n respired again, the drop in respiration rateto the defici ncy phase being only approximately13 %. Th drop in the P02 level from6.5 to 1 mmHg (0.87 to 0.13 kPa) is directlyr f1 ted in the record in Fig. 102 below. In thearne figure above, the course of the pH in thebi arbonate-free Krebs-Ringer solution is reorded.The absolute values of respiration andfermentation of the myocardiac tissue arerelatively low, evidently as a result of celldamage due to the manipulations undertaken.De pite this, the remaining metabolism sufficesto allow us to see clearly in the solution, whichi kept buffer-free, the time-point of the pHreduction due to the start of ferm.mt.atiimetabolism. It can be seen from the recordi_in Fig. 102 that in the myocardiac t~'!IIUeamined, the sudden change to fermenta .metabolism occurs as soon as the P0 2 lew .the solution sinks to below 3.5 mmHg 0.46kPa). Roughly the same level is also fo d'other cell types. It can be deduced from thesudden transition to fermentation metabo'that even a relatively small improvement in eoxygen supply in the critical area of the tisis usually enough to bring about respirationmetabolism again, and thereby to eliminate thetissue over-acidification.1.4.5 Over-acidification of the tissueIn order to become better acquainted with theover-acidification by glycolysis (caused by 02deficiency), we chose as a model the myocardialtissue of the rat under simulation ofamyocardial infarction. The pH measurementswere implemented by P. G. Reitnauer in thesupply area of a coronary vessel, partiallyligated, with a movable pH glass electrode onthe beating rat heart [146].Wistar rats placed on a thermostatically controlledstage under ethyl urethane anesthesiawere tracheotomized, artificially respirated,thoracotomized and pericardiotomized. Theexposed, strongly beating heart seemed at firstto make measurement impossible, but wasbrought into a position as favorable as possiblefor the implementation of the ligature ormeasurement, by placing a nylon loop just alittle way below the surface of the outermostapex of the heart. A thread under a left ventricularcoronary branch was fed through themyocardium with a bent surgical needle, andmade into a loose loop, in order to trigger lateran experimental myocardial infarction. In orderto throttle the large vascular trunks, the hearthad to be turned upwards and the ligaturepositioned on its dorsal side. However, sinceit was difficult to manipulate the loop, nolying beneath the heart, during measurement,smaller vascular branches of the ventral side 0the left ventricle were also ligated according 0the individual shape of the coronaries. The"low-noise" pH measurement on the bearrat heart was made possible by very fmemicroelectrodes (Figs 103 and 104) [190 2which had been developed in our Institute formeasurements of the pH profIles of optimallover-acidified cancer micrometastases [189 192]. The largest diameter of the inserted part ofsuch an electrode was only approximatel200 JJ.m, so injuries critical to the heart fun tion were avoided. A miniaturized (Pt/Ag/AgCl/0.9 % NaCI in H 2 0) unit served as referenelectrode. For the measurement the referenand the indicator electrode were placed on theheart concentrically from both sides. fterfirm contact of the reference electrode with hsurface of the heart, there followed the in rtion of the tip of the pH electrode in the upplarea of the coronary vessel branch prepared f rthe ligature, approximately 1 mm deep in hmyocardium. The position of the heartstabilized by the three point of contact apeloop, reference and pH electrode enoughFig. 03 Sch matic cross~tctiona pH micro lectrode
A100pmI IBFig. 104 Tip of a pH microelectrode before (A) and after (B) isolation with silicone rubber (free length of thesensitive tip is a few 100 /oLm)make possible the measurement and recordingof the pH values. Figure lOS shows this experimentin the stage before a small coronary vesselbranch on the ventral side of the left ventriclewas ligated. For the simulation of a coronarymyocardial infarction, the loop used for thispurpose could, after stabilization of the pHstarting level, be more or less tightly pulledtogether using two pairs of tweezers andavoiding any further influence on the positionof the heart; the loop could also, if necessary,be loosened again at a desired moment, byinserting a fine needle between the thread andthe myocardium.Using the experimental set-up discussed (Fig.106) we could record the pH course in the O2deficient region of the myocardium of rats inthe course of an experimentally generated infarction.In all experiments there occurred avery ub tantial drop in the pH immediatelyf er the triggering of the 02 deficiency in theyocardium, a a re ult of a local incr~a e ,inic acid concentration. It can be seen In Ig.6 how the P02 ill the supply ar a of the r I •ve el ink by ApH = 1 within 2 min.immediately after the constriction of a coronaryvessel branch of the left ventri Ie. A aresult of the incomplete ligature and a remainingsupply from other sources (collateral ve sels, diffusion from the environment) thereoccurs a pH level of 6.2. The remaining upplycan be proven by the fact that when artifi ialrespiration of the animal i topped the pH immediatelydrops further and then reache a Ie elof 5.2 within 16 min. This al 0 how how f tand how low the pH in the myocardium mu tdrop and cause damage to the ti ue (mi rocirculationinhibition, va cular ·poro it increasein red cell aggregation relea and a ti ation of the Iy osomal enzyme tol ti hainreaction etc.) when, a can be e pe ted in lar rhearts (in humans for example) th inf r tmechani m proceeds in u h a wa that th r ino remaining upply from th nvir nm nt.The method of pH r gi tratitemporarily brought und r 2w 11 uit d to giv inf rm ti nth damag au d b n dand dur ti n f th impairm nt
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