The Fine Structure of the Ventricular Muscle Cells of the Soft-Shelled Trutle Heart (Amyda), with Special Reference to the Sarcoplasmic Reticulum

1971 ◽  
Keyword(s):  
Fine Structure ◽  
Sarcoplasmic Reticulum ◽  
Special Reference ◽  
Muscle Cells ◽  
Ventricular Muscle

Fine Structure of Cardiac Muscle Cells after Injection of Normal and Thiouracil-Treated Rats with Triiodothyronine.

1975 ◽  
Vol 33 ◽  
pp. 536-537
Author(s):  
Eladio A. Nunez ◽  
Martin Hagopian ◽  
Roger L. Greif ◽  
Michael D. Gershon
Keyword(s):  
Drinking Water ◽  
Fine Structure ◽  
Thyroid Hormones ◽  
Cardiac Muscle ◽  
Muscle Cells ◽  
Left Ventricular ◽  
Ventricular Muscle ◽  
Cardiac Muscle Cells ◽  
Mitochondrial Number ◽  
Morphologic Changes

It has been reported that morphologic changes occur in mitochondria of cardiac muscle cells following treatment with thyroid hormones (thyroxine, triiodothyronine). These observations have been used to support the view that under normal conditions, thyroid hormones control mitochondrial metabolism. We have examined the effect of triiodothyronine on the fine structure of cardiac muscle from normal and thiouracil-treated rats. Rats were given thiouracil (0.1 percent in drinking water) for 10 weeks. Normal and thiouracil-treated rats were injected with triiodothyronine (75 ug of triiodo-L-thyronine i.p. per day) for three days. The left ventricular muscle of normal rats, and rats given thiouracil, triiodothyronine or thiouracil followed by triiodothyronine was examined ultrastructurally. Morphometric analysis of electron micrographs showed that mitochondrial number was not significantly different in the four groups of animals. The fine structure of normal cardiac muscle is illustrated in figure 1. Thiouracil treatment did not alter the fine structure of cardiac muscle cells (Fig. 3).

scholarly journals Evidence for the presence of calsequestrin in two structurally different regions of myocardial sarcoplasmic reticulum.

1984 ◽  
Vol 98 (4) ◽  
pp. 1597-1602 ◽  
Author(s):  
A O Jorgensen ◽  
K P Campbell
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Central Region ◽  
Protein A ◽  
Muscle Cells ◽  
Physiological Signals ◽  
Ventricular Muscle ◽  
Cardiac Muscle Cells ◽  
Band Region ◽  
Membrane Bound ◽  
Junctional Sarcoplasmic Reticulum

Localization of calsequestrin in chicken ventricular muscle cells was determined by indirect immunofluorescence and immuno-Protein A-colloidal gold labeling of cryostat and ultracryotomy sections, respectively. Calsequestrin was localized in the lumen of peripheral junctional sarcoplasmic reticulum, as well as in the lumen of membrane-bound structures present in the central region of the I-band, while being absent from the lumen of the sarcoplasmic reticulum in the A-band region of the cardiac muscle cells. Since chicken ventricular muscle cells lack transverse tubules, the presence of calsequestrin in membrane bound structures in the central region of the I-band suggests that these cells contain nonjunctional regions of sarcoplasmic reticulum that are involved in Ca2+ storage and possibly Ca2+ release. It is likely that the calsequestrin containing structures present throughout the I-band region of the muscle cells correspond to specialized regions of the free sarcoplasmic reticulum in the I-band called corbular sarcoplasmic reticulum. It will be of interest to determine whether Ca2+ storage and possibly Ca2+ release from junctional and nonjunctional regions of the sarcoplasmic reticulum in chicken ventricular muscle cells are regulated by the same or different physiological signals.

scholarly journals Choline Permeability in Cardiac Muscle Cells of the Cat

1970 ◽  
Vol 55 (5) ◽  
pp. 602-619 ◽  
Author(s):  
S. Bosteels ◽  
A. Vleugels ◽  
E. Carmeliet
Keyword(s):  
Cell Membrane ◽  
Cardiac Muscle ◽  
Paper Chromatography ◽  
Heart Muscle ◽  
Muscle Cells ◽  
Heart Cells ◽  
Ventricular Muscle ◽  
Cardiac Cell ◽  
Cardiac Muscle Cells ◽  
Rapid Phase

Permeability of the cardiac cell membrane to choline ions was estimated by measuring radioactive choline influx and efflux in cat ventricular muscle. Maximum values for choline influx in 3.5 and 137 mM choline were respectively 0.56 and 9 pmoles/cm2·sec. In 3.5 mM choline the intracellular choline concentration was raised more than five times above the extracellular concentration after 2 hr of incubation. In 137 mM choline, choline influx corresponded to the combined loss of intracellular Na and K ions. Paper chromatography of muscle extracts indicated that choline was not metabolized to any important degree. The accumulation of intracellular choline rules out the existence of an efficient active pumping mechanism. By measuring simultaneously choline and sucrose exchange, choline efflux was analyzed in an extracellular phase, followed by two intracellular phases: a rapid and a slow one. Efflux corresponding to the rapid phase was estimated at 16–45 pmoles/cm2·sec in 137 mM choline and at 1.3–3.5 pmoles/cm2·sec in 3.5 mM choline; efflux in 3.5 mM choline was proportional to the intracellular choline concentration. The absolute figures for unidirectional efflux were much larger than the net influx values. The data are compared to Na and Li exchange in heart cells. Possible mechanisms for explaining the choline behavior in heart muscle are discussed.

Sign in / Sign up

Export Citation Format

Share Document