Persisting zones of slow impulse conduction in developing chicken hearts.

Abstract

We performed a correlative electrophysiological and immunohistochemical study of embryonic chicken hearts during the septational period (Hamburger and Hamilton stages 13-31 [2-7 days of incubation]). The analyses yield conclusive evidence for slow conduction, up to 7 days of development, in the outflow tract, in the atrioventricular canal, and in the sinoatrial junction. The conduction velocity remains approximately 1 cm/sec in the outflow tract and increases in the ventricle 20-fold to approximately 20 cm/sec between 2 and 7 days of development. Transmembrane potentials of myocytes in the outflow tract and atrioventricular canal slowly rise (less than 5 V/sec), whereas in the atrium and ventricle, the upstroke velocity is eightfold to 13-fold higher. In the outflow tract, repolarization is completed only after the start of the next cycle. Because of the persistence of slow conduction, the myocardium flanking the developing atria and ventricle is thought to represent segments of persisting "primary" myocardium, whereas the more rapidly conducting "working" myocardium of the ventricle and atria is thought to represent more advanced stages of myocardial differentiation. The persisting primary myocardium was characterized by a continued coexpression of both the atrial and ventricular isoforms of myosin heavy chain. The developing atria and ventricle could be demarcated morphologically from the primary myocardium because the free walls of these segments only express their respective isoforms of myosin heavy chain. The slowly conducting myocardial zones appear to be essential for the function of the embryonic heart because 1) they provide the septating heart with alternating segments of slow and relatively fast conduction necessary for consecutive contraction of the atrial and ventricular segments and 2) their sphincterlike prolonged peristaltic contraction pattern can substitute for the adult type of one-way valves that start to develop at the end of septation.

Species‐specific differences of myosin content in the developing cardiac chambers of fish, birds, and mammals

“…4E). Control markers such as AMHC1 and VMHC1 (at both the mRNA and protein level) display an expression pattern confined to the atrial and ventricular myocardia, respectively, as previously described (De Jong et al, 1992;Yutzley and Bader, 1995). In the adult chicken heart, expression of MyHC mRNA and protein is similar to that observed in the embryonic stage, with higher expression being observed in the atrial myocardium as compared to the ventricular myocardium ( Fig.…”

“…With further development (H/H24), the heart acquires five morphological and functional segments: the inflow tract, atrium, atrioventricular canal, ventricle, and outflow tract (Argü ello et al, 1986;De Jong et al, 1992;Moorman and Lamers, 1994). Expression of MyHC transcripts is higher in the inflow tract/atrium region than in the ventricles/outflow tract region (Fig.…”

Bone Morphogenetic Protein Signaling Pathways in Heart Development and Disease

“…(See reviews, (Christoffels et al 2010;Moorman and Christoffels 2003)). The electrical impulse is carried from the atria, across the AVC to the ventricles (Valderrábano et al 2006;Rentschler et al 2002;de Jong et al 1992). The AVC has a slower conduction rate than the atria and delays the atrial-ventricular electrical impulse (de Jong et al 1992).…”

“…The electrical impulse is carried from the atria, across the AVC to the ventricles (Valderrábano et al 2006;Rentschler et al 2002;de Jong et al 1992). The AVC has a slower conduction rate than the atria and delays the atrial-ventricular electrical impulse (de Jong et al 1992). BMP2 is necessary for AVC specification and expression of Tbx2 (Yamada et al 2000;Ma et al 2005).…”

Ultrastructural changes of the myocardium in the embryonic rat heart

“…The intersegmental junctions have also been described as precursors of the conduction system of the heart (Virágh and Challice, 1977, 1982. Immunohistochemically, they differ from the atrial and ventricular working myocardium (Wessels et al, 1991;De Jong et al, 1992;Nakawaga et al, 1993;Sakai et al, 1994). Several reports have described ultrastructural changes in embryonic myocardium (Hibbs, 1956;Manasek, 1968bManasek, , 1970Virá gh and Challice, 1973;Chacko, 1976), and quantification of some cellular contents has been done in late fetal and postnatal stages (Anversa et al, 1975;Hirakow et al, 1980;Olivetti et al, 1980).…”