Summary
Experimental cardiopathies that are widely different in their histologic characteristics were studied in the albino rat. The main purpose of these comparative investigations was to determine the participation of various cations and anions (especially of K, Mg, Na and Cl) in the pathogenesis of metabolic cardiopathies that are induced by chemical means, but are not accompanied by histologically detectable changes of the coronary arteries.
It was observed that variations in dietary intake, not only of certain cations (K and Mg) but also of the anions (Cl and PO4), play an important role in the pathogenesis of certain necrotizing cardiopathies as well as in the mechanism of adaptive reactions that basically alter the disease-susceptibility of the myocardium. It was also noted that most of the agents that are capable of inducing cardiac lesions through some biochemical mechanism are potentially acting pathogens, whose cardiotoxicity largely depends upon other factors or conditions: some of which (i. e., corticoids, Na-salts, dietary deficiencies in K, Mg and Cl, sudden stress situations, age and coronary sclerosis) uniformly sensitize, while others (i. e., Cl-excess, Na-deficiency, adaptation to stressor agents and the condition produced by pregnancy) desensitize the myocardium to the production of cardiac lesions (necrosis, inflammation, calcification) by most diverse potentially pathogenic agents. On the other hand, the cardiac infarcts that can be produced by surgical occlusion of coronary arteries in the rat, differ basically in many respects from all metabolic cardiopathies studied. The latter are characterized precisely by the fact that they depend upon complex anion-cation interactions, not upon a single pathogen.
The importance of K, Mg, Na and Cl in the pathogenesis of cardiac necroses and the possible role of the ionic equilibrium in the production and prevention of necrotizing cardiac diseases are discussed on the basis of experimental studies performed by the author and of previous observations described by others.
Résumé
Nous avons étudié chez le rat diverses cardiopathies expérimentales à caractères histologiques différents. Ces études comparatives avaient pour objet d'évaluer le rôle de certains anions et cations (notament, le K, Mg, Na et le Cl) dans la pathogénèse des cardiopathies métaboliques provoquées par des agents chimiques mais en l'absence de toutes modifications histologiquement démontrables des artères coronaries.
Il fut observé que des variations du contenu en cations K et Mg ou encore en anions Cl et PO4 dans la diète, jouent un rôle important dans la pathogénèse de certaines cardiopathies nécrosantes tout autant que dans le mécanisme fondamental des réactions adaptives qui modifient la susceptibilité du myocarde. Nous avons constanté en outre que la plupart des agents capaples d'induire des lésions cardiaques par un mécanisme biochimique ont un potentiel pathogène et que leurs effets cardiotoxiques dépendent d'autres facteurs ou conditions. Ainsi, les hormones corticoïdes, les sels de Na, les déficiences alimentaires en K, Mg et Cl, les stress aigus, l'âge et la sclérose des artères coronaires tiennent lieu d'agents sensibilisateurs alors qu'un excès en Cl, une déficience en Na, une adaptation aux agents stressants et la gestation désensibilisent le myocarde à la production de lésions cardiaques (nécrose, inflammation, calcification) par des agents à potentiels pathogènes les plus divers. Par ailleurs, les infarctus cardiaques provoqués par l'occlusion chirurgicale des artères coronaires chez le rat, montrent des différences fondamentales avec les cardiopathies métaboliques que nous avons étudiées. Ces derniers, en effet, out pour caractéristique de dépendre essentiellement d'une interaction entre les anions et les cations et n'ont pas un seul agent pathogène.
L'importance du K, Mg, Na et du Cl dans la pathogénèse des nécroses du myocard et le rôle possible de l'équilibre ionique dans la production et la prévention des maladies cardiaques de type nécrosant sont discutés sur la base des études expérimentales effectuée par l'auteur et de diverses observations décrites par l'auteur.
Similar content being viewed by others
References
Lewitzky, A., Zbl. allg. Path.16, 532 (1905).
Selye, H., Krankheitsforschg.7, 289 (1929).
Erb, W., Arch. Exp. Path. Pharmakol.53, 173 (1906).
Fischer, B., Münch. med. Wschr.22, 235 (1905).
Schrader, G. A., C. O. Prickett undW. D. Salmon, J. Nutrition14, 85 (1937).
Büchner, F. undW. Lucadou, Beitr. Path. Anat.93, 169 (1934).
Selye, H., The Chemical Prevention of Cardiac Necroses (New York 1958).
Selye, H., The Pluricausal Cardiopathies (Springfield 1961).
Bajusz, E., Conditioning Factors for Cardiac Necroses (Ph. D. thesis, Université de Montréal) (Montreal 1962).
Bajusz, E., Z. angew. Bäder. Klimaheilk.5, 446 (1958).
Bajusz, E., Amer. J. Phys. Med.39, 153 (1960).
Bajusz, E. undH. Selye, Trans. N. Y. Acad. Sci.21, 659 (1959).
Selye, H. undE. Bajusz, Schweiz. med. Wschr.88, 1147 (1958).
Selye, H. undE. Bajusz, Acta physiol. latinoam.8, 147 (1958).
Selye, H. undE. Bajusz, Arzneimittelforschg.9, 281 (1959).
Selye, H., E. Bajusz, S. Renaud undN. Nádasdi, Ars Medici15, 831 (1960).
Cannon, P. R., L. E. Frazier undR. H. Hughes, Metabolism1, 49 (1952).
Follis, R. H., jr., Deficiency Disease. Functional and Structural Changes in Mammalia which Result from Exogenous or Endogenous Lack of One or More Essential Nutrients (Springfield 1958).
Grundner-Culemann, A., Arch. Kreislaufforschg.18, 185 (1952).
Meyer, J. H., R. R. Grunert, M. T. Zepplin, R. H. Grummer, G. Bohstedt undP. H. Phillips, Amer. J. Physiol162, 182 (1950).
Smith, S. G., B. Black-Schaffer undT. E. Lasater, A. M. A. Arch. Path.49, 185 (1950).
Thomas, R. M., E. Mylon undM. C. Winternitz, Yale J. Biol. Med.12, 345 (1940).
Liebow, A. A., W. J. McFarland undR. Tennant, Yale J. Biol. Med.13, 523 (1941).
Follis, R. H., jr., Bull. Johns Hopkins Hosp.71, 235 (1942).
Darrow, D. C., Proc. Soc. Exp. Biol. Med.55, 13 (1944).
Welt, L. G., W. Hollander, jr. undW. B. Blythe, J. Chronic Dis.11, 213 (1960).
Follis, R. H., Jr.,E. Orent-Keiles undE. V. McCollum, Amer. J. Path.18, 29 (1942).
Kronberg, A. undK. M. Endicott, Amer. J. Physiol.145, 291 (1946).
Poche, R., Arch. Path. Anat.331, 165 (1958).
Perkins, J. G., A. B. Petersen undJ. A. Riley, Jr., Amer. J. Med.8, 115 (1950).
Goodof, I. I. undC. N. MacBryde, J. Clin. Endocrin.4, 30 (1944).
Rodriguez, C. E., A. L. Wolfe undV. W. Bergstrom, Amer. J. Clin. Path.20, 1050 (1950).
Luft, R., N. Ringertz undB. Sjörgen, Acta endocrin.7, 196 (1951).
MaAllen, P. M., Brit. Heart J.17, 5 (1955).
Keye, J. D., Jr., Circulation5, 766 (1952).
Eppright, E. S. undA. H. Smith, J. Biol. Chem.118, 679 (1937).
Heppel, L. A., Amer. J. Physiol.127, 385 (1939).
Meyer, J. H., R. R. Grunert, M. T. Zepplin, R. H. Grummer, G. Bohstedt undP. H. Phillips, Amer. J. Physiol.162, 182 (1950).
Freed, S. C. undM. Friedman, Proc. Soc. Exp. Biol. Med.78, 74 (1951).
Cannon, P. R., L. E. Frazier undR. H. Hughes, Metabolism2, 297 (1953).
Rahman, M. H., L. E. Frazier, R. H. Hughes undP. R. Cannon, A. M. A. Arch. Path.63, 154 (1957).
Craig, J. M. undR. Schwartz, A. M. A. Arch. Path.64, 245 (1957).
Selye, H. undE. Bajusz, Proc. Soc. Exp. Biol. Med.98, 580 (1958).
Selye, H. undE. Bajusz, Brit. J. Pharmacol.14, 83 (1959).
Selye, H. undE. Bajusz, Amer.-J. Path.35, 525 (1959).
Follis, R. H., Jr., Proc. Soc. Exp. Biol. Med.51, 71 (1942).
Perdue, H. S. undP. H. Philipps, Proc. Soc. Exp. Biol. Med.81, 405 (1952).
Morrison, A. B., Proc. Soc. Exp. Biol. Med.103, 500 (1960).
Bois, P. undG. Jasmin, Rev. Canad. Biol.18, 358 (1959).
Kruse, H. D., E. R. Orent undE. V. McCollum, J. Biol. Chem.96, 519 (1932).
Barron, G. P., S. O. Brown undP. B. Pearson, Proc. Soc. Exp. Biol. Med.70, 220 (1949).
Brookfield, R. W., Brit. Med. J.1934, I, 848.
Cramer, W., Lancet1932, 174.
Greenberg, D. M. C. E.Anderson und E. V.Tufts, Proc. 30th Ann. Meet. Amer. Soc. Biol. Chem.(1936).
Lowenhaupt, E., M. P. Schulman undD. M. Greenberg, A. M. A. Arch. Path.49, 427 (1950).
Syllm-Rapoport, I., Klin. Wschr.36, 140 (1958).
Moore, L. A., E. T. Hallman undL. B. Sholl, A. M. A. Arch. Path.26, 820 (1938).
Mishra, R. K., Rev. Canad. Biol.19, 122 (1960).
Colby, R. W. undC. M. Frye, Amer. J. Physiol.166, 209 (1951).
Coltove, E., M. A. Holliday, R. Schwartz undW. M. Pallace, Amer. J. Physiol.167, 665 (1951).
Duckworth, J., W. Godden undG. M. Warnock, Biochem. J.34, 97 (1940).
Kunkel, H. O. undP. B. Pearson, J. Nutrition36, 657 (1948).
Patton, R. A., J. Comp. Physiol. Psychol.40, 283 (1947).
Tufts, E. V. undD. M. Greenberg, J. Biol. Chem.122, 693 (1938).
Vitale, J. J., P. L. White, M. Nakamura, D. M. Hedsted, N. Zanchek undE. E. Hellerstein, J. Exp. Med.106, 757 (1957).
Almquist, H. J., Proc. Soc. Exp. Biol. Med.49, 544 (1942).
Osborne, T. B. undL. B. Mendel, J. Biol. Chem.34, 131 (1918).
Fitzgerald, M. G. undP. Fourman, Clin. Sci.15, 635 (1956).
Barnes, B. A., O. Cope undT. Harrison, J. Clin. Invest.37, 430 (1958).
Klieber, M., M. D. Boelter undD. M. Greenberg, J. Nutrition21, 363 (1941).
Mishra, R. K., “Studies on experimental magnesium deficiency in the albino rat.” (D. Sc. thesis, Université de Montréal 1959).
Martin, H. E., J. Mehl undM. Wertman, Med. Clin. Amer.36, 1157 (1952).
Haury, V. G., J. Lab. Clin. Med.27, 1361 (1942).
Mader, I. J. undL. T. Inseri, Amer. J. Med.19, 976 (1955).
Blaxter, K. L., Bone Structure and Metabolism. P. 117. Ciba Found. Symp. (London 1956).
Hirschfelder, A. D., Proc. Soc. Exp. Biol. Med.30, 996 (1933).
Flink, E. B., R. McCollister, A. S. Prasad, J. C. Melby undR. P. Doe, Ann. Int. Med.47, 956 (1957).
Haury, V. G., J. Pharmacol. Exp. Ther.65, 453 (1939).
Székely, P., Brit. Heart J.8, 115 (1946).
Winkler, A. W., P. K. Smith undH. E. Hoff, J. Clin. Invest.21, 207 (1942).
Bernstein, M. undS. Sinkins, Amer. Heart J.17, 218 (1939).
Rothberger, C. J. undL. Zwillinger, Arch. Exp. Path. Pharmacol.181, 301 (1936).
Smith, P. K., A. V. Winkler undH. E. Hoff, Anesthesiology3, 323 (1942).
Malkiel-Shapiro,B., S. Afr. Med. J.32, 1211 (1958).
Perlia, A. N., Soviet. Med.20, 63 (1956).
Tufts, E. V. undD. M. Greenberg, J. Biol. Chem.122, 715 (1938).
Colby, R. W. undC. M. Frye, Amer. J. Physiol.166, 408 (1951).
Colby, R. W. undC. M. Frye, Amer. J. Physiol.166, 209 (1951).
Selye, H. undE. Bajusz, Z. Vitamin-Hormon.-Ferment-Forschg.10, 39 (1959).
Selye, H. undE. Bajusz, Cardiologia33, 305 (1958).
Bajusz, E. undH. Selye, Acta Pharmacol. (Kbh.),15, 235 (1959).
Selye, H. undE. Bajusz, Amer. J. Physiol.196, 681 (1959).
Bajusz, E. undH. Selye, Proc. Canad. Fed. Biol. Socs.2, 5 (1959).
Selye, H. undE. Bajusz, J. Nutrition72, 37 (1960).
Ellis, J. T., Amer. J. Path.32, 993 (1956).
Mefferd, R. B., Jr. und H. B.Hale, Air Univ. School of Med., USAF, Randolph AFB (Texas 1958).
Tapley, D. F., Bull. Johns Hopkins Hosp.96, 274 (1955).
Gray, I. undW. J. Jordan, Arch. Biochem.57, 521 (1955).
Meessen, H., Wien. Z. Inn. Med.39, 41 (1958).
Hellerstein, E. E., J. J. Vitale undN. Zamcheck, Fed. Proc.16, 359 (1957).
Hellerstein, E. E., J. J. Vitale, P. L. White, D. M. Hegsted, N. Zamcheck undM. Nakamura, J. Exp. Med.106, 767 (1957).
Vitale, J. J., P. L. White undM. Nakamura, Fed. Proc.16, 400 (1957).
Vitale, J. J., D. M. Hegsted, M. Nakamura undP. Connors, J. Biol. Chem.226, 597 (1957).
Vitale, J. J., M. Nakamura undD. M. Hegsted, J. Biol. Chem.228, 573 (1957).
Bajusz, E. undH. Selye, Amer. Heart J.60, 266 (1960).
Thacker, E. J., J. Nutrition26, 431 (1943).
Voris, L. undE. J. Thacker, J. Nutrition23, 365 (1942).
Selye, H. undE. Bajusz, Angiology10, 412 (1959).
Raab, W., Cardiologia36, 181 (1960).
Raab, W., E. Stark undW. R. Gigee, Circulation20, 754 (1959).
Bajusz, E. undH. Selye, Canad. Med. Assoc. J.82, 212 (1960).
Bajusz, E. undH. Selye, Acta endocr. (Kbh.)36, 295 (1961).
Selye, H. undE. Bajusz, Proc. Soc. Exp. Biol. Med.100, 11 (1959).
Bajusz, E. und H.Selye, 5th Internat. Congress on Nutrition (Washington, D. C., Sept. 1–5, 1960).
Bajusz, E. undH. Selye, Fed. Proc.19, 259 (1960).
Bajusz, E. undH. Selye, Kisérl. Orvostud.12, 283 (1960).
Selye, H. undE. Bajusz, Zvlas. Vesmir (Prague)37, 271 (1958).
Selye, H. undE. Bajusz, Acta endocr. (Kbh.),30, 183 (1959).
Bajusz, E. undR. Fitko, Pol. Tyg. Lek.15, 201 (1960).
Bajusz, E. undR. Fitko, Pol. Tyg. Lek.15, 6 (1960).
Bajusz, E., Z. Ges. Exp. Med.130, 13 (1958).
Bajusz, E. undM. Nadasdi, Folia Endocr. (Pisa)11, 446 (1958).
Selye, H. undE. Bajusz, Orv. Hetil.101, 168 (1960).
Seyle, H. undE. Bajusz, Lab. Invest.8, 1499 (1959).
Selye, H., E. Bajusz, S. Renaud undY. Lemire, Amer. Heart J.57, 88 (1959).
Selye, H. undE. Bajusz, Amer. J. Cardiol.4, 102 (1959).
Selye, H., E. Bajusz undS. Renaud, Z. Kreislaufforschg.48, 237 (1959).
Selye, H. undE. Bajusz, Virchows Arch. Path. Anat.332, 140 (1959).
Bajusz, E. undH. Selye, Amer. J. Physiol.199, 453 (1960).
Bajusz, E. undH. Selye, Folia Clin. Int.10, 260 (1960).
Selye, H. und E.Bajusz, Protection Afforded by Stress Against Humorally Induced Cardiac Necroses. Sodi-Pallares' Memorial Vol. (Mexico 1962).
Bajusz, E. undH. Selye, Naturwiss.47, 520 (1960).
Selye, H., P. Jean undE. Bajusz, Sem. Hop. Paris9, 331 (1961).
Selye, H. undE Bajusz, Arch. Int. Physiol67, 78 (1959).
Selye, H. undE. Bajusz, Beitr. Path. Anat.119, 333 (1958).
Selye, H. undE. Bajusz, Amer. J. Path.38, 481 (1961).
Selye, H., E. Bajusz undR. Strebel, Canad. J. Biochem.39, 519 (1961).
Strebel, R., H.Selye und E.Bajusz, Amer. J. Cardiol. (1962 im Druck).
Bajusz, E., H.Selye und R.Strebel, Proc. of 3rd World Congr. Psychiatr. (1962 im Druck).
Bajusz, E., Progr. Neurol. Psychiatr.15, 233 (1960).
Bajusz, E., Progr. Neurol. Psychiatr.16, 233 (1961).
Selye, H., E. Bajusz, S. Grasso undP. Mendell, Angiology11, 398 (1960).
Zsotér, T. und E.Bajusz, Cardiologia (1962 im Druck).
Selye, H., E. Bajusz undS. Renaud, Monit. Ostet. Ginec.30, 7 (1959).
Selye, H., A.Horava und G.Heuser, 1st–5th Vols. (Montreal 1951–55/56).
Conn, J. W., L. H. Louis, S. S. Fajans, D. H. P. Streeten undR. D. Johnson, Lancet1957/I, 802.
Smith, S. G., Arch. Biochem.20, 473 (1949).
Smith, S. G., Amer. J. Physiol.164, 702 (1951).
MacIntyre, I. undD. Davidsson, Biochem. J.70, 456 (1958).
Wolf, S., Mod. Conc. Cardiov. Dis.29, 599 (1960).
Hickam, J. B., W. N. Cargill undA. Golden, J. Clin. Invest.27, 290 (1948).
Stevenson, I. P., C. M. Duncan, undH. G. Wolff, J. Clin. Invest.28, 534 (1949).
Wolf, S., P. V.Cardon, E. M.Shepard und H. G.Wolff, Life Stress and Essential Hypertension: Study of Circularory Adjustments in Man. (Baltimore 1955).
Stevenson, I. P., C. M. Duncan undH. S. Ripley, J. Amer. Geriat. Soc.6, 104 (1951).
Duncan, C. M., I. P. Stevenson undH. G. Wolff, Psychosom. Med.13, 36 (1951).
Wolf, G. A., Jr. undH. G. Wolff, Psychosom. Med.8, 293 (1946).
Bard, P., Physiol. Rev. (Suppl. 4)40, 3 (1960).
Delgado, J. M. R., Physiol. Rev. (Suppl. 4)40, 148 (1960).
Karplus, J. P. undA. Kreidl, Arch. Ges. Physiol.215, 667 (1927).
Gellhorn, E., Autonomic Imbalance and the Hypothalamus (Minneapolis 1957).
Smith, C. A., Jr.,S. J. Jabbur undE. P. Lasher, Physiol. Rev. (Suppl. 4)40, 136 (1960).
Bard, P. A., Amer. J. Physiol.84, 490 (1928).
Folkow, B., Physiol. Rev. (Suppl. 4),40, 93 (1960).
Bajusz, E. und H.Selye, (not published observations).
Tanz, R. D., J. Pharmacol. Exp. Ther.128, 168 (1960).
Bajusz, E., Proc. Canad. Fed. Biol. Socs.1, 4 (1958).
Bajusz, E., Endocrinology64, 262 (1959).
Bajusz, E., Acta Neuroveg.20, 219 (1959).
Bajusz, E., Z. Vitamin-Hormon-Fermentforschg.10, 81 (1959).
Bajusz, E., Z. Vitamin-Hormon-Fermentforschg.10, 212 (1959).
Selye, H., E.Bajusz und M.Cantin, Z. Vitamin-Hormon-Fermentforschg. (1961 in press).
Selye, H. undE. Bajusz, Amer. J. Physiol.192, 297 (1958).
Danowski, T. S., Diabetes Mellitus, with Emphasis on Children and Young Adults (Baltimore 1957).
Kaiser, H., Münch. med. Wschr.102, 931 (1960).
Tanz, R. D., R. W. Whitehead undG. J. Voir, Jr., Proc. Soc. Exp. Biol. Med.94, 258 (1957).
Rogoff, J. M. undG. N. Steward, Amer. J. Physiol.78, 683 (1926).
Hench, P. S., C. H. Slocumb, A. R. Barnes, H. L. Smith, L. F. Polley undE. C. Kendall, Proc. Mayo Clin.24, 277 (1949).
Perera, G. A., K. L. Pines, H. B. Hamilton undK. Vislocky, Amer. J. Med.7, 56 (1949).
Sommerville, F., Brit. Med. J.1950/I, 860.
Selye, H., Canad. Med. Ass. J.42, 118 (1940).
Abrams, W. B. undT. N. Harris, Amer. Heart J.42, 876 (1951).
Hoffman, G., Arch. Exp. Path. Pharmakol.222, 224 (1954).
Emele, J. F. undB. D. Bonnycastle, Amer. J. Physiol.185, 103 (1956).
Booker, W. M., F. DeCosta, S. Mitchell undE. J. Robinson, J. Pharmacol. Exp. Ther.116, 8 (1956).
Cannon, C. undW. M. Booker, Fed. Proc.16, 187 (1957).
Shelton, M., W. M. Booker, A. Adoyene undG. Alles, Fed. Proc.15, 482 (1956).
Lacroix, E. undI. Leusen, Arch. Int. Pharmacodyn114, 103 (1958).
Bajusz, E. undH. Selye, Acta pharmacol. (Kbh.)15, 235 (1959).
Nasmyth, P. A., J. Physiol.139, 523 (1957).
Solomon, N., R. H. Travis undG. Sayers, Endocrinology64, 535 (1959).
Nahas, G., Circulat. Res.5, 48 (1957).
Crossfield, H. C., J. P. DaVanze undW. W. Swingle, Circulation18, 710 (1958).
Selye, H. und E.Bajusz, Orv. Hetil. (1962 im Druck).
Nickerson, M., G. W. Karr undP. E. Dresel, Fed. Proc.18, 427 (1959).
Gubner, R. S., Clin. Res.6, 209 (1957).
Turner, J. M., Biochem. J.70, 9 (1958).
Macchi, V. undM. Corti, Minerva Med.50, 4127 (1959).
Author information
Authors and Affiliations
Additional information
Part I: Z. Ernährungswiss.2, 229 (1962).
Rights and permissions
About this article
Cite this article
Bajusz, E. Nutritional factors in the pathogenesis of cardiac necroses. Z Ernährungswiss 3, 1–26 (1962). https://doi.org/10.1007/BF02021335
Received:
Published:
Issue Date:
DOI: https://doi.org/10.1007/BF02021335