Carnitine transport and exogenous palmitate oxidation in chronically volume-overloaded rat hearts

L-Carnitine transport and free fatty acid oxidation have been studied in hearts of rats with 3-month-old aorto-caval fistula. For carnitine transport experiments, the hearts were perfused via the ascending aorta with a bicarbonate buffer containing 11 mM glucose and variable concentrations L-[14C]carnitine (10-200 microM). In some experiments, the active component of carnitine transport was suppressed by the adjunction of 0.05 mM mersalyl acid. The subtraction of passive from total transport allowed reconstruction of the saturation curves of the carrier-mediated transport of L-carnitine. Our data suggest that at a physiological carnitine concentration (50 microM), the rate of [14C]carnitine accumulation was significantly depressed in mechanically overloaded hearts. In addition, according to Lineweaver-Burk analysis, the affinity of the membrane carrier for L-carnitine was considerably diminished (Km carnitine 125 instead of 83 microM, Vmax unchanged). The above alterations of L-carnitine transport did not result from a decrease of the transmembrane gradient of sodium, since the intracellular Na+ content of the hypertrophied hearts was quite similar to that of control hearts. The ability of atrially perfused, working hearts to oxidize the exogenous free fatty acids was assessed from 14CO2 production obtained in the presence of [U-14C]palmitate or [1-14C]octanoate. The total 14CO2 production, expressed per min per g dry weight, was significantly diminished in hearts from rats with the aorto-caval fistula if 1.2 mM palmitate was used. On the other hand, in the presence of 2.4 mM octanoate, a substrate which circumvents the carnitine-acylcarnitine translocase, no such reduction of the 14CO2 production could be detected. Our results suggest that the decrease of L-carnitine transport, resulting in a significant depression of tissue carnitine, may impair long-chain fatty acid activation and/or translocation into mitochondria. In contrast, the oxidation of short-chain fatty acids, the activation of which takes place directly in mitochondrial matrix, is not limited in volume-overloaded hearts.     

Catecholaminergic and peptidergic nerve components of intramural ganglia in the rat heart

Summary Immunohistochemical properties of the terminal nerve network in the rat heart were assessed by use of the elution-restaining method. The colocalization of the enzymes involved in catecholamine synthesis (tyrosine hydroxylase — TH, dopamine--hydroxylase — DBH) as well as the respective distributions of the neuropeptides associated with the adrenergic nervous system (neuropeptide tyrosine — NPY, C-terminal flanking peptide of neuropeptide Y — C-PON) were studied in series of serial sections throughout the interatrial septum and the atrioventricular junction. Our data suggest that ganglion cells of sulcus terminalis as well as the epicardial ganglia enclosed between the superior vena cava and ascending aorta are VIP- and TH-negative, but neuropeptide Y- and DBH-immunoreactive. They give rise to three intraseptal nerves directed towards the specialised structures of the atrioventricular junction. These nerve fascicles contain abundant, thick TH-immunoreactive nerve fibres and scarce, thin NPY- and DBH-immunoreactive fibres. The cell bodies of the intramural ganglion cells localized between the right and left branches of the bundle of His (Moravec and Moravec 1984) are strongly TH- and DBH-immunoreactive. They are innervated by thick nerve fibres having the same immunohistochemical properties (NPY- and DBH-immunoreactivities) as those of a subpopulation of the epicardial ganglion cells and seem to supply some of the TH-immunoreactive nerve fibres directed via the intraseptal nerves to the epicardial ganglia. The existence of a multicomponent nerve network, characterized by a reciprocal innervation of the sinus node and atrioventricular node areas, is suggested by our immunohistochemical data.     

Index of new names of syntaxa published in 1992

The present work collects the new names of syntaxa (in the sense of the Code of Phytosociological Nomenclature,Barkman et al. 1986) above subassociation, rank found in the literature received by the Library of the Conservatoire et Jardin botaniques in Geneva. For the year 1992, 658 names have been listed. For each one of them, an appreciation about its validity is given relating to the Code of Phytosociological Nomenclature. Fifteen names are given in addition to the Indexes 1987, 1990 and 1991 (Theurillat & Moravec 1990, 1993, 1994).     

Die submontanen krautreichen Buchenwälder auf Silikatböden der westlichen Tschechoslowakei

Die submontanen krautreichen Buchenwälder auf Silikatböden in der westlichen Tschechoslowakei (Tschechische Sozialistische Republik) zerfallen in vier Assoziationen: 1.Tilio cordatae-Fagetum Mráz 1960 em.Moravec 1977, 2.Tilio platyphylli-Fagetum Klika 1939, 3.Melico-Fagetum Seibert 1954 und 4.Carici pilosae-Fagetum Oberdorfer 1957. DasTilio cordatae-Fagetum ist an niedrigere Bergländer Mittel-, Süd- und Westböhmens gebunden. DasTilio platyphylli-Fagetum ist eine lokal bedingte Assoziation des Westteils des Gebirges ?eské st?edoho?í. DasMelico-Fagetum kommt in Nord- bis Ostböhmen und Nord- und Mittelmähren vor. DasCarici pilosae-Fagetum ist auf die Karpaten beschränkt (ausnahmsweise greift es auf den Ostrand des Böhmischen Hochlandes über). Die Buchenwälder des Hügellandes bei Jevany (Mittelböhmen) und des Gebirges ?elezné hory gehören, trotz dem Vorkommen in submontanen Lagen, demDentario enneaphylli-Fagetum Oberdorfer ex W. etA. Matuszkiewicz 1960 an. Die Zusammensetzung der Assoziationen ist durch pflanzensoziologische Tabellen belegt und ihre Verbreitung auf einer Punktkarte erfasst.     

Effect of inotropic stimulation on mitochondrial calcium in cardiac muscle.

Ca(2+)-dependent activation of citric acid cycle enzymes has been demonstrated in isolated cardiac mitochondria. These observations led to the hypothesis that Ca2+ is the signal coupling myofibrillar energy use to mitochondrial energy production in vivo. To test this hypothesis we have measured mitochondrial Ca2+ content during increased energy demand, using electron probe microanalysis. Mitochondrial Ca2+ was measured in hamster papillary muscles rapidly frozen at the peak rate of tension rise under control conditions and after stimulation with the beta-adrenergic agonist isoproterenol (10(-6) M). A third group of muscles was frozen after incubation in low (46.5 mM) Na+ solution to Ca2+ load the cells. Pyruvate dehydrogenase activity was measured in each of the muscles. Isoproterenol caused a 39% increase in force and a 43% increase in pyruvate dehydrogenase activity but no change in mitochondrial Ca2+ (0.46 +/- 0.19 (S.E.) mmol of Ca2+/kg, dry weight) compared with control (0.54 +/- 0.12). In contrast, low Na+ increased pyruvate dehydrogenase activity by 56% and also elevated mitochondrial Ca2+ to 1.28 +/- 0.31 (p less than 0.02). These results demonstrate that mitochondrial Ca2+ is not elevated after inotropic stimulation of cardiac muscle by beta-adrenergic agonists although pyruvate dehydrogenase activity is increased. We conclude that Ca2+ uptake by mitochondria is not a requirement for activation of mitochondrial respiration after increased energy demand.