1878 



II WIlHOIlK (II l'IIVSIll|ll(,V 



NEUROPIL Ml il ( IGY III 



modification of the experimental procedure in which 

 he was unable [u discover any change in P M uptake 

 in the cerebral hemisphere perfused with 50 cc. of 10 

 per cent saline. He presents this result as if it consti- 

 tuted a refutation of the conclusions of Schaltenbrand 

 & Bailey, but the pertinence of his study seems some- 

 what obscure. 



The panvascular nature of this phenomenon was 

 further emphasized by the demonstration that the 

 predominantly extracellular ion, chloride, required 

 48 min. to replace one third of the brain chloride after 

 intravenous administration in rabbits, whereas virtual 

 equilibrium with the plasma chloride was reached 

 within 11 min. for the majorit) of tissues (mm. 

 Halm & Hevesy (63) demonstrated that only 3 per 

 cent of the central nervous system sodium exchanged 

 after 1 1 min., 12 per cent after 2 hr., and equilibrium 

 was not reached for bj hr. following parenteral 

 administration of Na 24 . 



Experiments with radioactive potassium indicated 

 that this primarily intracellular ion exchanges be- 

 tween plasma and central nervous system somewhat 

 more rapidly than sodium, but still many times more 

 slowly than in intraneural tissues (118). Katzman & 

 Leiderman (89) used K.'-' to determine the influx and 

 outflux of brain potassium in rats. They found the 

 influx to be 2.8g mEq per kg per hr., the outflux rate 

 3.64 mEq per kg per hr., and the influx-outflux ratio 

 0.80. Since a steady state obtains, the outflux must be 

 equivalent to influx, and therefore these authors con- 

 clude that 211 mEq K. per kg wet brain is not exchange- 

 able with parenterally administered K.'-'. They 

 speculate that this nonexehangeablc potassium may 

 reside within a pool behind an impermeable mem- 

 brane either at the capillary, cellular or intracellular 

 level, or in. is represent chemically bound potassium, 

 as suggested by Folch (43) who established that there 

 is an excess of cations over common anions in the 

 brain amounting to 26 mEq and showed that this 

 .iiiiuii deficit is accounted lor by complex lipids 

 capable of binding potassium. 



Katzman & Leiderman found thai the potassium 

 influx-outflux ratios changed markedly with develop- 

 ment. Up to 35 davs of age, rats showed no binding 

 id potassium. Adrenalectomy did not appreciably 

 change the influx in adult animals, bin caused an 



increase in influX-OUtfluX ratio, indicating tli.it all 



brain potassium became exchangeable. Cortisone in 

 adrenalectomized animals restored the nonexehange- 

 ablc partment whereas deoxycorticosterone ami 



saline \t.n\ no effect 



Mi spur varying plasma potassium levels the pota 



siiim influx into the brain remained approximately 

 the same, leading to the suggestion that the inflow of 

 potassium in adult animals may lie a carrier-limited 

 one. These results arc similar to the behavior of glu- 

 cose in the isolated perfused cat brain (see below 1, 

 which also appears to be transported into the central 

 nervous system by .1 reaction which becomes carrier- 

 limited at high blood-glucose concentrations. 



Following intravenous administration of labeled 

 tracer doses, bromide, iodide, thiocvanate, phosphate 

 and chloride equilibrate throughout the body's extra- 

 cellular water within a few minutes, except in the 

 central nervous system where they are not even 

 approximately in equilibrium after 3 hours. 



Put as 



to CaUium Inn Ratio and Brain Function 



Main workers have investigated the relationship 

 between the ionic composition of the fluid environ- 

 ment of the central nervous system and various as- 

 pects of central nervous system function. The majority 

 of these studies have been conducted on anesthetized 

 animals, in which the relationship between central 

 ionic concentration and a) various autonomic func- 

 tions or A I the electrical activity of the brain was 

 observed. 



Two methods of altering central ionic concentra- 

 tions have been employed: intracarotid injection of 

 solutions of varying ionic composition; and direct 

 central introduction of such solutions either by injec- 

 tion into the cisterna magna or the lateral ventricles, 

 or by perfusion of the ventricular sv stem of the brain 

 with .111 artificial cerebrospinal fluid appropriately 

 modified. Some differences exist between the results 

 observed with these procedures and are tn lie attrib- 

 uted to differences in the distribution of materials 

 presented via these different routes. In general, how- 

 ever, the results are in agreement. It is clear that the 

 ionic composition of the cerebrospinal fluid plavs an 

 important role in the maintenance and variation of 



membrane potentials in the central nervous system, 

 and in the function of central mechanisms involved in 

 behavior and in the regulation of autonomic pi messes. 

 In 1899 Meltzer ( 11 ", ) described the effects of 

 intracerebral injections of potassium chlorate iii rab- 

 bits in an effort to ascribe die toxicology of this sub- 

 stance iii its action on tlie central nervous svsiem. lie 



observed thai: "I he injection of I minims of a 5% 

 solution o| ECClOi in 10 1 he brain of rabbits causes at 



once a long series of convulsions, forced movements, 

 opisthotonus, coordinated movements, uncoordinated 



1 li line ,ind lunii convulsions, etc This state of excita- 



