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E Leniger-Follert

Publications and source records attributed to E Leniger-Follert.

15 recordsLinked to original sources
PubMed1979

Simultaneous measurements of microflow and evoked potentials in the somatomotor cortex of the cat brain during specific sensory activation.

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.

Animals↗
PubMed1978

Time course of changes of extracellular H+ and K+ activities during and after direct electrical stimulation of the brain cortex.

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.

Animals↗
PubMed1978

The effect of papaverine on local tissue PO2 and microflow in cat brain cortex.

The effect of intracarotid and intravenous administration of papaverine on local tissue PO2 and microflow in the cat's brain surface was studied. Local tissue PO2 was measured with a multiwire surface electrode polarographically, and microflow by local hydrogen clearance method. The intracarotid infusions were made for 1, 2 and 5 min with doses of 0.1, 0.2 and 0.5 mg/kg/min papaverine, and the intravenous ones for 5 min with doses of 0.2, 0.5 and 1 mg/kg/min. The continuous intracarotid infusions showed that papaverine in the doses used distinctly increased local tissue PO2 and microcirculation of the brain surface. With the doses applied, systemic arterial pressure (SAP) changed little. It slightly decreased only during the 5 min infusions containing 0.5 mg/kg/min. The duration of the effect increased with increases in the duration of the infusion and of the dose. The maximum duration was observed with 5 min infusions and lasted for 10--15 min after drug administration was discontinued. During the i.v. infusions, tissue PO2 and microflow rose less than with intracarotid ones. No redistribution of capillary flow was observed.

Animals↗
PubMed1977

Direct determination of local oxygen consumption of the brain cortex in vivo.

A method is described to determine local oxygen consumption quantitatively in the brain cortex under in vivo conditions. Local oxygen consumption is calculated from the slope of local tissue PO2 decrease during a few seconds of total ischemia of the brain for each second after the stop of circulation. The decrease of tissue PO2 is recorded simultaneously at several measuring sites. To be independent of oxygen chemically bound to hemoglobin, tissue PO2 values are raised above 100 Torr. The calculation of local oxygen consumption for each second during the short period of ischemia showed that the O2 consumption remains constant only for a few seconds ranging from 5 to maximally 15 s at different locations. The O2 consumption decreases continuously although the tissue PO2 values are still above the full saturation of hemoglobin. The rate of local oxygen consumption varies considerably at different measuring sites of the superficial layers of the brain cortex (cat). The mean value amounts to 3 +/- 1.5 ml O2/100 g tissue and minute.

Animals↗
PubMed1976

Behavior of microflow and local PO2 of the brain cortex during and after direct electrical stimulation. A contribution to the problem of metabolic regulation of microcirculation in the brain.

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.

Animals↗
PubMed1975

[Regulation of local tissue PO2 in the cerebral cortex of the cat].

Local PO2 was measured in the cat cortex on adjacent sites with a platinum multiwire surface electrode both during steady state conditions and with varying arterial oxygen supply. Concomitantly, PO2 in the sinus sagittalis was recorded continuously through the vascular wall. Under normoxia and steady state conditions local tissue PO2 values varied between O Torr and almost arterial levels of 85 Torr in accordance with theoretical calculations. With increased arterial oxygen supply local tissue PO2 as measured on agjacent sites was found to react fairly differently. Linear increases in local tissue PO2 as compared with arterial PO2, as well as constant levels, or only very small increases, were recorded. The constancy of local PO2 (="local PO2 autoregulation") was caused by local vasoconstriction. With reduced supply of arterial oxygen, however, tissue PO2 dropped in all studied sites down to hypoxia and anoxia. PO2 autoregulation during a decrease in arterial PO2, as described by Bicher (1973) could not be found.

Animals↗