Spennede studie som nevner mange viktige prinsipper rundt CO2 og hinter til at det er veldig mye vi har misforstått.
Beskriver spesielt godt hvordan lav CO2 (alkalose) gjør at cellemembraner blir mer permeabal (slipper ting lettere igjennom) for å balansere pH inne i cellen. Noe som fører til at også Ca2+ slippes inn i cellene og f.eks. muskelceller trekker seg mer sammen og nerveceller fyrer av lettere. Kroppen trenger mer oksygen og den setter igang en negativ spiral hvor økt pustefrekvens gir mindre CO2 som gir mer behov for oksygen og dermed en videreføing av økt pustefrekvens. Høy CO2 (acidose) gjør det motsatte, muskler slapper av, nervene roes ned og cellen beskyttes.
The role of carbon dioxide (CO2) is underestimated in the pathomechanism of neuropsychiatric disorders, though it is an important link between psyche and corpus.
The actual spiritual status also influences respiration (we start breathing rarely, frequently, irregularly, etc.) causing pH alteration in the organism;
on the other hand the actual cytosolic pH of neurons is one of the main modifiers of Ca2+-conductance, hence breathing directly, quickly, and effectively influences the second messenger system through Ca2+-currents. (Decreasing pCO2 turns pH into alkalic direction, augments psychic arousal, while increasing pCO2 turns pH acidic, diminishes arousal.)
One of the most important homeostatic function is to maintain or restore the permanence of H+-concentration, hence the alteration of CO2 level starts cascades of contraregulation. However it can be proved that there is no perfect compensation, therefore compensational mechanisms may generate psychosomatic disorders causing secondary alterations in the «milieu interieur».
Authors discuss the special physico-chemical features of CO2, the laws of interweaving alterations of pCO2 and catecholamine levels (their feedback mechanism), the role of acute and chronic hypocapnia in several hyperarousal disorders (delirium, panic disorder, hyperventilation syndrome, generalized anxiety disorder, bipolar disorder), the role of «locus minoris resistentiae» in the pathomechanism of psychosomatic disorders. It is supposed that the diseases of civilization are caused not by the stress itself but the lack of human instinctive reaction to it, and this would cause long-lasting CO2 alteration. Increased brain-pCO2, acidic cytosol pH and/or increased basal cytosolic Ca2+ level diminish inward Ca2+-current into cytosol, decrease arousal–they may cause dysthymia or depression. This state usually co-exists with ATP-deficiency and decreased cytosolic Mg2+ content. This energetical- and ion-constellation is also typical of ageing-associated and chronic organic disorders. It is the most important link between depression and organic disorders (e.g. coronary heart disease). The above-mentioned model is supported by the fact that H+ and/or Ca2+ metabolism is affected by several drugs (catecholemines, serotonin, lithium, triaecetyluridine, thyroxine) and sleep deprivation, they act for the logically right direction.
If we take our breath deeply or frequently our pulse speeds up proving that CO2 has left the pacemaker cells of heart, and the alkalic cytoplasm allowes Ca2+ to enter in the cytosol. If we keep on this kind of breathing for a long time, our pulse will slowly come back to the incipient frequency because the organism compensates the alteration of pH in the cytosol. The lack of H+ in cytosol increases conductance of Ca 2+ and some other ions (Harvey et al.), thus it increases contraction, metabolism and O2 requirement (Laffey et al.), and also increases excitability of neurons in the peripherium (Macefield et al.) and in the brain (Stenkamp et al.). All these events can be explained by the simple fact that lack of H+ (=alkalosis) increases transmembrane conductance of ions and (consequently) increases active ion-pumping mechanisms too (because the original ion-status has to be restored). By contrast, acidosis decreases the transmembrane Ca 2+-conductance (Tombaugh & Somjen), decreases excitability of neurons, and the decreased Ca 2+-conductance can dramatically affect neurotransmitter re- lease (Dodge et al..).
Then chronic hypocapnia or hypercapnia is followed by cascades which alter the whole ionmileu in the cells, they may alter even the neurotransmitter/endocrine sta- tus (Dodge et al.). Therefore, it is inappropriate to call that process a “compensational mechanism”, this name suggests that it is all right, while it is not! According to Claude Bernard alteration of milieu interieur can result in illness. It is very important that the new ion milieu is similarly stable as the original one and it does not allow the organism to restore the original status. Therefore we should name this happening a „complication” (in- stead of “compensation”).