 2 , and locally produced PGE 2 and PGI 2 (24, 43). Failure of DA closure after birth is a common complication of premature delivery that is still presenting challenges in terms of diagnosis, assessment, and treatment options (43).Although the isolated DA is sensitive to a wide range of contractile agonists, the major factor actively stimulating contraction at birth is increasing O 2 tension, which has a profound effect on the DA, both directly and by modulating its response to vasodilators and vasoconstrictors (43). To constrict properly after birth, the DA prepares itself for this specific task from a quite early onset during development (3). This preparation is reflected by changes in responsiveness with advancing gestational age. These have been extensively characterized in numerous mammalian specie...

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mentioning

confidence: 97%

Ontogeny of chicken ductus arteriosus response to oxygen and vasoconstrictors

Ågren¹,

Cogolludo²,

Kessels³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

108

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“…The possibility of studying fetal physiology in the absence of direct maternal effects has made the chicken embryo a valuable and increasingly used model to study hypoxic effects on prenatal growth and development (18,24,37,45,47). In common with the sheep fetus, the chicken embryo also shows a CO redistribution and an initial bradycardic response to acute hypoxia (12,32), but the chemoreflex that activates both the vagal and sympathetic pathways causing bradycardia and hypertension in the sheep (16) is not present in the chicken embryo, which shows a significant hypotensive response to acute hypoxia (12).…”

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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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“…The 'fetal origins' hypothesis proposes that adverse intrauterine environment results in developmental adaptations that permanently change structure, physiology, and metabolism, thereby predisposing individuals to cardiovascular, metabolic, and endocrine disease in adult life [7] . The chick embryo seems to be an interesting animal model to study mechanisms in the intriguing new fi eld of developmental physiology that deals with the prenatal programming of cardiovascular pathology [7,12] .…”

Section: Discussionmentioning

confidence: 99%

“…The chick embryo model provides an advantageous system for the study of the infl uence of prenatal adverse events on cardiovascular development [7] . Since the embryo develops outside the mother, effects of external stresses can be studied independently of any confounding infl uences from alterations in maternal hormonal, metabolic, or hemodynamic status [7] .…”

mentioning

confidence: 99%

“…Since the embryo develops outside the mother, effects of external stresses can be studied independently of any confounding infl uences from alterations in maternal hormonal, metabolic, or hemodynamic status [7] . Previous studies of our group characterized the structure and reactivity of pulmonary and systemic arteries of the chick from embryonic day 15 (of the 21 days of incubation) and evaluated the cardiovascular effects of the exposure to hypoxia, tobacco smoke extract, or malnutrition [8][9][10][11][12][13][14] .…”

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confidence: 99%

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Cardiopulmonary Effects of Chronic Administration of the NO Synthase Inhibitor L-NAME in the Chick Embryo

Villamor

Kessels

Suylen³

et al. 2005

Neonatology

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Background: Experimental observations in mammalian models suggest that endothelial nitric oxide (NO) synthase (NOS) content and activity are decreased in persistent pulmonary hypertension of the newborn. Objectives: To test the hypothesis that disruption of NO signaling in the developing chick embryo lung may contribute to pulmonary hypertension. Methods: We analyzed pulmonary arterial reactivity and structure and heart morphology of 19-day chick embryos (incubation time 21 days) that received a daily injection of the NOS inhibitor Nω-nitro-L-arginine methyl ester (L-NAME, 20 µg per gram egg) or vehicle from day 12 until day 18. Results: Exposure to L-NAME did not affect embryonic survival or body mass of the embryos. The contractile responses to KCl, endothelin-1, the thromboxane A₂ mimetic U46619, noradrenaline, and electrical-field stimulation were not affected by exposure to L-NAME. In contrast, in ovo L-NAME exposure reduced the sensitivity of pulmonary arteries to acetylcholine (pD₂: 6.53 ± 0.14 vs. 6.96 ± 0.13; p < 0.05) and this effect was reversed by the NOS substrate L-arginine. Relaxations induced by sodium nitroprusside or forskolin were not altered by chronic L-NAME. Pulmonary vessel density was not different, but the percentage medial wall area of small pulmonary arteries (external diameter 10–50 µm) was slightly but significantly increased in the embryos exposed to L-NAME. In addition, hearts of L-NAME-exposed embryos showed an increase in right and left ventricular wall area. Conclusions: Chronic inhibition of NOS produced, in the chick embryo, impairment of endothelium-dependent relaxation, structural remodeling of the pulmonary vascular bed and biventricular cardiac enlargement.

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The Chicken Embryo in Developmental Physiology of the Cardiovascular System: A Traditional Model with New Possibilities

Cited by 33 publications

References 36 publications

Ontogeny of chicken ductus arteriosus response to oxygen and vasoconstrictors

Ontogeny of chicken ductus arteriosus response to oxygen and vasoconstrictors

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

Cardiopulmonary Effects of Chronic Administration of the NO Synthase Inhibitor L-NAME in the Chick Embryo

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