[Xeftt of,t"". Respiratorv... standstill117, 1 ~pHl210'"fr-..."f11JiJ1lppt6rtJITttfiaIItlttionpoltnfiIJ/.s in EeGE*11M\,~ r.. 37·C,\ pHA-imlor~ ~ '~sfiIItJf• 6.40\\\,69,76~,l I-.-....- -I1etut tr:'tWR" ""t- 430 405 JIK) "60 30 ominoto 1 2 3 4 5 6 7 8 9 10 11 " 13 14 15mint ..~pH·5,87finilimum)Fig. 108 Recording of the pH incerebral cortex of a rat in the pre-fiand final stage of prolonged etheranesthesia at a normal blood glucoselewl. Result: a spontaneous, rapiddrop of cerebral pH leads to exituslethalis within ~ 6 min(eg. flI19iTapet:lrrir)~myrxrutIitr irfurctJ1ysoso11KJ/ qloIytic t:IKtincytolySismJt'lion1KJI1-anl/uenftrunsitiontrJI1f1uent Q/'eosmimi •I'/flllalt:rJrtrr' smtlll-focus necroses Il11it:rocJrculotionrlisturbedififlfJisfatJe i tfJ/1 -f:&N,focliS t.crosis tlifh Copi rtJr.l doma~.....--.........,.......---~I1 10 10 2 10 3 '2,0' 10 5 10 6 10 7 'n:Iir l'tIs6.----..,....L.----r-.L-----r-...L---..,......L----r-...L---r-~-~..:i....:;£=:::.;:=-=.::::..imasinrJo'inhib Hail 'Y'T4 b;::---+----+----+----+----+------l-------l-------l---~~2 :::-+-----+-----+-------+-------+-------+-~ ~ fCfivtIiionol71---+----+-+--"----"'Il~~~~--+_----+---__l__-----+-____l 'I:Y::f1:~p1 1 ~--+---+-----+---+--6~--+----+---+---+---+--=-,~---+----+---+---+---+---+--'6 L---~J,.o.--~....--~.-----:+-.,...---+,---,.J.,O--....,,~OO---,00...L.-O",,-...J..Fig. 109 Guidelines for the dependency of the tissue pH on the size of volume V with total 02 deficiency. Meurements on cancer micro-metastases as models for glycolyzing tissue, with glass micro-electrodes under CMT cditions [2, 191]; V ~ volume with 02 utilization deficit•solid line in Fig. 109. We must allow for a normalblood glucose concentration for ourproblem (except for badly stabilized diabetic,ee below). Different fermentation capacity andupply ituation of the cell a well a oth rm tabolic exchange rate con tant are al 0
1000S! p.!!.. levelsmeasurtd inlerctlfli/lari/]79872f~XiOtlity oferythrocytes1 CMT • tumor tissue under cancer multistep therapy(CMT) conditions..iJ. g. metlSlUtd fisSIle -pHin OIT 1inforcl-I IV /.~ V 1/~ ~~~ ~ 'IV ~R·50 151""65 2 4 6 8 6 2 4 6 8 7pHR •Fig. 111 The pH at the venous end of capillaries (pHcv)in tissues under glycolysing conditions as function ofthe tissue pH at a given capillary distance R. Approximationaccording to [140]very small and very large volumes of O2 deficiencyin the myocardium, which are includedin Fig. 109. These measurements gave us thep values for the upper and lower boundarylevel of the transition curve for normal cellswith fermentation metabolism.ccording to our model, the followin~ as es ment should not be very far from reahty: the67472811,8oFig. 110 The pH as function of the distancefrom the capillary axis r in the venous capillaryarea of tissue volumes lJ ;;;. 10 mm 3 , underglycolysing conditions (lactic acid formation)of different intensity; calculated accordingto [140]. The lactic acid accumulation occurringin strongly inhibited microcirculation(e.g. case IV) is neglected. It brings about asignificant pH reduction in capillary andcapillary vicinitylactic acid formation in the space of the narrowglycolytic zone (cf. Fig. 99) of a single intercapillaryarea is not enough to lead to a considerablereduction of the mean pH level in theinterstitium (and at the venous end of thecapillary wall). Only when the glycolytic zonesof many intercapillary areas come together(V > 0.2 mm 3 ) can the reduction of the meanpH in the tissue exceed 0.5 pH units. pH reductionsof more than 1 unit in the tissue (andsevere pH reductions also at the venous endof the capillary walls), which finally trigger theblood microcirculation inhibition and capillarydamage, do not occur until the volume of theOrdeficient area exceeds 10 mm 3 .The consequences of an O 2 deficit in thevarious organs and tissues of the human areoften determined by the relation presentedhere. The connection between the size of thevolume affected by O 2 deficiency, and the levelof the pH reduction which occurs, is thus oneof the elementary pathophysiological bases ofO 2 deficiency diseases and conditions. It annow be understood why critical con equen e(e.g. large-area necrosis after a myo ardial infarction,tissue degradation in inflammati nprocesses) only occur when the aff t d ti uarea exceeds a certain volume (e.g. _ 10mm 3 ).pH profiles in the intercapillary spaccan be expected for the venouglycolysing ti u r gionmention d minimum volum[140), can be n in Fig. 110.
- Page 1 and 2:
sand functl ni ove d cellular capil
- Page 3:
8 1. Physiological fou~dationsmmHga
- Page 6 and 7:
Basic mechanisms and functions 11e
- Page 8 and 9:
Basic mechanisms and functions 13pr
- Page 11 and 12:
500r-T_-+5__r-_-+1O__,....-_~15.1O-
- Page 13 and 14:
~IUI1!J ~atpWorMs---~~·tIIlDkeJ \I
- Page 15 and 16:
y r na onabS,olu'te clla.ra~t ri ti
- Page 17 and 18:
100907065"I 4y iological foundation
- Page 19 and 20:
1. hy lologlcal foundations70"''''J
- Page 21 and 22:
CII'Cli8LC outl)ut VAr;lllil i e re
- Page 23 and 24:
-'0 y 101091cai oundatlons80%6050l~
- Page 25 and 26:
,..._........,.--~"'!""!!'!~~----_.
- Page 27 and 28:
hi v d in h arrangement shown above
- Page 29 and 30:
34 1. Physiological foundations70%6
- Page 31 and 32:
logical foundationsu .on in the opt
- Page 33 and 34:
1. Physiological foundations. ~ la~
- Page 35 and 36:
II foundationsI tem IBPtrsons with
- Page 37:
1. Physiological foundationsAirdosi
- Page 40 and 41:
110N.ttJJOt~1. Physiological founda
- Page 42 and 43:
1. Phy iological foundationsAnoO;HT
- Page 44 and 45:
hysiological foundations...fJJHT(JI
- Page 46 and 47:
1. Physiological foundationsCOCOM I
- Page 48 and 49:
g r d, whi h con iderably contribut
- Page 50 and 51:
logical foundations13IrPtz12.......
- Page 52 and 53:
,. Physiological foundationsIf-RoN
- Page 54 and 55: 1. Physiological foundationsAll"i1t
- Page 56 and 57: ~~itItINitIIJq/s N 31 54 52~IBIP~-.
- Page 58 and 59: BDuring OzMTprocedurecAfter OzMTpro
- Page 60 and 61: A Bi3lrfss 1'1oafofmovement 8 0pl'r
- Page 62 and 63: Table 6 PO b measurements of unsele
- Page 64 and 65: serert~ hyperoxia pure 0 } .distres
- Page 66 and 67: IIstress qirI/iII mn wryhJI1IJSISLo
- Page 68 and 69: A/JtfJtnk«P~1Mtrr'ttriIWIItJfIS~.~
- Page 70 and 71: Table 7 The change in the architect
- Page 72 and 73: nsMslor rotd'1uI.-Jl!Jg1"/11(J(Jrfr
- Page 74 and 75: IonsFig. 74 Histological pictures s
- Page 76 and 77: IonseM' Selecfofherm equipment-_s1S
- Page 78 and 79: .....-------................',..,-n
- Page 80 and 81: eM/rot gro"/!.Histologicallyconfirm
- Page 82 and 83: A1er tnit,almonipulotionsand III«l
- Page 84 and 85: Q'CSlNltftning1A. QfQ/-fJlf1inguQ
- Page 86 and 87: otllm'lv.2 h th ju tifi d pro p ct
- Page 88 and 89: t48xlD J WsEhmmahooofMe ~crdieal, c
- Page 90 and 91: old°z-/ImitMW mode of calcu/aflonC
- Page 92 and 93: he cylindr'cal area upplied by the'
- Page 94 and 95: Tn-T-~-----1~--~--~JaluralttJtranSi
- Page 96 and 97: aPI)Ii:lcati?n with a patially very
- Page 98 and 99: are triggered. At the same site, ho
- Page 100 and 101: n respired again, the drop in respi
- Page 102 and 103: Exholationtubeloop aroundcmebroncll
- Page 106 and 107: ventieFig. 112 pH decrease between
- Page 108 and 109: BIncorporation ofJ5s-slI"ate intofh
- Page 110 and 111: ~LFig. 115 Electron micrograph of h
- Page 112 and 113: 12111098V ~ .-"~"' .....b""", ".1Tt
- Page 114 and 115: ,,,;tt cola;, ofH1e 88JIJitKIJIIl "
- Page 116 and 117: "-1r-180 I'\112007(J)Jr' '- jwry¥I