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Journal articles on the topic 'Chick heart'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Boehm, C., T. R. Johnson, J. D. Caston, and R. J. Przybylski. "Cardiac hypertrophy in chick embryos induced by hypothermia." American Journal of Physiology-Cell Physiology 252, no. 1 (January 1, 1987): C97—C104. http://dx.doi.org/10.1152/ajpcell.1987.252.1.c97.

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A decrease in incubation temperature from 38 to 32 degrees C elicits a decrease in chicken embyro size and weight with concomitant heart enlargement if done after day 10 of incubation. When assayed at day 18 of incubation with the hypothermia started on day 11 or 14, evidence is presented that the heart enlargement is an hypertrophy with no detectable hyperplasia. Supporting data are presented for various physical parameters showing increases in heart wet and dry weight, volume, area, wall thickness, and cell size. There was little difference in DNA content and nuclear [3H]thymidine labeling index between hearts of control and hypothermic embryos. Hearts of hypothermic embryos showed a slight increase in water content and considerable increases in RNA, protein, and glycogen content per unit DNA. The average size of polysomes isolated from hypothermic hearts was larger than that of polysomes isolated from controls. Microscopic studies showed no obvious increase in amount of capillary beds, connective tissue, and myocardial cells. Annulate lamellae were found only in myocardial cells of hypothermic embryos in sparse amounts and low frequency but always associated with large deposits of glycogen.

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2

Anderson, R. H. "The developing heart in chick embryos." Circulation 82, no. 4 (October 1990): 1542–43. http://dx.doi.org/10.1161/circ.82.4.2401086.

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3

Janikovičová, L., Z. Demčišáková, L. Luptáková, and Petrovová E. "Pre-Incubation and its Effect on the Development and Malformations of The Chick Embryo." Folia Veterinaria 63, no. 1 (March 1, 2019): 24–31. http://dx.doi.org/10.2478/fv-2019-0004.

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Abstract This study was conducted to evaluate the effect of eggs stored with and without pre-incubation on chick embryos with emphasis on: embryo body, heart weight, malformations, and mortality. For this study, a total of 120 chick embryos were divided into three groups, based on the length of storage before hatching (3, 7 and 10 days). Observations of the weight of chick embryo bodies, chick embryo hearts, and the level of mortality and appearance of malformations were noted. With an increase in days stored, the chick embryo’s weight decreased. The pre-incubation period had a positive effect on the weight of chick embryo, and chick hearts. Malformations, including: hydrocephalus, open body cavity and underdeveloped wings, were observed in all three groups, with the highest proportion seen in the pre-incubated hatching eggs stored for 10 days; this group also displayed the highest level of mortality. Non-pre-incubated eggs showed the most promise with better results in all experimental groups. In conclusion, the research suggests the optimal storage for chick embryos to be 3 days, with lowest levels of mortality, malformations and limited effects on the body and heart weight.

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4

Hoyle, C., N. A. Brown, and L. Wolpert. "Development of left/right handedness in the chick heart." Development 115, no. 4 (August 1, 1992): 1071–78. http://dx.doi.org/10.1242/dev.115.4.1071.

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The chick heart tube develops from the fusion of the right and left areas of precardiac mesoderm and in almost all cases loops to the embryo's right-hand side. We have investigated whether any intrinsic difference exists in the right and left areas of precardiac mesoderm, that influences the direction of looping of the heart tube. Chick embryos incubated to stages 4,5 and 6 were cultured by the New method. Areas of precardiac mesoderm were exchanged between donor and host embryos of the same stage and different stages to form control, double-right and double-left sided embryos. Overall, double-right sided embryos formed many more left-hand loops than double-left sided embryos. At stages 4 and 5 a small percentage of double-right embryos formed left-hand loops (13%) whereas at stage 6 almost 50% of hearts had left-hand loops. Control embryos formed right-hand loops in 97% of cases. The stability of right-hand heart looping by double-left sided embryos, may be related to the process of ‘conversion’, whereas the direction of looping by double-right sided embryos has become randomised. There is some indication that an intrinsic change occurred in the precardiac mesoderm between stages 5 and 6 that later influenced the direction of looping of the heart tube. The direction of body turning is suggested to be linked to the direction of heart looping.

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5

Bkaily, G., A. Sculptoreanu, D. Jacques, D. Economos, and D. Menard. "Apamin, a highly potent fetal L-type Ca2+ current blocker in single heart cells." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 2 (February 1, 1992): H463—H471. http://dx.doi.org/10.1152/ajpheart.1992.262.2.h463.

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Apamin, a bee venom polypeptide, was reported to block the naturally occurring Ca2+ slow action potentials (APs) in cultured cell reaggregates from old chick hearts [Bkaily, G. et al. Am. J. Physiol. 248 (Heart Circ. Physiol. 17): H961-H965, 1985] as well as the tetrodotoxin (TTX)- and Mn(2+)-insensitive slow Na+ current in young embryonic chick heart cells (Bkaily, G. In Vitro Toxicology. Academic, In press; Bkaily et al. J. Mol. Cell. Cardiol. 23: 25-39, 1991). With the use of the whole cell voltage-clamp technique in single ventricular cells from 10-day-old chick embryos and 17- to 20-wk-old human fetuses, two types of Ca2+ currents (ICa), T and L, were found. These two types of slow inward current in both heart preparations were nearly similar in their voltage, kinetics, and pharmacology. Apamin, a slow Ca2+ action potential blocker in old embryonic chick heart, was found to block the L-type ICa (IL) in a dose-dependent manner without affecting the T-type ICa in both heart cell preparations. The blockade of the IL by apamin was completely reversible upon washout with apamin-free solution. Therefore, when compared with nifedipine or to PN 200-110, apamin seems to be a highly potent L-type Ca2+ channel blocker in heart cells.

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6

Barnett, J. V., M. Taniuchi, M. B. Yang, and J. B. Galper. "Co-culture of embryonic chick heart cells and ciliary ganglia induces parasympathetic responsiveness in embryonic chick heart cells." Biochemical Journal 292, no. 2 (June 1, 1993): 395–99. http://dx.doi.org/10.1042/bj2920395.

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We have developed a system for the co-culture of embryonic chick heart cells obtained from embryos at 3.5 days in ovo with ciliary ganglia from chick embryos at 7 days in vivo. After 3 days of co-culture, removal of the ciliary ganglia resulted in complete degeneration of axons within 6-8 h, leaving the post-innervated heart cell culture devoid of neurons. Embryonic chick heart cells at 3.5 days in ovo are unresponsive to muscarinic stimulation. However, following 3 days of co-culture with ciliary ganglia, the heart cells developed a negative chronotropic response to muscarinic stimulation (paired t test, P < 0.02) which persisted for at least 24 h after removal of the ciliary ganglion. The development of muscarinic responsiveness was associated with an increase in the levels of specific alpha-subunits of the guanine nucleotide binding proteins (G-proteins), with a 3-fold increase in the level of alpha 39 (39 kDa subunit) and a 2.5-fold increase in the level of alpha 41. The level of the G-protein subunit alpha s remained unchanged. Culture of embryonic chick heart cells at 3.5 days in ovo with medium conditioned by the growth of embryonic chick heart cells and ciliary ganglia had an effect on the chronotropic response to muscarinic stimulation and on alpha 39 and alpha 41 levels identical to that of co-culture. These data suggest that a soluble factor released during the co-culture of embryonic chick heart cells and ciliary ganglia is capable of inducing muscarinic responsiveness. These studies suggest that innervation of the heart may induce parasympathetic responsiveness by increasing the availability of G-proteins which couple the muscarinic receptor to a physiological response.

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7

Raddatz, E., M. Servin, and P. Kucera. "Oxygen uptake during early cardiogenesis of the chick." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1224—H1230. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1224.

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Oxidative metabolism of the isolated embryonic heart of the chick has been determined using a spectrophotometric technique allowing global as well as localized micromeasurements of the O2 uptake. Entire hearts, excised from embryos of 10 somites (primordia fused, stage 10 HH) and 40 somites (S shaped, stage 20 HH) were placed in a special chamber under controlled metabolic conditions where they continued to beat spontaneously and regularly. During the 32 h of development, the O2 consumption of the whole heart increased from 0.9 +/- 0.1 to 5.3 +/- 0.8 nmol O2/h. These values corrected for protein content were, however, comparable (0.45 nmol O2.h-1.micrograms-1). At stage 10-12, the O2 uptake varied along the cardiac tube (from 0.74 to 1.0 nmol O2.h-1.mm-2). From stage 10 to 20, the O2 uptake per unit area of ventricle wall increased from 0.7 +/- 0.2 to 1.8 +/- 0.2 nmol O2.h-1.mm-2, and the O2 uptake per myocardial volume during one cardiac cycle varied from 7 to 2.5 nmol O2/cm3. These results indicate that, despite an intense morphogenesis, the cardiac tissue has a rather low and stable oxidative metabolism, although the O2 requirement of the whole heart increases significantly. Moreover, the normalized suprabasal aerobic energy expenditure decreases throughout early cardiogenesis. The functional integrity of the isolated embryonic heart combined with the experimental possibilities of the microtechnique make the preparation appropriate for studying the changes in cardiac metabolism during development.

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8

Taber, Larry A., and Renato Perucchio. "Stress-Strain Relations in Embryonic Chick Heart." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (July 1, 2001): H463—H466. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h463.

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9

STONE, BRADLEY A., MELVYN LIEBERMAN, and WANDA KRASSOWSKA. "Field Stimulation of Isolated Chick Heart Cells." Journal of Cardiovascular Electrophysiology 10, no. 1 (January 1999): 92–107. http://dx.doi.org/10.1111/j.1540-8167.1999.tb00646.x.

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10

Kagawa, K., and H. Kagawa. "DNA modification in chick heart and cerebrum." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 138, no. 2 (June 2004): 147–60. http://dx.doi.org/10.1016/j.cbpb.2004.03.001.

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11

Hu, H., and F. Sachs. "Mechanically Activated Currents in Chick Heart Cells." Journal of Membrane Biology 154, no. 3 (December 1, 1996): 205–16. http://dx.doi.org/10.1007/s002329900145.

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12

Choy, Michael, Sharon Oltjen, Dorothy Ratcliff, Margaret Armstrong, and Peter Armstrong. "Fibroblast behavior in the embryonic chick heart." Developmental Dynamics 198, no. 2 (October 1993): 97–107. http://dx.doi.org/10.1002/aja.1001980204.

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13

Yamagishi, Toshiyuki, Yuji Nakajima, Shin-Ichiro Nishimatsu, Tsutomu Nohno, Katsumi Ando, and Hiroaki Nakamura. "Expression oftbx20 RNA during chick heart development." Developmental Dynamics 230, no. 3 (2004): 576–80. http://dx.doi.org/10.1002/dvdy.20076.

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14

Moriya, Kenji, Yuya Chiba, and Yoshiko Maruyama. "Spectrum Analysis of Heart Rate Fluctuations in Hatched and Unhatched Prenatal Chick Embryos." Journal of the Institute of Industrial Applications Engineers 6, no. 3 (July 25, 2018): 107–11. http://dx.doi.org/10.12792/jiiae.6.107.

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15

Sedmera, David. "HLHS: Power of the Chick Model." Journal of Cardiovascular Development and Disease 9, no. 4 (April 11, 2022): 113. http://dx.doi.org/10.3390/jcdd9040113.

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Background: Hypoplastic left heart syndrome (HLHS) is a rare but deadly form of human congenital heart disease, most likely of diverse etiologies. Hemodynamic alterations such as those resulting from premature foramen ovale closure or aortic stenosis are among the possible pathways. Methods: The information gained from studies performed in the chick model of HLHS is reviewed. Altered hemodynamics leads to a decrease in myocyte proliferation causing hypoplasia of the left heart structures and their functional changes. Conclusions: Although the chick phenocopy of HLHS caused by left atrial ligation is certainly not representative of all the possible etiologies, it provides many useful hints regarding the plasticity of the genetically normal developing myocardium under altered hemodynamic loading leading to the HLHS phenotype, and even suggestions on some potential strategies for prenatal repair.

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16

Oštádalová, I., and B. Oštádal. "85Sr uptake by the chick embryonic heart: Effect of high doses of isoproterenol." Canadian Journal of Physiology and Pharmacology 70, no. 7 (July 1, 1992): 959–62. http://dx.doi.org/10.1139/y92-131.

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The aim of the present study was to establish whether intraamnial administration of toxic doses of isoproterenol to chick embryos increases cardiac accumulation of strontium, the homologue element of calcium. It has been shown that the ability of embryonic tissues (blood, heart, and liver) to accumulate 85Sr decreases significantly during ontogeny. Administration of isoproterenol to chick embryos did not elevate the concentration of 85Sr in the heart. It seems, therefore, that isoproterenol-induced developmental changes in the chick embryonic myocardium are not necessarily due to intracellular calcium (as measured by 85Sr) overload.Key words: heart, isoproterenol, radiostrontium, chick embryo.

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17

Höchel, Joachim, Ryuichi Akiyama, Takuya Masuko, James T. Pearson, Martin Nichelmann, and Hiroshi Tazawa. "Development of heart rate irregularities in chick embryos." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 2 (August 1, 1998): H527—H533. http://dx.doi.org/10.1152/ajpheart.1998.275.2.h527.

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Heart rate (HR) irregularities in chick embryos were defined as large fluctuations (>10 beats/min) comprising irregular, brief deceleration and/or acceleration of instantaneous HR (IHR). IHR was determined directly from the arterial blood pressure while adequate gas exchange was maintained through an eggshell and chorioallantoic membrane. Five embryos were examined on each day from day 11 to day 19 of incubation. Baseline HR was stable until day 12–13, and on around day 13–14 transient, rapid deceleration of HR (termed V pattern) began to appear, with a subsequent increase in its frequency and magnitude. The acceleration patterns (lambda, avian omega, and periodic patterns) appeared later, and the IHR became increasingly irregular, with additional, spontaneous deceleration and acceleration patterns toward hatching. Additional experiments with intravenous administration of autonomic drugs clearly showed that rapid deceleration of HR was mediated by parasympathetic nervous function but did not always show clear relations of sympathomimetic and sympathetic blocking agents to the acceleration patterns.

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18

Clay, J. R., C. E. Hill, D. Roitman, and A. Shrier. "Repolarization current in embryonic chick atrial heart cells." Journal of Physiology 403, no. 1 (September 1, 1988): 525–37. http://dx.doi.org/10.1113/jphysiol.1988.sp017262.

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19

Abu-Issa, Radwan, and Margaret L. Kirby. "Patterning of the heart field in the chick." Developmental Biology 319, no. 2 (July 2008): 223–33. http://dx.doi.org/10.1016/j.ydbio.2008.04.014.

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20

DUNLOP, JOHN, PETER S. WHITTON, JULIAN A. DOW, and ROBIN H. C. STRANG. "Taurine concentration in cultured embryonic chick heart cells." Biochemical Society Transactions 15, no. 6 (December 1, 1987): 1042–43. http://dx.doi.org/10.1042/bst0151042.

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21

Piwnica-Worms, D., R. Jacob, C. R. Horres, and M. Lieberman. "Potassium-chloride cotransport in cultured chick heart cells." American Journal of Physiology-Cell Physiology 249, no. 3 (September 1, 1985): C337—C344. http://dx.doi.org/10.1152/ajpcell.1985.249.3.c337.

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The polystrand preparation of cultured chick heart cells has a unidirectional transmembrane Cl- efflux that is twice K+ efflux. However, Cl- conductance of this heart cell membrane is low [regardless of extracellular K+ (K+o)], suggesting the existence of electroneutral Cl--dependent transport mechanisms. Furosemide (10(-3) M) decreases the 36Cl tracer efflux rate constant from a control value of 0.67 to 0.33 min-1. Extracellular Na+--free solution, which depletes intracellular Na+ within 1 min, has no significant effect on 36Cl efflux. K+o-free solution plus 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 10(-4) M) promotes the loss of Cl- against the Cl- electrochemical gradient; Cl- loss is furosemide sensitive in a dose-dependent manner. Incubating polystrands in 133 mM K+o, normal extracellular Cl- (Cl-o) solution causes net K+ and Cl- uptake in a 1:1 stoichiometry as well as a furosemide-sensitive volume increase; 130 mM extracellular choline or Li+ cannot mimic this high-K+o-induced volume increase. Removal of Cl-o from 133 mM K+o solution prevents K+ uptake and causes a Cl- loss as well as a furosemide-sensitive volume decrease. Adjusting Cl-o concentrations in high-K+o solution plus DIDS, so that the Cl- chemical gradient equally opposes the K+ chemical gradient, prevents high-K+o-induced volume changes. These data suggest that the cardiac cell membrane contains a furosemide-sensitive K+-Cl- cotransport mechanism.

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22

Chuck, Emil T., David M. Freeman, Michiko Watanabe, and David S. Rosenbaum. "Changing Activation Sequence in the Embryonic Chick Heart." Circulation Research 81, no. 4 (October 1997): 470–76. http://dx.doi.org/10.1161/01.res.81.4.470.

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23

Osmond, M. K., A. J. Butler, F. C. Voon, and R. Bellairs. "The effects of retinoic acid on heart formation in the early chick embryo." Development 113, no. 4 (December 1, 1991): 1405–17. http://dx.doi.org/10.1242/dev.113.4.1405.

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The vitamin A derivative retinoic acid has previously been shown to have teratogenic effects on heart development in mammalian embryos. The craniomedial migration of the precardiac mesoderm during the early stages of heart formation is thought to depend on a gradient of extracellular fibronectin associated with the underlying endoderm. Here, the effects of retinoic acid on migration of the precardiac mesoderm have been investigated in the early chick embryo. When applied to the whole embryo in culture, the retinoid inhibits the craniomedial migration of the precardiac mesoderm resulting in a heart tube that is stunted cranially, while normal or enlarged caudally. Similarly, a local application of retinoic acid to the heart-forming area disrupts the formation of the cardiogenic crescent and the subsequent development of a single mid-line heart tube. This effect is analogous to removing a segment of endoderm and mesoderm across the heart-forming area and results in various degrees of cardia bifida. At higher concentrations of retinoic acid and earlier developmental stages, two completely separate hearts are produced, while at lower concentrations and later stages there are partial bifurcations. The controls, in which the identical operation is carried out except that dimethyl sulphoxide (DMSO) is used instead of the retinoid, are almost all normal. We propose that one of the teratogenic effects of retinoic acid on the heart is to disrupt the interaction between precardiac cells and the extracellular matrix thus inhibiting their directed migration on the endodermal substratum.

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24

Alser, Maha, Samar Shurbaji, and Huseyin C. Yalcin. "Mechanosensitive Pathways in Heart Development: Findings from Chick Embryo Studies." Journal of Cardiovascular Development and Disease 8, no. 4 (March 26, 2021): 32. http://dx.doi.org/10.3390/jcdd8040032.

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The heart is the first organ that starts to function in a developing embryo. It continues to undergo dramatic morphological changes while pumping blood to the rest of the body. Genetic regulation of heart development is partly governed by hemodynamics. Chick embryo is a major animal model that has been used extensively in cardiogenesis research. To reveal mechanosensitive pathways, a variety of surgical interferences and chemical treatments can be applied to the chick embryo to manipulate the blood flow. Such manipulations alter expressions of mechanosensitive genes which may anticipate induction of morphological changes in the developing heart. This paper aims to present different approaches for generating clinically relevant disturbed hemodynamics conditions using this embryonic chick model and to summarize identified mechanosensitive genes using the model, providing insights into embryonic origins of congenital heart defects.

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25

Fioranelli, Massimo, Alireza Sepehri, Maria Grazia Roccia, Cota Linda, Chiara Rossi, Amos Dawod, Petar Vojvodic, et al. "Recovery of Brain in Chick Embryos by Growing Second Heart and Brain." Open Access Macedonian Journal of Medical Sciences 7, no. 18 (August 30, 2019): 3085–89. http://dx.doi.org/10.3889/oamjms.2019.777.

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To recover chick embryos damaged the brain, two methods are presented. In both of them, somatic cells of an embryo introduced into an egg cell and an embryo have emerged. In one method, injured a part of the brain in the head of an embryo is replaced with a healthy part of the brain. In the second method, the heart of brain embryo dead is transplanted with the embryo heart. In this mechanism, new blood cells are emerged in the bone marrow and transmit information of transplantation to subventricular zone (SVZ) of the brain through the circulatory system. Then, SVZ produces new neural stem cells by a subsequent dividing into neurons. These neurons produce new neural circuits within the brain and recover the injured brain. To examine the model, two hearts of two embryos are connected, and their effects on neural circuits are observed.

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26

Qi, Z., K. Naruse, and M. Sokabe. "3R1030 Effects of amphipaths on a stretch activated BK channel(SAKCa) cloned from chick heart." Seibutsu Butsuri 42, supplement2 (2002): S206. http://dx.doi.org/10.2142/biophys.42.s206_3.

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27

Männer, Jörg. "Embryology of congenital ventriculo-coronary communications: a study on quail-chick chimeras." Cardiology in the Young 10, no. 3 (May 2000): 233–38. http://dx.doi.org/10.1017/s1047951100009161.

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AbstractVentriculo-coronary arterial communications are rare congenital heart defects which have been explained traditionally on the basis of abnormal persistence of such communications found in the normal developing heart. Recent studies, however, have suggested that these embryonic communications might be an incidental finding rather than a normal feature. Thus, it has been suggested that congenital ventriculo-coronary communications do not represent remnants of normal embryonic vessels, but rather represent acquired lesions. In the present study, hearts were constructed in embryonic chicks in which the coronary vasculature was almost completely derived from a quail-donor. After immunohistochemical staining of the quail-derived coronary endothelium, chimeric hearts were analysed with respect to the presence of embryonic ventriculo-coronary communications, and with respect to the origin of these structures from either coronary arteries or endocardium. The results demonstrate the normal presence of ventriculo-coronary communications in avian embryonic hearts. They show, furthermore, that these structures are of coronary endothelial origin. The findings are in accord with the traditional view on the pathogenesis of congenital ventriculo-coronary communications. The roles of elevated ventricular pressure, abnormal remodelling of the developing myocardium, and of abnormal growth of the coronary vasculature are discussed relative to the pathogenesis of congenital ventriculo-coronary communications.

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28

Zamir, Evan A., Varahoor Srinivasan, Renato Perucchio, and Larry A. Taber. "Mechanical Asymmetry in the Embryonic Chick Heart During Looping." Annals of Biomedical Engineering 31, no. 11 (December 2003): 1327–36. http://dx.doi.org/10.1114/1.1623487.

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29

Ruknudin, A., F. Sachs, and J. O. Bustamante. "Stretch-activated ion channels in tissue-cultured chick heart." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 3 (March 1, 1993): H960—H972. http://dx.doi.org/10.1152/ajpheart.1993.264.3.h960.

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With use of single-channel patch-clamp recording, we found five distinct types of stretch-activated ion channels (SACs) in tissue-cultured embryonic chick cardiac myocytes. With 140 mM K+ saline in the pipette, four channels had linear conductances of approximately equal to 25, 50, 100, and 200 pS and other channel was an inward rectifier of approximately equal to 25 pS at 0 mV membrane potential. The 100- and 200-pS channels were K+ selective, whereas the others passed alkali cations and Ca2+. From reversal potentials, the permeability ratio of K+/Na+, PK/PNa, was 3–7 for nonselective channels and 7–16 for K(+)-selective channels. Channel density was approximately equal to 0.3/microns2 for linear conductances and approximately equal to 0.1/microns2 for inward rectifier. Open-channel noise was a function of pipette filling solution with root-mean-square (RMS) noise increasing in the order K+ < isosmotic sucrose (plus trace ions) < Na+, probably reflecting short-lived block by extracellular ions. All channels were blocked by 20 microM Gd3+. The 25-pS linear channel was also blocked by 12.5 microM tetrodotoxin and 10 microM diltiazem, but the others were insensitive at these concentrations. Extracellular Cs+ and tetraethylammonium chloride did not block any channels. We saw no SAC activity in cells grown without embryo extract (EE), which demonstrates that channel expression, or some necessary cofactor, is under control of growth factors. Basic fibroblast growth factor (FGF) could replace EE in supporting channel expression. The presence of SACs capable of generating inward currents might explain how stretch increases automaticity in the heart. Because some SACs were permeable to Ca2+, they could contribute to the Starling curve and perhaps to initiating stretch-induced hypertrophy.

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30

Clapham, D. E., and D. E. Logothetis. "Delayed rectifier K+ current in embryonic chick heart ventricle." American Journal of Physiology-Heart and Circulatory Physiology 254, no. 1 (January 1, 1988): H192—H197. http://dx.doi.org/10.1152/ajpheart.1988.254.1.h192.

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Single ventricular cells from 7- to 10-day-old embryonic chicks were studied with the use of whole cell, outside-out, and cell-attached patch-clamp techniques. The macroscopic delayed rectifier current, IK, activated at membrane potentials above -25 mV. Peak IK at +40 mV was 103 +/- 20 pA (5.7 +/- 1 microA/cm2). IK was selective for K ions with reversal potentials close to the Nernst equilibrium potentials. The onset of current during a voltage step was sigmoidal and was fit by the function IK = IKoo (1-e-t/tau)2. The peak time constant of activation was greater than 6 s at -25 mV (22 degrees C). Significant inactivation was not observed. IK was blocked by intracellular cesium, extracellular 1 mM 4-aminopyridine, 20 mM tetraethylammonium chloride, and 1 mM barium chloride. Single-channel recordings revealed a K+-selective channel with a slope conductance of 15 pS (extracellular [K+] = 4 mM, intracellular [K+] = 145 mM). An ensemble average of consecutive single-channel traces reproduced the whole cell current. The single-channel density was approximately 0.04/micron 2 based on frequency of patches containing the 15-pS single conductance. Approximately 100 channels/cell would sum to account for the net IK. We have described for the first time a channel underlying the main delayed rectifier current and, as such, a main repolarization current in chick ventricle.

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31

Yamagishi, Toshiyuki, Yuji Nakajima, Katsumi Ando, Masahide Sakabe, and Hiroaki Nakamura. "Expression patterns of sox9 gene during chick heart development." Developmental Biology 319, no. 2 (July 2008): 604. http://dx.doi.org/10.1016/j.ydbio.2008.05.443.

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32

Shrier, A., and J. R. Clay. "Repolarization currents in embryonic chick atrial heart cell aggregates." Biophysical Journal 50, no. 5 (November 1986): 861–74. http://dx.doi.org/10.1016/s0006-3495(86)83527-5.

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33

Sedmera, David, Michel Grobéty, Christophe Reymond, Pascal Baehler, Pavel Kucera, and Lukas Kappenberger. "Pacing-Induced Ventricular Remodeling in the Chick Embryonic Heart." Pediatric Research 45, no. 6 (June 1999): 845–52. http://dx.doi.org/10.1203/00006450-199906000-00011.

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34

Romano, Roberto, Anne-Catherine Rochat, Pavel Kucera, Yves de Ribaupierre, and Eric Raddatz. "Oxidative and Glycogenolytic Capacities within the Developing Chick Heart." Pediatric Research 49, no. 3 (March 2001): 363–72. http://dx.doi.org/10.1203/00006450-200103000-00010.

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35

Ahmed, N. A., N. M. Radwan, A. S. Al-Zahaby, and M. M. Abd El-Salam. "Reserpine effects on neurotransmitters in chick heart during growth." Journal of Physiology-Paris 91, no. 2 (April 1997): 81–90. http://dx.doi.org/10.1016/s0928-4257(97)88942-5.

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36

Lin, I.-En, and Larry A. Taber. "Mechanical effects of looping in the embryonic chick heart." Journal of Biomechanics 27, no. 3 (March 1994): 311–21. http://dx.doi.org/10.1016/0021-9290(94)90007-8.

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37

Anderson, Claire, Bill Hill, Hui-Chun Lu, Adam Moverley, Youwen Yang, Nidia M. M. Oliveira, Richard A. Baldock, and Claudio D. Stern. "A 3D molecular atlas of the chick embryonic heart." Developmental Biology 456, no. 1 (December 2019): 40–46. http://dx.doi.org/10.1016/j.ydbio.2019.07.003.

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38

Murphy, E., D. M. Wheeler, A. LeFurgey, R. Jacob, L. A. Lobaugh, and M. Lieberman. "Coupled sodium-calcium transport in cultured chick heart cells." American Journal of Physiology-Cell Physiology 250, no. 3 (March 1, 1986): C442—C452. http://dx.doi.org/10.1152/ajpcell.1986.250.3.c442.

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In cultured embryonic chick heart cells, alterations of extracellular Na (Nao) and Ca (Cao), intracellular Na (Nai) and Ca, extracellular pH, and membrane potential resulted in changes in Na and Ca contents that were consistent with sarcolemmal Na-Ca exchange. 24Na efflux measurements revealed a large ouabain-insensitive component, one-third of which was inhibited by removal of Cao. Incubating the cells in Na-free solution resulted in a rapid, 1.5- to 2-fold increase in total cell Ca that remained elevated for at least 15 min. Cells exposed for 15 min to Nao less than or equal to 20 mM became maximally loaded with Ca, whereas Ca loading fell off sharply at values of Nao greater than 20 mM. The movement of Na against its electrochemical gradient was shown to be associated with Ca accumulation. During Na-K pump inhibition (in 10(-4) M ouabain), Na initially rose 2- to 3-fold to a level below its equilibrium value; then, lowering Cao for 30 min from 1.25 to 0.75 mM caused a 26% elevation in Nai, whereas raising Cao from 1.25 to 2.7 mM resulted in a 25% fall in Nai against its electrochemical gradient. These data are consistent with Nai being maintained by a Na-Ca exchange during Na-K pump inhibition. In the presence of ouabain (10(-4) M), Ca uptake into intracellular organelles, e.g., mitochondria, was suggested by an increase in total cell Ca as well as the occurrence of mitochondrial matrix granules, which were shown qualitatively by X-ray analysis to contain Ca. Although matrix granules also occurred in mitochondria during Na-free incubation, they did not contain detectable amounts of Ca when examined under identical conditions of fixation and analysis.

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39

Rotevatn, S., E. Murphy, L. A. Levy, B. Raju, M. Lieberman, and R. E. London. "Cytosolic free magnesium concentration in cultured chick heart cells." American Journal of Physiology-Cell Physiology 257, no. 1 (July 1, 1989): C141—C146. http://dx.doi.org/10.1152/ajpcell.1989.257.1.c141.

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Cytosolic free magnesium (Mgi) was measured in embryonic chick heart cells loaded with one of two newly developed 19F nuclear magnetic reasonance (NMR)-sensitive magnesium chelators, 4-methyl,5-fluoro-2-aminophenol-N,N,O-triacetate (MF-APTRA) and 5-fluoro-2-aminophenol-N,N,O-triacetate (5F-APTRA). The cells, embedded in strands of collagen, were superfused at a rate that allowed for solution changes in 2 min. In this preparation 19F- and 31P-NMR spectra were stable for at least 3.5 h. Because Na-coupled Mg countertransport may be a possible mechanism of Mg transport, in some experiments extracellular Na was reduced to 1 mM (choline substituted). This manipulation caused a 2.5-fold increase in Mgi from the basal level of 0.56 mM. A significant proportion of this increase in Mgi could be secondary to an increase in Cai that occurs with low extracellular Na (Nao) perfusion (Nai-Cao exchange). Perfusing cells with nominally Ca-free, 1 mM Na salt solution substantially attenuated the increase in Mgi that occurred with Ca present (1.25 mM) in the low Na (1 mM) solution. Furthermore, perfusion with 1 mM Na, Mg-free salt solution caused a 1.5-fold increase in Mgi, which cannot be attributable to Nai-Mgo exchange. Therefore attempts to describe the regulation of Mgi in heart cells must differentiate between the effects of Nai-Mgo exchange and competition for binding sites that are secondary to stimulation of ion gradient-coupled mechanisms.

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40

Cayré, R., P. Valencia-Mayoral, V. Coffe-Ramírez, C. Sánchez-Gómez, P. Angelini, and M. V. de la Cruz. "The Right Atrioventricular Valvular Apparatus in the Chick Heart." Cells Tissues Organs 148, no. 1 (1993): 27–33. http://dx.doi.org/10.1159/000147519.

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41

Liang, Bruce T., and Brett Haltiwanger. "Adenosine A2aand A2bReceptors in Cultured Fetal Chick Heart Cells." Circulation Research 76, no. 2 (February 1995): 242–51. http://dx.doi.org/10.1161/01.res.76.2.242.

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42

Martinsen, Brad J. "Reference guide to the stages of chick heart embryology." Developmental Dynamics 233, no. 4 (2005): 1217–37. http://dx.doi.org/10.1002/dvdy.20468.

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43

Al Naieb, Sarah, Christoph M. Happel, and T. Mesud Yelbuz. "A detailed atlas of chick heart development in vivo." Annals of Anatomy - Anatomischer Anzeiger 195, no. 4 (July 2013): 324–41. http://dx.doi.org/10.1016/j.aanat.2012.10.011.

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44

Ford, Byron D., Jeffrey A. Loeb, and Gerald D. Fischbach. "Neuregulin Stimulates DNA Synthesis in Embryonic Chick Heart Cells." Developmental Biology 214, no. 1 (October 1999): 139–50. http://dx.doi.org/10.1006/dbio.1999.9394.

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45

Kern, Christine B., Stanley Hoffman, Ricardo Moreno, Brook J. Damon, Russell A. Norris, Edward L. Krug, Roger R. Markwald, and Corey H. Mjaatvedt. "Immunolocalization of chick periostin protein in the developing heart." Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology 284A, no. 1 (2005): 415–23. http://dx.doi.org/10.1002/ar.a.20193.

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46

Shepherd, Neal, Victoria Graham, Bhavya Trevedi, and Tony L. Creazzo. "Changes in regulation of sodium/calcium exchanger of avian ventricular heart cells during embryonic development." American Journal of Physiology-Cell Physiology 292, no. 5 (May 2007): C1942—C1950. http://dx.doi.org/10.1152/ajpcell.00564.2006.

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It has been suggested that the sodium/calcium exchanger NCX1 may have a more important physiological role in embryonic and neonatal hearts than in adult hearts. However, in chick heart sarcolemmal vesicles, sodium-dependent calcium transport is reported to be small and, moreover, to be 3–12 times smaller in hearts at embryonic day (ED) 4–5 than at ED18, the opposite of what would be expected of a transporter that is more important in early development. To better assess the role of NCX1 in calcium regulation in the chick embryonic heart, we measured the activity of NCX1 in chick embryonic hearts as extracellular calcium-activated exchanger current ( INCX) under controlled ionic conditions. With intracellular calcium concentration ([Ca2+]i) = 47 nM, INCX density increased from 1.34 ± 0.28 pA/pF at ED2 to 3.22 ± 0.55 pA/pF at ED11 ( P = 0.006); however, with [Ca2+]i = 481 nM, the increase was small and statistically insignificant, from 4.54 ± 0.77 to 5.88 ± 0.73 pA/pF ( P = 0.20, membrane potential = 0 mV, extracellular calcium concentration = 2 mM). Plots of INCX density against [Ca2+]i were well fitted by the Michaelis-Menton equation and extrapolated to identical maximal currents for ED2 and ED11 cells (extracellular calcium concentration = 1, 2, or 4 mM). Thus the increase in INCX at low [Ca2+]i appeared to reflect a developmental change in allosteric regulation of the exchanger by intracellular calcium rather than an increase in the membrane density of NCX1. Supporting this conclusion, RT-PCR demonstrated little change in the amount of mRNA encoding NCX1 expression from ED2 through ED18.

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47

George, Rajani M., Gabriel Maldonado-Velez, and Anthony B. Firulli. "The heart of the neural crest: cardiac neural crest cells in development and regeneration." Development 147, no. 20 (October 15, 2020): dev188706. http://dx.doi.org/10.1242/dev.188706.

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ABSTRACTCardiac neural crest cells (cNCCs) are a migratory cell population that stem from the cranial portion of the neural tube. They undergo epithelial-to-mesenchymal transition and migrate through the developing embryo to give rise to portions of the outflow tract, the valves and the arteries of the heart. Recent lineage-tracing experiments in chick and zebrafish embryos have shown that cNCCs can also give rise to mature cardiomyocytes. These cNCC-derived cardiomyocytes appear to be required for the successful repair and regeneration of injured zebrafish hearts. In addition, recent work examining the response to cardiac injury in the mammalian heart has suggested that cNCC-derived cardiomyocytes are involved in the repair/regeneration mechanism. However, the molecular signature of the adult cardiomyocytes involved in this repair is unclear. In this Review, we examine the origin, migration and fates of cNCCs. We also review the contribution of cNCCs to mature cardiomyocytes in fish, chick and mice, as well as their role in the regeneration of the adult heart.

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48

Männer, Jörg, Wolfgang seidl, and Gerd Steding. "Complete transposition in a chick embryo demonstrated by scanning electron microscopy." Cardiology in the Young 8, no. 3 (July 1998): 396–99. http://dx.doi.org/10.1017/s1047951100006958.

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AbstractChick embryos are frequently used as animal models when researching the developing heart. In the past, every attempt to induce complete transposition (the combination of concordant arrioventricular and discordant ventriculo-arterial connections) failed in chicks, suggesting that it might be impossible to develop a chicken modle for this malformation. We demonstrate, to the best of our knowledge, the first well-documented case of complete transpositon occourrine in the chick

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49

Pawlak, K., and J. Niedzióka. "Non-invasive measurement of chick embryo cardiac work." Czech Journal of Animal Science 49, No. 1 (December 11, 2011): 8–15. http://dx.doi.org/10.17221/4265-cjas.

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This study used a non-invasive method of ballistocardiography to investigate cardiac work of chick embryos. In this method, an eggshell with electric charges on it is one capacitor plate, the other being a receiving antenna of the measuring equipment. Chick embryo cardiac work induces micro-movements of the whole egg, resulting in changes in the distances between the plates and thus in the difference of potentials between the shell and the receiving antenna. This is registered by the measuring equipment. The first single signals of cardiac work were registered on day 7 of incubation. Starting from day 9, the signal was recorded from all embryos. During the study, the heart rate decreased from 248 to 161 beats per minute and signal amplitude was found to steadily increase from 6.3 to 432.7 mV/m. Great disturbances in ballistocardiograms were observed on days preceding embryonic deaths.  

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50

Wang, D. Z., R. S. Reiter, J. L. Lin, Q. Wang, H. S. Williams, S. L. Krob, T. M. Schultheiss, S. Evans, and J. J. Lin. "Requirement of a novel gene, Xin, in cardiac morphogenesis." Development 126, no. 6 (March 15, 1999): 1281–94. http://dx.doi.org/10.1242/dev.126.6.1281.

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A novel gene, Xin, from chick (cXin) and mouse (mXin) embryonic hearts, may be required for cardiac morphogenesis and looping. Both cloned cDNAs have a single open reading frame, encoding proteins with 2,562 and 1,677 amino acids for cXin and mXin, respectively. The derived amino acid sequences share 46% similarity. The overall domain structures of the predicted cXin and mXin proteins, including proline-rich regions, 16 amino acid repeats, DNA-binding domains, SH3-binding motifs and nuclear localization signals, are highly conserved. Northern blot analyses detect a single message of 8.9 and 5.8 kilo base (kb) from both cardiac and skeletal muscle of chick and mouse, respectively. In situ hybridization reveals that the cXin gene is specifically expressed in cardiac progenitor cells of chick embryos as early as stage 8, prior to heart tube formation. cXin continues to be expressed in the myocardium of developing hearts. By stage 15, cXin expression is also detected in the myotomes of developing somites. Immunofluorescence microscopy reveals that the mXin protein is colocalized with N-cadherin and connexin-43 in the intercalated discs of adult mouse hearts. Incubation of stage 6 chick embryos with cXin antisense oligonucleotides results in abnormal cardiac morphogenesis and an alteration of cardiac looping. The myocardium of the affected hearts becomes thickened and tends to form multiple invaginations into the heart cavity. This abnormal cellular process may account in part for the abnormal looping. cXin expression can be induced by bone morphogenetic protein (BMP) in explants of anterior medial mesoendoderm from stage 6 chick embryos, a tissue that is normally non-cardiogenic. This induction occurs following the BMP-mediated induction of two cardiac-restricted transcription factors, Nkx2.5 and MEF2C. Furthermore, either MEF2C or Nkx2.5 can transactivate a luciferase reporter driven by the mXin promoter in mouse fibroblasts. These results suggest that Xin may participate in a BMP-Nkx2.5-MEF2C pathway to control cardiac morphogenesis and looping.

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