Chapter-1 / Physiological Foundations - WHNLive Public Library

of clerogenou noxae. 1 Di turbing factors which, according to W.H. Hauss, regularly trigger thenchyme reaction (172), detected by the increased rate of 3SS-sulfate incorporation into the sulfo­-lPOly accharide of the ground substance of connective tissue in various organs (animal experiments)I of oxygen 2h pOtensiony rtension (Fig. 39)rationsinsi factionsnicotineforeign proteinallergic reactionso foreign substancesover4xertion2 mechanical stress13 interbrein stimulationemotional stimuli6 noise6 hormones17 influences of dietDisturbing factorshypobaric chamber with P0 2values < 150 mmHgblood pressure amplitude too low (e.g. < 25 mmHg)reduced kidney circulation; hypertension (systol. blood pressure> 200 mmHg)anesthesia etc.endotoxins, staphylococcus toxin, diphtheria toxinpasteurella multocida, staphylococciinhalation of cigarette smokealbumin injectionserum shock, Arthus' phenomenoncroton oil, plastic productsexcessive movement in the treadmilllaceration of muscle, dilatation of the aortathalamus stimulation by means of electric.currentbinding, restricted movementroaring, uniform random noiseadrenaline, testosterone, thyroxine, cortisone, glucagonsclerogenous diets1 Most of these noxae deteriorate the oxygen status2 Subnormal values of Po or '11; locally reduced 02 delivery to the vessel wall; mechanical irritation at ramificationsin the arterial systir:t rtsclerogenous irritation or O 2 deficiency lastsfor a long time (reduced clearance capacity dueto energy deficiency) and particularly if suchong-lasting conditions frequently recur, thenthe non-decomposable deposition productsfrom the metabolism (collagen fibre bundles,calcification etc.) accumulate in the way shownby the electron micrographs in [I 72]. Thedamage to the vessel wall caused by thesebreakdown products no longer recedes (irreversiblephase), as the increase of the diffusionength in both directions of the vessel wallradial, central) begins definitively to limit theetabolism there. A final stabilization of theypertrophic structure thus oc~urs. We ther~forebelieve that the pathologIcal changes Intructure of the vessel wall remain reversible fora long time. The important th~ng is. that thearteriosclerosis be combatted In thIS phase,fore the irreversible wall degeneration finallyes place. We have already seen [2, 8, 106]e reversal of the sclerogenous noxa "oxygenficiency" as a method of renormalization of'he velieI wall structure in the reversible phase,the 02MT in a highly intensive variant. ted to the part of the body in question.ct f ting discussed in Paragraph 5.3.9Ie 42) hould al 0 be mentioned as aIUf'tl'llfll!r method for the renormalization oftt8Jiosci rotically degenerated wall of arterieand arterioles, and of degenerated layers of thealveocapillary system of the lung.According to [172] the pathological changes inthe vessel wall structure caused by the nonspecificmesenchyme reaction affect mainlarterial vessels and their ramifications. Despitethis, this reaction could always re ult in adeterioration of the O 2 supply to the ti sue viacapillaries, above a certain intensity. Thideterioration should result from the reductionof the blood flow (cross-section narrowingreduction in vasomotoric adaptability and inthe air chamber effect) in sclerotically degeneratedarteries.A related reaction in the fine blood capillariecauses the vessel wall thickening di cos ed in1.1.1, and thereby a narrowing of the lumenand even a direct hampering of oxygen and ubstratediffusion to the intercapillar pa . Thbasal membrane thickening of the capillori sdue to protein depo its i a w ll-kno n ph nomenonin diabetic (mi ro)angi pathi andkidney di ea e. Th me pro an Ioccur in th m mbran f th m lin h(Paragraph 1.4.11) and th n I d t th n ur ­pathie of th diab ti . In nn ti nih hiwe hould mention that th patho ni b Imembran thi k nin n b br n dtri t fa ting ( nd I