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.

Local tissue oxygen pressure (PO2) was recorded with a platinum multiwire surface electrode at adjacent sites of the cat cortex under steady-state conditions and with different arterial oxygen supply. Simultaneously PO2 in the sinus sagittalis was continuously recorded through the vascular wall in some experiments. Under normoxic and steady-state conditions local PO2 values varied between 0 Torr and almost arterial levels of 90 Torr. This was in accordance with the assumption of a diffusive transport of oxygen in tissue. With increased arterial oxygen supply local tissue PO2 reacted quite differently at adjacent sites. Linear increases in local tissue PO2 as compared to arterial PO2 as well as constant levels, very small increases and even small decreases were recorded. Constancy or small changes, respectively, of local PO2 (= local PO2 regulation) may be caused by changes in microflow, but changes in oxygen consumption cannot be excluded completely. The regulation of local PO2 could be abolished by adding CO2 to the gas mixture or by producing tissue anoxia. With severely reduced arterial oxygen supply local tissue PO2 dropped down to hypoxic or anoxic levels at all sites measured.

The behaviour of both microflow and evoked potentials was investigated in the right somatomotor cortex of the cat (anaesthetized with chloralose) during electrical stimulation of the contralateral left forepaw. Frequency, amplitude, and time of stimulation were varied. Using the local hydrogen clearance method the changes of microflow were continuously monitored in the same cortical area from which the evoked potentials were recorded. The experiments have shown that activation of the somatomotor cortex by somatic stimulation of the contralateral forepaw results in changes of microflow which clearly correlate to the side and amplitude of the primary evoked potentials. An increase in flow as well as in amplitude of the potentials depends on the stimulation parameters. The changes of microflow are limited to a small area of 1--2 mm in diameter. We conclude that a tight coupling of flow to functional activity exists in the microcirculatory range.

Summary: Before, during, and after bicuculline-induced seizures, changes in microflow, local tissue Po" and ex tracellular H+ and K + activities were contimiously re corded in the suprasylvian gyrus of the cat in parallel with electrical activity, Additionally, the patterns of microflow during seizures after blockade of the l3-adrenergic and cholinergic receptors and after phentolamine application were studied, With the onset of discharges, microflow increased at all sites, The maximum increase was ob served when the electrical activity was the strongest. During the period of alternating silent and non silent phases, microflow oscillated in parallel with functional activity, When the discharges ceased, microflow de creased to a new steady-state leveL Tissue hypoxia was It is well accepted from many experimental studies in animals and clinical studies in humans that epileptic seizures are accompanied by an in creased cerebral metabolism and an increased ce rebral blood flow, and that a tight coupling exists between cerebral metabolism and blood flow during seizures [for review see Kuschinsky and Wahl (1978) and Sokoloff (1978Sokoloff ( , 1981] . A good correla tion has also been found between the epileptic dis charges in the electroencephalogram and the in creased cortical blood flow during both generalized and focal seizures. As most of the studies of cere bral blood flow have been performed with methods that do not allow a continuous registration of blood flow, little information is available about the ki netics of cerebral blood flow during and after sei zures and especially in the silent phases of the elec trocorticogram (ECoG).

Microflow was continuously recorded at four sites of the brain cortex (cat) during and after direct electrical stimulation of the brain. In some experiments local oxygen partial pressure (PO2) was additionally measured with a new combined element in the same capillary area where microflow was determined. This simultaneous measurement of both microflow and local PO2 in the tissue enabled us to analyze the kinetics of microflow and its dependence on local PO2 during activation. Microflow increased at all sites measured, in most cases within 1-2 s after the beginning of stimulation, reached the maximum of hyperemia after the end of stimulation and then gradually returned to the initial level within 30 s up to several minutes according to the intensity of the stimulation. The reaction pattern of microflow was uniform. As local PO2 normally did not decrease and did not even show an initial decrease after the onset of stimulation, the hyperemia could not be caused by local hypoxia. On the contrary, local PO2 always increased with the increase of microflow. This PO2 increase is necessary, because the tissue which consumes more oxygen needs higher PO2 gradients to transport the oxygen to the mitochondria.