Summary
In adaptation of rats to repeated stress exposure, a mechanism gradually forms at the level of heart to provide a considerable increase in the organ resistance to reperfusion paradox and toxic concentrations of catecholamines and Ca2 +. Sarcoplasmic reticulum and mitochondria isolated from the hearts of adapted animals are highly resistant to autolysis, and nuclei to the damaging action of one-chain DNA. These changes are named phenomenon of the adaptive stabilization of structures (PhASS). An important role of myocardial heat shock protein (HSP) accumulation in the mechanism of PhASS is shown. The development of PhASS is accompanied by an increased resistance of myocardium to ischemic necrosis.
Key words
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Aschenbrenner V, Druyan R, Albin R, Rabinovitz M (1970) Haem a, cytochrome c and total protein turnover in mitochondria from rat heart and liver. Biochem J 119: 157–168
Currie RW, White FP (1981) Trauma-induced protein in rat tissues: a physiological role for a “heat shock protein”? Science 214: 72–73
Hammond DL, Lai JK, Markert CL (1982) Diverse forms of stress lead to a new pattern of gene expression through a common and essential metabolic pathway. Proc Natl Acad Sci USA 79: 3485
Hearse DJ, Humphrey SM, Chain EB (1973) Abrupt reoxygenation of the anoxic potassium arrested perfused rat heart. J Mol Cell Cardiol 5: 395–401
Malyshev IYu (1989) Adaptation of the organism to stress exposure increases the heart resistance to adrenotoxic damage (in Russian). Bull Exper Biol Med 4: 411–413
Meerson FZ (1988) The role of lipid peroxidation in the myocardium in stress and the antioxidant protection of the heart. In: Singal PK (ed) Oxygen radicals in the pathophysiology of heart disease. Kluwer Academic Publishers, Boston, pp 285–301
Meerson FZ (1991) Adaptive protection of the heart: protecting against stress and ischemic damage. CRC Press, Boca Raton
Meerson FZ (1990) Phenomenon of the adaptive stabilization of structures and protection of the heart (in Russian). Kardiologiya 3: 6–12
Meerson FZ, Malyshev IYu, Sazontova TG (1990) Adaptation to stress exposure prevents arrhythmogenic and contractural effects of the excess of Ca’ on the heart by increased activity of sarcoplasmic reticulum. Basic Res Cardiol 85: 96–103
Meerson FZ, Pshennikova MG, Belkina LM, Abdikaliev NA, Malyshev IYu (1989) Prevention of ischemic arrhythmias by activation of stress-limiting systems of the organism. CV World Report 2: 205–212
Meerson FZ, Sazontova TG, Arkhipenko YuV (1990) Increased resistance of cardiac sarcoplasmic reticulum Cat + pump to autolysis after adaptation of rats to stress. Biomed Sci 1: 373–378
Schwartz K, Boheler KR, Chassagne C, Bastie D, Mercadier JJ (1990) The mechanogenic transduction of the hypertrophied mammalian myocardium. J Mol Cell Cardiol 22 (Suppl II): 8
Watson JV, Nakeff A, Chambers SH, Smith PS (1985) Flow cytometric fluorescence emission spectrum analysis of Hoechst 33343 strained DNA in chicken thymocytes. Cytometry 6: 310–315
Zak R, Aschenbrenner V, Rabinowitz M (1971) Synthesis and degradation of myosin in cardiac hypertrophy. J Clin Invest 50: 1020
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1991 Springer-Verlag Berlin Heidelberg
About this chapter
Cite this chapter
Malyshev, I.Y., Shneider, A.B., Meerson, F.Z. (1991). Phenomenon of the adaptive stabilization of sarcoplasmic and nuclear structures in myocardium. In: Gülch, R.W., Kissling, G. (eds) Current Topics in Heart Failure. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-662-30769-4_20
Download citation
DOI: https://doi.org/10.1007/978-3-662-30769-4_20
Publisher Name: Steinkopff, Heidelberg
Print ISBN: 978-3-7985-0894-1
Online ISBN: 978-3-662-30769-4
eBook Packages: Springer Book Archive