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.

scholarly journals Structure of myofibrils at extra-junctional membrane attachment sites in cultured cardiac muscle cells

1988 ◽  
Vol 89 (1) ◽  
pp. 97-106
Author(s):  
B.T. Atherton ◽  
M.M. Behnke
Keyword(s):  
Cell Membrane ◽  
Cardiac Muscle ◽  
Muscle Cells ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Cardiac Muscle Cells ◽  
Lateral Contact ◽  
Attachment Sites ◽  
Membrane Attachment ◽  
Actin Cables

The composition and organization of myofibrils at extra-junctional membrane attachment sites in cultured neonatal rat cardiac muscle cells were analysed by immunofluorescence and electron microscopy. When myofibril terminals attached to the cell membrane via focal contacts at regions of the sarcolemma that lacked intercalated discs, they appeared to be non-striated and resembled thick actin cables. Although the non-striated terminals contained actin, myosin and alpha-actinin, the proteins were not organized into recognizable sarcomeres at the light microscopic level. Analysis of the structure of the terminals in the electron microscope confirmed that the usual sarcomeric organization and attachments to the sarcolemma were markedly modified. The non-striated myofibril terminals differed in structure from both stress fibres in non-muscle cells and stress fibre-like structures present in embryonic heart cells in culture. Non-striated myofibril terminals attached to the cell membrane by lateral contact with extra-junctional electron-dense membrane plaques rather than by insertion by their ends into the fascia adherens. It is proposed that the structure and composition of membrane-attachment points for myofibrils may have an influence on the structure, organization or stability of contractile elements in cardiac muscle.

Coaggregation and formation of a joint myocardial tissue by embryonic mammalian and avian heart eel Is

Development ◽  
1980 ◽  
Vol 59 (1) ◽  
pp. 263-279
Author(s):  
Asish C. Nag ◽  
Mei Cheng ◽  
Christopher J. Healy
Keyword(s):  
Cardiac Muscle ◽  
Tritiated Thymidine ◽  
Muscle Cells ◽  
Intercellular Adhesion ◽  
Heart Cells ◽  
Embryonic Cells ◽  
Cardiac Muscle Cells ◽  
Electron Microscopic Autoradiography ◽  
Stage Of Development ◽  
Mixed Aggregates

Intercellular adhesion and tissue reconstruction from homologous dissociated embryonic cells from two species were studied. Dissociated 12-day-old embryonic rat heart cells and 50-h-old embryonic chick heart cells were labeled with tritiated thymidine and allowed to aggregate in Erlenmeyer flasks during rotation culture on a gyratory water-bath shaker. The cultures were continued for 72 h. Cell aggregates were examined microscopically for evidence of contractility and subsequently processed at intervals between 1 and 72 h for transmission electron microscopic autoradiography. Rat and chick hearts used in this study appeared comparable in their stage of development and cellular composition. With the exception of mature blood cells and some fibroblastic non-muscle cells, all chick cardiac muscle cells were labeled with tritiated thymidine. As the cultures continued, aggregates increased in size by continuous accretion of cells and joining of small clusters. The cells within these mixed aggregates exhibited synchronous contractility from 1 h until the cultures were terminated. Most of the aggregation in both control and mixed aggregates was completed within 24 h. Control aggregates consisted of cells from a single species, either chick or rat. Approximately 18 % of labeled chick cardiac muscle cells established intercellular contacts and junctions with unlabeled rat cardiac muscle cells after 6 h of culture. This increased to 72 % after 72 h in culture. The junctions observed between chick and rat cardiac muscle cells were desmosomes and hemidesmosomes. Approximately 13 % of the cardiac muscle cells of one species either chick or rat were found scattered within clusters which contained .15 % of the cells from the other species after 72 h of culture. These scattered cells did not form junctions with monospecific cell groups. The implications of these intercellular adhesions between the same and different species are discussed, bearing two hypotheses in mind: (1) Moscona and collaborators, (2) Burdickand Steinberg. This study suggests that cellular as well as species identity plays an important role in the determination of intercellular adhesion among the embryonic cells from different species.

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).

Effects of oligomycin and acidosis on rates of ATP depletion in ischemic heart muscle

1986 ◽  
Vol 250 (3) ◽  
pp. H503-H508 ◽  
Author(s):  
W. Rouslin ◽  
J. L. Erickson ◽  
R. J. Solaro
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Muscle ◽  
Heart Muscle ◽  
Ph Dependence ◽  
Muscle Cells ◽  
Atp Depletion ◽  
Ischemic Heart ◽  
Mitochondrial Atpase ◽  
Cardiac Muscle Cells ◽  
Tissue Ph

The perfusion of canine cardiac muscle with 10 microM oligomycin produced a nearly 90% slowing of the net rate of tissue ATP depletion from 0.200 to 0.025 mumol X min-1 X g wet wt-1 of tissue during a subsequent myocardial autolytic interval during which tissue pH was held constant. Moreover, lowering the tissue pH during the autolytic process by 0.6 unit from approximately 6.8 to approximately 6.2 produced a nearly 60% slowing of the net rate of tissue ATP depletion from 0.200 to 0.087 mumol X min-1 X g wet wt-1. The pH dependence of the net rate of tissue ATP depletion (by an oligomycin-sensitive process) was that predicted from the mitochondrial ATPase pH-inhibition profiles reported earlier (J. Biol. Chem. 258: 9657-9661, 1983). When taken together with our observation that the mitochondrial ATPase comprises approximately 90% of the total of all of the ATP hydrolyzing activities present in cardiac muscle cells, data reported here suggest that the protonic inhibition of the mitochondrial ATPase plays a major role in regulating the rate of tissue ATP depletion during myocardial ischemia.

scholarly journals Uniform sarcomere shortening behavior in isolated cardiac muscle cells.

1980 ◽  
Vol 76 (5) ◽  
pp. 587-607 ◽  
Author(s):  
J W Krueger ◽  
D Forletti ◽  
B A Wittenberg
Keyword(s):  
Cardiac Muscle ◽  
Heart Muscle ◽  
Sarcomere Length ◽  
Maximum Velocity ◽  
Diffraction Method ◽  
Muscle Cells ◽  
Adult Rats ◽  
Cardiac Muscle Cells ◽  
Ventricular Tissue ◽  
Intact Heart

We have observed the dynamics of sarcomere shortening and the diffracting action of single, functionally intact, unattached cardiac muscle cells enzymatically isolated from the ventricular tissue of adult rats. Sarcomere length was measured either (a) continuously by a light diffraction method or (b) by direct inspection of the cell's striated image as recorded on videotape or by cinemicroscopy (120--400 frames/s). At physiological levels of added CaCl2 (0.5--2.0 mM), many cells were quiescent (i.e., they did not beat spontaneously) and contracted in response to electrical stimulation (less than or equal to 1.0-ms pulse width). Sarcomere length in the quiescent, unstimulated cells (1.93 +/- 0.10 [SD] micrometers), at peak shortening (1.57 +/- 0.13 micrometers, n = 49), and the maximum velocity of sarcomere shortening and relengthening were comparable to previous observations in intact heart muscle preparations. The dispersion of light diffracted by the cell remained narrow, and individual striations remained distinct and laterally well registered throughout the shortening-relengthening cycle. In contrast, appreciable nonuniformity and internal buckling were seen at sarcomere lengths < 1.8 micrometers when the resting cell, embedded in gelatin, was longitudinally compressed These results indicate (a) that shortening and relengthening is characterized by uniform activation between myofibrils within the cardiac cell and (b) that physiologically significant relengthening forces in living heart muscle originate at the level of the cell rather than in extracellular connections. First-order diffracted light intensity, extremely variable during sarcomere shortening, was always greatest during midrelaxation preceding the onset of a very slow and uniform phase of sarcomere relengthening.

THE EFFECTS OF ACUPUNCTURE ON CARDIAC MUSCLE CELLS AND BLOOD PRESSURE IN SPONTANEOUS HYPERTENSIVE RATS

2004 ◽  
Vol 29 (1) ◽  
pp. 83-95 ◽  
Author(s):  
Hung-Chien Wu ◽  
Jaung-Geng Lin ◽  
Chun-Hsien Chu ◽  
Yung-Hsien Chang ◽  
Chung-Gwo Chang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Muscle ◽  
Muscle Cells ◽  
Hypertensive Rats ◽  
Cardiac Muscle Cells

Dendroaspis Natriuretic Peptide Induces the Apoptosis of Cardiac Muscle Cells

2005 ◽  
Vol 27 (1) ◽  
pp. 33-51 ◽  
Author(s):  
Ki-Chan Ha ◽  
Han-Jung Chae ◽  
Cheng-Shi Piao ◽  
Suhn-Hee Kim ◽  
Hyung-Ryong Kim ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Natriuretic Peptide ◽  
Muscle Cells ◽  
Cardiac Muscle Cells
Sign in / Sign up

Export Citation Format

Share Document