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Publications and source records attributed to E Page.

At least 91 records · Page 5Linked to original sources
PubMed1981

Development of dyadic junctional complexes between sarcoplasmic reticulum and plasmalemma in rabbit left ventricular myocardial cells. Morphometric analysis.

Dyadic junctional couplings between cardiac sarcoplasmic reticulum (SR) and plasma membrane presumably are implicated in release of Ca2+ from terminal cisterns of SR during excitation-contraction coupling. We measured the areas of SR and plasma membrane involved in such couplings in late embryonic and neonatal rabbit left ventricles during a developmental period characterized by rapid cell growth and rapid accumulation of myofibrils. By morphometric methods previously applied to adult hearts, it could be shown that from the inception of the nascent T-system the surface density of dyadic couplings at T-tubular plasmalemma exceeds by about four-fold that at the external plasmalemmal envelope. Before the development of a T-system (similar to or approximately 10 days after birth) surface density of dyads, as well as total dyad areas per unit cell volume and per unit myofibrillar volume, increase progressively during embryonic life until they approach constancy at near adult values one day after birth. Constancy of total dyadic membrane area per unit myofibrillar volume during neonatal cell growth confirms that the membrane area of the activating system and the volume of myofibrils to be activated accumulate in a constant proportion.

Animals↗
PubMed1980

Accumulation of technetium-99m pyrophosphate in experimental infarctions in the rat.

Cardiac accumulation patterns of pyrophosphate labelled with techetium-99m (TcPyP) in rats one hour to 7 days after coronary artery ligation were studied by light microscopy, myocardial scintigraphy, imaging the isolated heart and by direct measurement of tissue activity. Results suggest that myocardial cells taking up TcPyP are irreversibly damaged and that the disappearance of TcPyP uptake coincides with the removal of necrotic cells by phagocytes.

Animals↗
PubMed1980

Chloride distribution and exchange in rat ventricle.

The cellular Cl content and concentration ([Cl]cell) and the cellular uptake of 36Cl have been measured in the rat left ventricle in vivo. The in vitro efflux of 36Cl from perfused contracting ventricles preequilibrated with 36Cl in vivo was also determined at 22, 30, and 38 degrees C. [Cl]cell was 8.2 +/- 0.5 mmol/kg cell water, corresponding to a calculated equilibrium potential of Cl of -70 to -80 mV. This figure for [Cl]cell is significantly lower than previous estimates in the literature, which were subject to an analytical error leading to overestimation of muscle Cl content obtained coulometrically. At 38 degrees C, Cl exchange under quasi-steady-state conditions was 31.2 mumol . (g dry ventricle . min)-1 or 42.5 pmol . (cm2 plasma membrane . s).-1 Apparent activation energy of the flux was 10.4 kcal/mol. At 22 degrees C, no dependence of the exchange on contraction frequency was detectable over a range of 80-160 contractions/min. The Cl exchange flux is among the fastest, if not the fastest. known for myocardial ion transport.

Animals↗
PubMed1980

Quantitative studies on plasmalemmal folds and caveolae of rabbit ventricular myocardial cells.

Plasmalemmal folds and caveolae were investigated by qualitative and quantitative analysis of electron micrographs obtained by freeze fracture and transmission electron microscopy (TEM) of rabbit right ventricular papillary muscles whose mean sarcomere lengths ranged from 1.64 to 2.28 micron. In passively extended muscles, folds were observed at sarcomere lengths of 2.3 micron and could be shown by extrapolation to become completely extended at a maximum sarcomere length of 2.8 micron. It was concluded that the plasmalemma does not contribute to resting tension in the physiological range of sarcomere lengths. Caveolae are present in both the external plasmalemmal envelope and T-tubular plasmalemma. They show no preferential distribution with respect to underlying myofibrillar striations or membrane folds and are nearly devoid of membrane particles in freeze-fractured material. The surface density of caveolar necks (4.0/micron2 apparent plasmalemmal area) is only 16-20% of that reported for frog skeletal muscle. Caveolae augment plasmalemmal area by 21-32%, assuming two or three caveolae per neck, respectively. Caveolar membrane does not serve as a reservoir of membrane to be recruited into external plasmalemma, at least over the physiological range of sarcomere lengths. In heart muscle they do not account for the T-tubular access resistance, and their function in this tissue remains unknown.

Animals↗
PubMed1979

Interstitial anion distribution in striated muscle determined with [35S]sulfate and [3H]sucrose.

The distributions of a charged and an uncharged extracellular tracer in the interstitial spaces of skeletal and heart muscles were examined in vivo by a double-labeling technique. 35SO4(2-) and [3H]sucrose were simultaneously injected intraperitoneally into rats and toads, and extracellular volume was determined in the rat gastrocnemius and left ventricle and in the toad semitendinosus. In nephrectomized rats and in toads with intact kidneys, sucrose and SO4(2-) spaces were constant for several hours. Sucrose and SO4(2-) spaces did not significantly differ in rat ventricle (P greater than 0.80); in rat gastrocnemius the sucrose space was much larger than SO4(2-) space (2P less than 0.0005), while in toad semitendinosus sucrose space was somewhat smaller than SO4(2-) space (2P less than 0.005). These observations suggest that fixed charges in the interstitial compartment can lead to extracellular anion exclusion in some tissues and perhaps to accumulation in others. The magnitude and direction of these effects differ for different striated muscles.

Animals↗
PubMed1979

Distribution, surface density, and membrane area of diadic junctional contacts between plasma membrane and terminal cisterns in mammalian ventricle.

The surface density of diadic junctional complexes (DJC) between plasmalemma and terminal cisternal membrane, as well as the areas of plasmalemmal and cisternal membrane involved in DJC, have been determined morphometrically in external plasmalemmal envelope and T-system of rabbit, rat, and mouse ventricular heart muscle. In all three species, both the surface density and the plasmalemmal area of DJC are 4- to 6-fold greater in the T-system than in the external plasmalemmal envelope. The surface density and DJC membrane area per unit cell volume and per unit myofibrillar volume increase in the order rabbit less than rat congruent to mouse and are not related simply to basal heart rate or intraventricular pressure. The results show that if Ca2+ release is a function of terminal cisterns, then, in ventricular heart muscle, most of the Ca2+ thus released for myofibrillar activation must originate from cisterns associated with the T-system. They make it necessary to consider the possibility that the 20--50% of plasmalemma in the T-system that is involved in excitation-contraction coupling may be unavailable for other processes; and they show that interspecies differences in surface density and membrane area of DJC/unit cellular and myofibrillar volume correlate with differences in Ca2+- activated Ca2+ release in skinned fibers and with differences in rate of tension development described for intact rat and rabbit ventricular muscle.

Anatomy, Comparative↗
PubMed1978

Cellular Cl content and concentration of amphibian skeletal and heart muscle.

Toads (Bufo marinus) and frogs (Rana pipiens pipiens) were given intraperitoneal injections of Na36Cl and Na235SO4. After in vivo equilibration for 20--180 min, the animals were pithed, and their ventricular and semitendinosus muscles were excised. Measurements of total Cl (by titrimetry) and 36Cl (by radioassay) showed that specific radioactivities of plasma and mus les approached equality within 1 h after injection for toad skeletal and heart muscle and frog ventricles, indicating complete exchange of cellular Cl with 36Cl. From the simultaneously measured muscle water contents and 35SO4 spaces, intracellular Cl concentrations in vivo (in mumol/g cell water) for semitendinosus and ventricular muscles were calculated to be, respectively, 1.4 +/- 0.3 and 2.3 +/- 0.8 for Bufo and 1.7 +/- 0.7 and 4.8 +/- 2.4 for Rana. In view of these low values, active cellular Cl accumulation seems improbable, but cannot be rigorously excluded without simultaneous membrane potential and intracellular ion activity measurements. A high concentration of Cl in the sarcoplasmic reticulum of skeletal muscle is also inconsistent with these measurements.

Animals↗
PubMed1978

Quantitative ultrastructural analysis in cardiac membrane physiology.

Quantitative measurements on electron micrographs of heart muscle can yield information useful for cellular physiologists and at present not obtainable in other ways. These methods are subject to preparative artifact, sampling problems, and problems inherent in the mathematical description of ultrastructure. Nevertheless they provide the best available data for membrane areas of the plasmalemma and its components, as well as for membrane areas of the sarcoplasmic reticulum and mitochondria. Morphometric methods can be used to study growth of membranes. Changes in the volumes of intracellular membrane-limited subcompartments can also be measured. Quantitative analysis of freeze-fractured membrane replicas can be carried out either by a statistical approach or by optical diffraction. In this way, physiological perturbations or developmental events leading to changes in membrane permeability can be studied for correlated changes in membrane structure.

Animals↗
PubMed1977

Volume changes in sarcoplasmic reticulum of rat hearts perfused with hypertonic solutions.

To explore whether morphometry of intracellular membrane-limited subcompartments can be used to follow physiological volume changes in such subcompartments in hearts rapidly fixed by perfusion fixation, we have measured osmotically induced volume changes in electron micrographs of longitudinally oriented sarcoplasmic reticulum (LSR) and terminal cisterns (TC) of rat left ventricular myocardial cells. Vascular perfusion with solutions whose osmolality varied from 0.67 to 1.88 isomolal showed that in the hyperosmolal range LSR volume decreased linearly. Approximately 79% of LSR luminal volume participated in the osmotic rey unresponsive. By contrast, we found that the TC responded by dilation when hearts were perfused with hypersomolal NaCl, NaI, LiCl, or sucrose. Furthermore, with hyperosmolal NaCl the dilation developed within 1 minute; its rate and extent of development were concentration-dependent; it manifested an obligate association with prior or concomitant T-tubular dilation and was not readily reversible. We conclude that (1) the technique sensitively measures in situ changes of LSR volume; (2) most of LSR luminal water is osmotically responsive, but a significant fraction may not be; (3) exposure to hyperosomolal solutions may bring about (perhaps irreversible) structural changes in the diadic membrane complex, leading to changes in its solute permeability.

Animals↗