Ventilatory responses to hypoxia. Inspired oxygen was lowered while Pao2 was held at 43 mm Hg by adding CO2 to the inspired air. If this had not been done (lower curve), hypocapnia secondary to the hypoxic hyperventilation would have reduced the ventilatory response. The numbers next to the lower curve are Pao2 values measured at each point on the curve. (Based on Loeschke HH, Gertz KH. Einfluss des O2-Druckes in der Einatmungsluft auf die Atemtätigkeit des Menschen, geprüft unter Konstanthaltung des alveolaren CO2-Druckes. Pflugers Arch Gesamte Physiol Menschen Tiere 1958;267:460-477.)
by the blood-brain barrier (capillary endothelium), which has its own transport capability.
Because of the properties of the limiting membranes, CSF is essentially protein-free, but it is not just a simple ultrafiltrate of plasma. CSF differs most notably from an ultrafiltrate by its lower bicarbonate and higher sodium and chloride ion concentrations. Potassium, magnesium, and calcium ion concentrations also differ somewhat from plasma,- moreover they change little in response to marked changes in plasma concentrations of these cations. Bicarbonate serves as the only significant buffer in CSF, but the mechanism that controls bicarbonate concentration is controversial.
Most proposed regulatory mechanisms invoke the active transport of one or more ionic species by the epithelial and endothelial membranes. Because of the relative impermeabilities of the choroidal epithelium and capillary endothe-lium to H + , changes in H+ concentration of blood are poorly reflected in CSF. By contrast, molecular carbon dioxide diffuses readily,- therefore, blood Pco2 can influence the pH of CSF. The pH of CSF is primarily determined by its bicarbonate concentration and Pco2. The relative ease of movement of molecular carbon dioxide in contrast to hydrogen ions and bicarbonate is depicted in Figure 22.8.
. Movement of H+, HCO 3 , and molecular CO2 between capillary blood, brain interstitial fluid, and CSF. The acid-base status of the chemoreceptors can be quickly changed only by changing Paco2.
In healthy people, the Pco2 of CSF is about 6 mm Hg higher than that of arterial blood, approximating that of brain tissue. The pH of CSF, normally slightly below that of blood, is held within narrow limits. Cerebrospinal fluid pH changes little in states of metabolic acid-base disturbances (see Chapter 25)—about 10% of that in plasma. In respiratory acid-base disturbances, however, the change in pH of the CSF may exceed that of blood. During chronic acid-base disturbances, the bicarbonate concentration of CSF changes in the same direction as in blood, but the changes may be unequal. In metabolic disturbances, the CSF bicarbonate changes are about 40% of those in blood but, with respiratory disturbances, CSF and blood bicarbonate changes are essentially the same. When acute acid-base disturbances are imposed, CSF bicarbonate changes more slowly than does blood bicarbonate, and it may not reach a new steady state for hours or days. As already noted, the mechanism of bicarbonate regulation is unsettled. Irrespective of how it occurs, the bicarbonate regulation that occurs with acid-base disturbances is important because, by changing buffering, it influences the response to a given Pco2.
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