Inbred C3H male mice in 20 groups of 10 each were studied to identify the trace mineral element essential to the prevention of "paralysis" in vitamin E deficiency. Cobalt, copper, manganese, and zinc were studied by employing several possible combinations of omissions and additions. Highly purified vitamin E-deficient diets were employed and α-tocopheryl acetate added as the source of vitamin E. It was found that in vitamin E deficiency a concomitant lack of Mn invariably resulted in 100% incidence of early paralysis. Lack of no other element had this effect. After onset of symptoms, additions of vitamin E or Mn, or both, did not reverse the damage, but life spans were increased. The mechanisms of the effect of Mn in protecting against early onset of paralysis in the mouse has not been explained. Body weights were higher in Mn-fed, E-deficient mice than in groups lacking Mn but receiving other minerals.
The positive inotropic action of glucagon on the cat heart is dependent upon the extracellular Ca concentratiod. The inotropic effect is proportionately greater, the lower the concentration of Ca in the perfusate (above zero, at which glucagon is without significant effect). Nevertheless, Ca influx (as measured with "Ca) into the myocardium is not demonstrably influenced by glucagon, except at 0.09 mM Ca, where the interpretation of the effect is complicated by the fact that there is mechanical asystole at that Ca concentration in the absence of glucagon, while excitation-contraction coupling still occurs when the hormone is added. The possibility is suggested that glucagon may influence intracellular movement of Ca, even when its transmembrane movement is affected only slightly.It has been shown that glucagoji has the capacity to increase tension and work production by heart muscle. The mechanism of the positive inotropic action has not been clarified. Beta-blocking agents do not abolish the action (1-4). It has also been reported that the glucagon effect is unaltered by catecholamine depletion due to treatment with reserpine (2).A possible link with Ca stores is suggested by studies (5) that showed that glucagon caused an increase in Ca stores in microsomal preparations from canine myocardium.The present study was undertaken to ascertain the effects of altered extracellular Ca concentration upon the positive inotropic effect of glucagon, and to measure possible changes in the rate of Ca influx into heart-muscle cells under the influence of glucagon. METHODSMale cats weighing about 3-4 kg were anesthetized with sodium pentobarbital. Artificial respiration with oxygen was applied via an intratracheal cannula. Heparin was injected via the jugular vein. After thoracotomy, the aorta was immediately cannulated for coronary perfusion. The heart was removed from the chest during continuous perfusion with oxygenated, modified Kreb's solution at 37°C, and the mitral valve was quickly incised to prevent distension of the heart. by fluid accumulation. The perfusate from the heart was discarded until it was free from blood. Thereafter, a closedcircuit Langendorff perfusion, as modified by use of a Sigmamotor pump, was performed. The perfusate contained 116 mM NaCl, 5 mM KCl, 25.4 mM NaHCO, 1.24 mM NaHr P04 H20, 1.8 mM CaCI2, and 5.56 mM glucose, and was aerated with 95% 02-5% Co2. Flow rate was 18 ml/min. After 30 min of perfusion, the hearts were perfused with experimental solutions containing various amounts of calcium, with and without glucagon. Reservoirs in the water bath were connected to the perfusion line by three-way stopcocks, so that 463 the desired solutions at identical temperature could be introduced into the perfusion system at any time. Isometrictension development and electrograms were recorded as described (6). The effects of glucagon upon tension production were observed at various concentrations of Ca in the perfusate. When a constant heart rate was required during the Ca-influx study, artificia...
Abstract. In the first 150 seconds after contracture of rabbit myocardium has been induced by shifting from perfusion with zero [Ca2+1 and low [K+] to solutions with normal levels of those cations, there is a large influx of Ca2+ as measured both by isotopic tracer flux and by total tissue [Ca]. Tracer studies indicate that the influx is 90 per cent complete in 90 seconds. Contracture due to substitution of either Li+ or Ki for Na+ in perfusion fluids is also associated with an increased influx, but of lesser magnitude. The latter typ( s of contracture are reversible while the former is not. It seems probable that the irreversible contracture is induced by the large Ca2 + influx.Previous studies' have shown that the net influx of Ca2+ into heart muscle after a period of exposure to zero [Ca2+] [Ca2+] in the perfusate effluent and the extravascular, extracellular fluid. 45Ca was employed as a tracer for calcium movement by switching the perfusate source to a reservoir containing the isotope at the time of beginning the Ca2+ uptake period. After this period the perfusion was instantaneously shifted to solutions of identical composition except for the Ca2+ isotope. Nonradioactive perfusion was continued for exactly 180 sec in order to eliminate the majority of the high activity perfusate. The perfusate effluent was collected at short intervals and it was assumed that the extracellular space was in equilibrium with the perfusate during the final collection period. The 180 sec washout was employed because Ca2+ entrance into muscle cells is slow and large errors could be introduced into 45Ca values for the intracellular compartments by small errors in sucrose-space measurements. According to previous studies on dog papillary muscle by Langer4 and others, the half time for the 603
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.