[Glutamatergic excitation of cortical neurons depending on site of origin on the neuronal membrane and cholinergic regulation under hypothermic condition].

In sensorimotor cortical slices of guinea pig in the course of cooling of incubating fluid from 34 to 21-22 delta C it was shown that hypothermia does not influence on the evoked spike reactions to iontophoretic application of glutamate to the soma, but glutamate action on the dendritic locus causes the shot latency somatic spike response during hypothermic increasing of the rate of spontaneous activity and long latency spike response--during hypothermic fall of activity. While the cooling rate of spontaneous activity in the slow firing neurons was mainly increasing and in the high firing neurons (above 4 spikes per second)--decreasing. The changes in spontaneous activity began at 30 degrees C along with the decreased spike reactions to iontophoretic applications of acetylcholine and efficacy of dendro-somatic propagation. At the same temperature the fall of spike amplitude was initiated and increased with further hypothermia. It is proposed that the basis for hypothermic changes of neuronal activity.is the decreased rate of M-cholinergic process at 27-29 degrees C. Neurons of different physiological properties display different sensitivity to hypothermic factor.

[The temperature regulation of the spontaneous activity frequency and the concomitant changes of the cortical neurons' spike amplitude].

In the sensorimotor cortical slices of guinea pigs, the rate of neurons' spike activity increased at 27-29 and 34-36 degrees C. The change of the firing rate was accompanied by a drop in the spike amplitude at the temperature below 27 and above 34 degrees C. Usually after cooling to 24 degrees C the spike amplitude fully restored when the temperature increased to 32-34 degrees C. The fall of spike amplitude at t >35 degrees C could not be stopped by temperatyre decrease. The data obtained indicate the important role of the neuron membrane K+ permeability.

Endogenous Na/K-ATPase inhibitors in patients with preeclampsia.

Although preeclampsia (PE) is a major cause of maternal and fetal mortality, its pathogenesis is not fully understood. Digitalis-like cardiotonic steroids (CTS) are believed to be involved in the pathophysiology of PE, as illustrated by clinical observations that DIGIBIND, a digoxin antibody which binds CTS, lowers blood pressure in PE. Recently we reported that plasma levels of marinobufagenin (MBG), a vasoconstrictor CTS, are increased fourfold in patients with severe PE. In the present study, we tested whether anti-MBG, or anti-ouabain antibodies, or DIGIBIND can reverse inhibition of erythrocyte Na/K-ATPase (NKA) from patients with mild PE (blood pressure, 149 +/- 3/93 +/- 3 mm Hg; age, 28 +/- 2 years; gestational age, 37 +/- 1 weeks). Development of PE was associated with twofold rise in plasma MBG levels (1.58 +/- 0.15 vs. 0.80 +/- 0.11 nmol/L; P<0.01). The activity of erythrocyte NKA in 12 patients with PE was lower than in 6 normotensive gestational age-matched subjects (1.56 +/- 0.18 vs. 3.11 +/- 0.16 micromol Pi/ml/hr; P<0.001). In vitro treatment of erythrocytes from PE patients with anti-MBG antibody fully restored the NKA activity (3.26 +/- 0.41 micromol Pi/ml/hr; P<0.01). The effects of DIGIBIND was marginally significant (2.53 +/- 0.32 micromol Pi/ml/hr), while the anti-ouabain antibody was not effective (2.25 +/- 0.25 micromol Pi/ml/hr, P>0.5). The present observations provide evidence for a role for MBG in the pathogenesis of PE, and suggest that antibodies against MBG may be useful in the treatment of this syndrome.