~LFig. 115 Electron micrograph of hypertrophic myocardium; O 2 deficiency in parts of the intercapillary space,high density of Iysosomes L in this specimen [197]the site of the greatest capillary distances. TheO 2 metabolism of the myocardiac cells isthereby unsaturated (supply deficiency), andthere finally follows the sudden change of themetabolism of the myocardiac cells to fermentation(lactic acid formation) at P02 ~ 3.5mmHg (0.46 kPa). The spontaneous lysosomeformation evidently begins as soon as the cell isonly deficiently supplied with 02, and gl _colysis looms [199]. Thi should be een aprocess occurring in the living organi m hi hdeserve great attention due to it pr babIuniver al character.By Iy 0 ome formation and b thchange to ferm ntation m tab Ii mstrong pH reduction a a r uIt, aturudd nithm
dislloblti(Jln (dige tion)ma,terial. ........... a becomed ration of 02drawn intocf. ig. 109) then,~lJralrall~h 1.4.5, he red ction canreach level near pH = 6.0 63, at which hemembrane of the ly 0 orne b come permeable,the ly 0 omal enzyme are relea ed, andat which, furthermore, a trong acti ation ofthe pH dependent enzyme occur. he finalstage is the dissoluti()n of the ce necro is .Irna cytolysi and cytolytic chain reactionautocytolysis. The death of cells isn d to several as yet unsolved problems.o currence of cell death can be defined ast' epoint at which the outer cell membrane, .. g the intracellular space becomes irre'b y permeable and the cell interior therebyomes stainable (e.g, trypan blue test [2].e activity of the hydrolytic enzymes existing, a single cell (and stored there initially in theomes) is usually enough, after intracellulare e and a certain reaction time in O 2 defi-'ency, to damage the outer cell membraneirreversibly, even at almost neutral cellular pH,,e. to kill the cell. Autocytolysis does notOCCUl, however, as experiments show, if theouter noxae (e.g. extreme O 2 deficiency, overacidification,hyperthermia) cease soon aftere intracellular release of enzymes, as is shownin Fig, 116, left. In such a case, the releasedysosomal enzymes are evidently quickly re-entrapped in newly-formed lyso omes. Such acompartmentalization demands energy, henceoxygen, for thermodynamic reasons. Th ,inthis aspect, too, O 2 deficiency should stronglypromote autocytolysis. The site where celldecline occurs mainly as a result of auto.cytolysis can be considered to be the lethalcomer" at the venous end of the intercapillaryspace. We understand this, for example, for theelementary process of the ageing organism'sadaption to the drop in the 02 supply capaciin older age.Lysosomal cytolytic chain reaction. e dermethe lysosomal cytolytic chain reaction [2] as amechanism of cell damage, by hich I so omalenzymes entering the extracellular space from adying cell contribute to the death of neighboringcells. The extracellular appearance of theenzymes only occurs (Fig. 116) after a certaint•% A" - ........9tJ\• I1rI...... .,'J ~~1,,'·A~~14· tJHI/I1H§ f--'JIJ~/l......o-'~pH. 6.3'---2D ~"'"' T -31°'10"- J,.•1-0', I I I'IIZJ3DIA5060708090fJOWJ12O 13D UO 50 1fIJ 11rJ • .,n·t -"V/l.oo"'""",.lfF61 ~~~ V 11IJfJf.'fIi*al3!1J• ~..1 "'~' -.dIJ? [17 Ce#u·s·"..gmr'V(z • 5·f(J-JI--flO'Yo90tIJ~60solI"'13D201)o8JOofly onnllenzYn11Sof p = ,0 i xtnlDOf n If • _en(jl8nt
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1. Physiological foundationsCOCOM I
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,. Physiological foundationsIf-RoN
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1. Physiological foundationsAll"i1t
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BDuring OzMTprocedurecAfter OzMTpro
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