Urbanics R, Leniger-Follert E, Lübbers D W
Pflugers Arch. 1978 Dec 15;378(1):47-53. doi: 10.1007/BF00581957.
The kinetics of H+ and K+ activities were recorded during and after direct electrical activation of the brain cortex (cat). H+ activity was measured with H+-sensitive glass microelectrodes (tip diameters of 1--4 micron) and K+ activity was registered with double-barrelled ion-sensitive microelectrodes (tip diameters of 1--3 micron). It could be shown that extracellular H+ activity initially decreased for a few seconds and increased only after the 7.s. Maximum acidosis was always noticed after stimulation ended. Alkalotic as well as acidotic changes were the higher the stronger the stimulation parameters were. K+ activity increased very rapidly after stimulation began, reached its maximum when stimulation ended and then decreased to its initial value with an undershoot. It is concluded that the functional hyperemia of microflow could be triggered by the rapid increase in K+ activity, whereas the initial alkalotic change of extracellular pH means that H+ activity does not play a role in the first phase of this kind of hyperemia. The alkalotic shift is interpreted to be caused by the washout of C02 due to the rapid increase in microflow. In the further course, H+ activity obviously contributes to the maintenance of functional hyperemia. In this later period K+ activity is always below the control value.
在对猫的大脑皮层进行直接电刺激期间及之后，记录了H⁺和K⁺活性的动力学变化。使用尖端直径为1 - 4微米的H⁺敏感玻璃微电极测量H⁺活性，并用尖端直径为1 - 3微米的双管离子敏感微电极记录K⁺活性。结果表明，细胞外H⁺活性最初会在几秒内下降，仅在7秒后才会升高。刺激结束后总会出现最大酸中毒情况。刺激参数越强，碱中毒和酸中毒变化就越明显。刺激开始后K⁺活性迅速升高，刺激结束时达到最大值，然后出现下冲并降至初始值。研究得出结论，微血流的功能性充血可能由K⁺活性的快速增加引发，而细胞外pH值最初的碱中毒变化意味着H⁺活性在这种充血的第一阶段不起作用。碱中毒转变被解释为由于微血流快速增加导致CO₂被冲走所致。在后续过程中，H⁺活性显然有助于维持功能性充血。在这个后期阶段，K⁺活性始终低于对照值。
