Development of the ventricular myocardial trabeculae in Scyliorhinus canicula (Chondrichthyes): evolutionary implications.

The development of the ventricular myocardial trabeculae occurs in three steps: emergence, trabeculation and remodeling. The whole process has been described in vertebrates with two different myocardial structural types, spongy (zebrafish) and compact (chicken and mouse). In this context, two alternative mechanisms of myocardial trabeculae emergence have been identified: (1) in chicken and mouse, the endocardial cells invade the two-layered myocardium; (2) in zebrafish, cardiomyocytes from the monolayered myocardium invaginate towards the endocardium. Currently, the process has not been studied in detail in vertebrates having a mixed type of ventricular myocardium, with an inner trabecular and an outer compact layer, which is presumptively the most primitive morphology in gnathostomes. We studied the formation of the mixed ventricular myocardium in the lesser spotted dogfish (Scyliorhinus canicula, Elasmobranchii), using light, scanning and transmission electron microscopy. Our results show that early formation of the mixed ventricular myocardium, specifically the emergence and the trabeculation steps, is driven by an endocardial invasion of the myocardium. The mechanism of trabeculation of the mixed ventricular myocardium in chondrichthyans is the one that best reproduces how this developmental process has been established from the beginning of the gnathostome radiation. The process has been apparently preserved throughout the entire group of sarcopterygians, including birds and mammals. In contrast, teleosts, at least those possessing a mostly spongy ventricular myocardium, seem to have introduced notable changes in their myocardial trabeculae development.

[Morphometric features of cardiomyocytes in the ventricular septum of patients with hypertrophic cardiomyopathy]. / Morfometricheskie osobennosti kardiomiotsitov mezhzheludochkovoi peregorodki u bol'nykh gipertroficheskoi kardiomiopatiei.

AIM: to determine the diameter and length of cardiomyocytes (CMC) in the ventricular septum (VS) of patients with hypertrophic cardiomyopathy (HCM) and to analyze correlations of a change in CMC sizes with the anatomical features of the heart in the patients. MATERIAL AND METHODS: Longitudinal sections of intraoperative myocardial biopsy specimens taken from 23 patients aged 15-59 years with HCM were treated using immunohistochemical detection of connexin 43; the sizes of 50 CMCs were measured; a 4-point scale was used to assess the degree of myofibril loss (MFL) in these cells. The change in the diameter and length of the cells during their rearrangement as MFL gradually increased, as well as the correlations of CMC sizes with the anatomical parameters of the heart were analyzed. RESULTS: VS CMCs from the patients with HCM were hypertrophic and were in the early stages of rearrangement accompanied by MFL. During this rearrangement, CMCs in some patients grew in length and, less frequently, diameter. The average diameter of CMCs was directly correlated with VS thickness. The average length of the cells in the CMC population with a considerable degree of MFL also directly correlated with VS thickness. CONCLUSION: The findings could suggest that the factor raising VS thickness in HCM may be an increase in not only diameter of CMCs, but also in length of CMCs, which had impaired orientation in the VS - which are oriented perpendicular to their normal tangential position. The presence of such CMCs in the VS myocardium in patients with HCM can be discussed due to the typical large number of myocardial areas with the impaired parallel arrangement of CMCs.

Angiotensinergic and noradrenergic neurons in the rat and human heart.

Although the physiological and pharmacological evidences suggest a role for angiotensin II (Ang II) with the mammalian heart, the source and precise location of Ang II are unknown. To visualize and quantitate Ang II in atria, ventricular walls and interventricular septum of the rat and human heart and to explore the feasibility of local Ang II production and function, we investigated by different methods the expression of proteins involved in the generation and function of Ang II. We found mRNA of angiotensinogen (Ang-N), of angiotensin converting enzyme, of the angiotensin type receptors AT(1A) and AT2 (AT(1B) not detected) as well as of cathepsin D in any part of the hearts. No renin mRNA was traceable. Ang-N mRNA was visualized by in situ hybridization in atrial ganglial neurons. Ang II and dopamine-ß-hydroxylase (DßH) were either colocalized inside the same neuronal cell or the neurons were specialized for Ang II or DßH. Within these neurons, the vesicular acetylcholine transporter (VAChT) was neither colocalized with Ang II nor DßH, but VAChT-staining was found with synapses en passant encircle these neuronal cells. The fibers containing Ang II exhibited with blood vessels and with cardiomyocytes supposedly angiotensinergic synapses en passant. In rat heart, right atrial median Ang II concentration appeared higher than septal and ventricular Ang II. The distinct colocalization of neuronal Ang II with DßH in the heart may indicate that Ang II participates together with norepinephrine in the regulation of cardiac functions: produced as a cardiac neurotransmitter Ang II may have inotropic, chronotropic or dromotropic effects in atria and ventricles and contributes to blood pressure regulation.

The structural characteristics of the heart ventricle of the African lungfish Protopterus dolloi: freshwater and aestivation.

This paper reports on the structure and ultrastructure of the ventricular myocardium of the African lungfish Protopterus dolloi in freshwater (FW), in aestivation (AE), and after the AE period. The myocardium shows a conventional myofibrillar structure. All the myocytes contain large intracytoplasmic spaces occupied by a pale material that could contain glycosaminoglycans and/or glycogen, which may be used as food and water reservoirs. In FW, the myocytes in the trabeculae associated with the free ventricular wall show structural signs of low transcriptional and metabolic activity (heterochromatin, mitochondria of the dense type). These signs are partially reversed during the AE period (euchromatin, mitochondria with a light matrix), with a return to the FW appearance after arousal. The myocytes in the septum show, in FW conditions, nuclear polymorphism (heterochromatin, euchromatin), and two types (colliquative and coagulative) of necrosis. In AE, all the septal myocytes show euchromatin, and the number of necrotic cells increases greatly. Cell necrosis appears to be related to the septal architecture. After arousal, the septal myocytes exhibit a heterochromatin pattern, the number of necrotic cells decreases, cell debris accumulates under the endocardium, and phagocytosis takes place. Despite being a morphologic continuum, the trabeculae associated with the free ventricular wall appear to constitute a different compartment from that formed by the trabeculae in the ventricular septum. Paradoxically, AE appears to trigger an increase in transcriptional and synthetic myocardial activities, especially at the level of the ventricular septum. This activity may be involved in mechanisms of autocrine/paracrine regulation. Aestivation cannot be regarded as the result of a general depression of all cellular and organic activities. Rather, it is a much more complex state in which the interplay between upregulation and downregulation of diverse cell activities appears to play a fundamental role.