Electron microscopic visible ischemic changes of the mitochondrial ATPases in human myocardial cells during extracorporal circulation

1981 ◽  
Vol 76 (1) ◽  
pp. 106-113 ◽  
Author(s):  
F. Beyersdorf ◽  
C. Gauhl ◽  
O. Elert ◽  
P. Satter
2005 ◽  
Vol 67 (2) ◽  
pp. 225-233 ◽  
Author(s):  
A BORBELY ◽  
A TOTH ◽  
I EDES ◽  
L VIRAG ◽  
J PAPP ◽  
...  

2004 ◽  
Vol 50 (5) ◽  
pp. 45-48
Author(s):  
L. E. Panin ◽  
V. F. Maksimov ◽  
A. R. Kolpakov ◽  
I. M. Korostyshevskaya

An electron microscopic study of a model of the rat contracting heart perfused by the Langendorf procedure has indicated the myo¬cardial effects of epinephrine, corticosterone, high density lipoproteins (HDL), and low density lipoproteins (LDL) and revealed a role of hormones in the uptake and intercellular distribution of colloidal gold-labeled lipoproteins. Epinephrine enhanced LDL dis¬solution onto the endothelial surface, by slowing down their myocardial penetration, but failed to affect the penetration and distribution of labeled HDL that did not leave the capillary walls. Corticosterone drastically increased receptor-mediated absorption of HDL by the capillary endothelium and ensured their penetration into the interstitial macrophages, but it did not affect the myocardial pene¬tration of labeled LDL. In all experiments, corticosterone caused the lowered content of glycogen in the myocardial cells, sarcoplasmic sequestration of its residues and their interstitial release. Epinephrine and corticosterone differently affect the myocardial penetration and distribution of atherogenic and antiatherogenic lipoproteins. Under stress, it ensures mobilization of different metabolic pathways for myocardial energy supply.


1976 ◽  
Vol 21 (1) ◽  
pp. 1-12
Author(s):  
Helge Jensen ◽  
Hogne Engedal ◽  
Thv Selmer Saetersdal

1990 ◽  
Vol 46 (5) ◽  
pp. 495-498
Author(s):  
Y. Kawamoto ◽  
T. Hanaichi ◽  
M. Naito ◽  
A. Miyama

Author(s):  
Larry F. Lemanski

A naturally-occurring genetic mutation, designated c for “cardiac lethal”, was discovered in Ambystoma meximanum. The effect of homozygosity for recessive gene c is the absence of a heart beat, even though initially heart development appears normal. Mutant embryos are first distinguishable form their normal siblings at Harrison stage 34, when the normals develop contracting hearts. The mutant hearts at this stage, upon gross examination appear structurally normal but fail to beat. Nevertheless, the mutants survive through stage 41, which is about 20 days beyond the heart-beat stage and exhibit normal swimming movements indicating that gene c does not affect skeletal muscle. Electron microscopic studies of normal hearts at stage 34 reveal that the myocardial cells contain organized myofibrils; these myofibrils first form directly beneath the plasma membrane. By stage 41, the normal myocardial cells contain numerous well-organized myofibrils and thus have now become highly differentiated muscle cells.


Author(s):  
Tetsuo Morita ◽  
Tatsuo Shimada

From light and transmission electron microscopic studies, it has been long known that Purkinje cells of mammalian hearts have morphological characteristics different from ordinary myocardial cells. In the present study, not only Purkinje cells and myocardial cells but also connective tissue sheaths surrounding these cells were investigated by combined scanning electron microscopy(SEM) and chemical digestion.The moderator band of adult sheep heart was used because it possessed both Purkinje cells and myocardial cells (Fig.1). Tissue blocks were immersed in Karnovsky’s fixative for 3hr or longer. Some fixed tissues were inrrtersed in a 3-5% aqueous solution of NaClO for 1 min to digest the endocardial endothelium, and then were treated with 8N HCl for 30 min at 60°C to remove connection tissue elements. The others were iirmersed in a 2N NaOH or KOH solution for 7 days at room temperature to digest cellular elements. After freeze-cracking in a 40% dimethyl sulfoxide solution, the tissues were washed throughout in a saline solution containing tween 20, placed in a 1% aqueous solution of tannic acid for 2hr and conductive-stained with 1% OsO4 for 2hr.


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