Chapter-1 / Physiological Foundations - WHNLive Public Library

p h rapyn inhibition of theocc:urs d to th m chani mcall~illa:ryl pill ry blood v el occlu-Gislcussed (f. ig. 75), the drainage ofid f rm d by f rm ntation i also'hi:ndlere:d i d n acido i ). This accumulation. i a id triggers a further feedback promthe MT procedure, in myocardial ininand aloin the late phase of shock. home temporal delay: the deceleration orpping of the drainage of lactic acid leads to aadual reduction in the pH at the venous andthe capillary from at first approximately6.6 to 6.7 down to 6.0. Linked with this is anincrease in the vascular leakage and red cell aggregation,and also a further loss in blood cellfl xibility, Le. an intensification of the occluion.The time required for this pH reductionwas determined at 150-200 min by in vivo pHrecordings for CMT conditions. The time-spanuntil steady-state overacidification is reachedseems to be considerably shorter under infarctionconditions (high-rate formation of acidicmetabolites by the permanently working heartmuscle).This double feedback process explains the sud- .denness with which the infarction overcomesthe victim. At the same time it can also beunderstood, however, that the infarction can beeliminated with the same suddenness in theinitial phase of the acute ischemia, by a measurewhich increases the tissue pH. The portrayeddouble feedback process in the triggeringor interruption of the infarction is a theoreticallysignificant characteristic of the myocardialinfarction which has hardly been discussedin cardiology as yet, perhaps because,although its pathogenetic rank in medicine wasprobable from observation, it is and can be seenin its functional context much more clearly byphy iology and physics.fter the reduction of the pH in the myocardiactissue concerned, there follows in thecourse of some 10 min the cellular release ofy 0 omal enzymes, which are activated with afetor of virtually lOat pH values of around 6,nd instigate the destruction of the relevant11 [141]. As soon as the outer cell membranebeen destroyed after about 100 min, theomal enzyme which then enter the extralIularpace contribute to the damage ofi boring cell, and the lysosomal cytolytich in reaction of the myocardiac infarction4] di cu. d below, proce ds after a furth rd lay of one to everal hours, which inmally I ad to th homogen ou larg -ar an cro i In the affected regIon f the heartmu cleoThe answer to the question of how long thecourse of the infarction mechanism remainsreversible in the given temporal course i ofcrucial practical significance for the de ign ofa causal therapy for the initial pha e of theacute myocardiac infarction. It is only po siblein the reversible initial phase to bring the acuteinfarction to a halt by therapeutic measure .Measures which are not applied until later, inthe irreversible phase, particularly in the clinic,can only spatially limit the self-maintainingmechanism, ameliorate it, and support theorganism so that it can better survive, or surviveat all, the time-span with reduced cardiac performance.In animal experiments we ascertainedthe amount of time up to the beginningof the irreversible tissue damage in the rat, bymeans of pH measurements in the rat heart,described below, under the conditions of amyocardiac infarction triggered by a coronaryligature. We found that the transition from thereversible to the irreversible phases occurs approximately20 min after the infarction is triggered.If we use as a basis our estimation thatpharmacologically therapeutic measures, withthe aim of interrupting the infarction in itreversible phase, must be taken within 20 minthen it necessarily follows that only the patienthimself can undertake this primarily helpfulmeasure, as medical treatment is only in veryrare cases available within 20 min of the infarction.It follows from this that only a therapywhich has been prepared by the cardiologi t inattendance (especially for high-risk patient)and which can be carried out by the patienthimself, can restrict the triggering and pread ofthe infarction mechanism in an acute case. Thisconclusion practically force u to restrict thesetherapeutic measures to drugs with a fast andreliable effect when given orally or perlingually.