Cellular changes in mechanically overloaded heart

Hatt, P. Y.

doi:10.1007/978-3-642-85299-2_17

Cited by 17 publications

(5 citation statements)

References 10 publications

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“…Thus, even though a rich net of vasa vasorum has been demonstrated in the extrapulmonary veins, a capillarization appears to be totally absent in the subendothelial layer of the intrapulmonary veins [20]. Furthermore, the cellular changes presented here by electron microscopy after 4 weeks of LVI are in some ways similar to those previously reported of the enlarging ventricular myocardium [4,5,7,27]. In the hypertrophic human myocytes of the latter studies, processes of lysis of the cytoplasm in combination with structural changes indicative of increased protein synthesis, were observed within the same cytoplasmic area.…”

Section: Discussionsupporting

confidence: 83%

Striated myocytes and atrial specific granules in the pulmonary veins of chronically infarcted rat hearts

1987

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The ultrastructure of the striated myocytes in the pulmonary myocardium of the Wistar rat, was studied following left ventricular infarction (LVI) for 4 days and 4 weeks, respectively. Ischemia was provided by ligating of the left coronary artery which successively produces left ventricular dysfunction and congestion of the left atrium and pulmonary veins. In general, the striated myocytes of the extrapulmonary veins of the control groups displayed ultrastructural characteristics similar to those of the left atrium. However, in the former, transverse tubules commonly occurred making interior couplings with the SR at the I-band levels. Also, between striated myocytes of the intrapulmonary veins of the controls nexus-like junctions of about 2 micron length were observed. Further, in the same groups atrial specific granules (ASG), including A-granules and B-granules, were present in about 20%-30% of the striated myocytes of the extrapulmonary veins as shown in single sections. The ASG tended to decrease by number in areas approaching the lung hilus and were not observed in the intrapulmonary veins of the controls. After 4 days of ventricular ischemia granules also appeared in the intrapulmonary veins. They were mostly seen in single and randomly spread in the cytoplasm of a limited number of cells, i.e., in between 0% and 5% of the myocytes as seen in single sections. Four days of LVI produced only minor cellular injuries to the extrapulmonary and intrapulmonary venous wall, while more severe lesions appeared in both areas following 4 weeks of LVI. Such lesions were preferably localized to the adluminal surface and consisted mainly of Z-band and sarcomere anomalies, vacuolization of the cytoplasm and mitochondrial swelling.

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Section: Discussionsupporting

confidence: 83%

Striated myocytes and atrial specific granules in the pulmonary veins of chronically infarcted rat hearts

1987

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“…Because the expression of HSPs in myocytes from overloaded hearts was, as described above, associated with an increase in total protein synthesis, it could be hypothesized that HSPs are specifically expressed by a subpopulation of damaged myocytes. Such a population was observed 2-4 d after hemodynamic overload by Hatt (48). However, this hypothesis does not fit with the results ofimmunocytochemical labeling of HSP 70 that failed to depict any emergence of a new myocyte population that exhibited changes in its cellular distribution after hemodynamic overload (Fig.…”

Section: Discussionmentioning

confidence: 87%

Synthesis of stress proteins in rat cardiac myocytes 2-4 days after imposition of hemodynamic overload.

Delcayre

Samuel²,

Marotte³

et al. 1988

J. Clin. Invest.

109

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Isolated adult myocytes incubated with I35Slmethionine were used to study the expression of proteins in the rat heart during the first 2 wk after either pressure or volume overload. In both models an early (24 d) and transient expression of three major stress proteins (heat shock protein [HSPJ HSP 70, HSP 68, and HSP 58) was observed together with an increased synthesis of putative ribosomal proteins. Only traces of 35S-labeled HSPs were detected in controls and sham-operated animals. The three stress proteins were identified by their migration in two-dimensional gels, by comigration with HSPs, which had been induced in myocytes by incubation at 41°C and immunoblot analysis using antisera directed against the 70-kD protein.Immunohistochemical staining of HSP 70 in rod-shaped myocytes and detection by immunoblot showed that HSP 70 was equally present and distributed in both sham-operated and overloaded hearts, and provided no evidence for a subpopulation of myocytes acutely involved in the increased expression of HSP 70. It is suggested that the transient expression of HSPs that occurs during the early adaptation of the myocardial cells to overload could confer some degree of protection to the actively growing myocytes.

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“…ANF is normally constitutively secreted from the ventricular myocytes (Bloch et al 1988;, whereas in volume-overloaded hearts the synthesis and secretion is upregulated. Accordingly, increased levels of ANF mRNA are observed (Lattion et al 1986) and secretory granules similar to those seen in the atria occur (Hatt 1975;Takemura et al 1990;. Characteristically, the expression of ANF immunoreactivity is most significant in the regions close to the infarcted myocardium .…”

Section: Discussionmentioning

confidence: 88%

Regional activation of the immediate‐early response gene c‐fos in infarcted rat hearts

Larsen

Skar

Frotjold

et al. 1998

Int J Experimental Path

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Regional infarction of the left ventricle is followed by hypertrophy of the viable myocardium. This compensatory growth of cardiac myocytes requires induction of gene transcription and synthesis of proteins. In this study, we examined the expression of the immediate-early response gene c-fos following ligation of the left coronary artery in rat hearts. RNase protection assay demonstrated a rapid increase in the c-fos mRNA level in the ventricular myocardium. After two days of infarction, the c-fos expression was attenuated and was comparable to that observed in sham-operated control hearts. In situ tissue distribution of Fos protein-like immunoreactivity revealed the appearance of positively stained cells adjacent to the lateral border of the ischaemic myocardium, in the left ventricular subendocardial areas, in the papillary muscles of the left ventricle, in the proximity of great transmural vessels, and focally in the normo-perfused subepicardial myocardium. Double staining using antibodies recognizing the Fos protein and alpha-actinin, confirmed that the accumulation of nuclear Fos protein-like immunoreactivity was mainly seen in the cardiac myocytes. However, double staining of the Fos protein and Hoechst DNA labelling showed that detectable immunoreactivity occurred only in a limited proportion of the total nuclei present in these myocardial regions. Moreover, the regions showing c-fos activation correspond to the areas in which the appearance of subsequent growth responses are most pronounced following myocardial infarction. The present results therefore indicate that an early and regional c-fos activation is taking place in viable cardiac myocytes following left coronary artery ligation, and that c-fos is a possible regulating factor of sequential events leading to altered pattern of gene expression and protein synthesis in the hypertrophying heart.

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Cellular changes in mechanically overloaded heart

Cited by 17 publications

References 10 publications

Striated myocytes and atrial specific granules in the pulmonary veins of chronically infarcted rat hearts

Striated myocytes and atrial specific granules in the pulmonary veins of chronically infarcted rat hearts

Synthesis of stress proteins in rat cardiac myocytes 2-4 days after imposition of hemodynamic overload.

Regional activation of the immediate‐early response gene c‐fos in infarcted rat hearts

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