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Biomedical subjects

E Sommer

Publications and source records attributed to E Sommer.

At least 55 records · Page 3Linked to original sources
PubMed1978

[Hemispheric dominance in schizophrenics as determined on extrapyramidal side effects of neuroleptics].

Phenomena observed during treatment with neuroleptics were clinically measured in an attempt to determine the difference in vulnerability of the two hemispheres and the relation between this difference and schizophrenic diseases. In the group of systematic schizophrenias the increase in tonus was significantly higher in the dominant hemisphere. This finding is considered a verification of the nosological hypothesis of schizophrenias.

Brain↗
PubMed1976

[Investigations in streaming blood of the alert animal and man. II. Investigations on the mechanism of water resorption from the gut into the portal vein blood in the rat (author's transl)].

Arteriovenous differences (AVD) of electrolyte concentration in the gut are followed by continuous conductometry of ultrafiltrates of portal venous and aortic blood. Intraduodenal application of tap water amounting to 0.5, 1,0 or 2,0% body weight lead to extremely variable reactions both in time course and dimension of AVD. Whereas large and fast changes can be described by a single exponential term, small and slow changes show saturation effects. Evidence is presented, that these differences correspond to permeability changes, both for water in the direction: lumen to blood and for electrolytes in the direction: blood to lumen. Thirst has an enhancing effect on AVD. A dual resorptive pathway is proposed to fit the data.

Animals↗
PubMedDate not supplied

The influence of arterial pressure changes on blood volume replacement after acute hemorrhage in the alert rat.

The fluid content of circulating blood was followed continuously by conductometric measurement of large vein hematocrit in the alert rat. Arterial pressure was registered simultaneously. 2.5-23% of the determined blood volume was withdrawn rapidly and the changes of fluid content (delta v) calculated. Determinations of plasma protein showed that calculated delta v(delta vapp) may exceed true delta v due to transvascular fluid inflow by maximally 38%. A very fast phase of fluid inflow into the circulation (delta vfapp, within 1 min) was observed at the beginning, followed by a slow phase (delta vsapp), the magnitude of both being proportional to the concomitant arterial pressure drop (delta p). At delta p = 0, delta vfapp was 20% of the volume of blood withdrawn, total replacement (delta vfapp + delta vsapp = volume withdrawn) being complete in 60 min. At delta p = -20 mm Hg the figures were 40% and 20 min, respectively. Experiments on splenectomized animals showed essentially the same relations, excepting that delta vsapp may have been underestimated in normal rats. An arterial pressure rise after hemorrhage may attenuate complete replacement. The results are discussed in terms of capillary fluid conductivity. Thus CFC may be in the order of 0.029 ml/min x mm Hg x 100 g.

Acute Disease↗
PubMedDate not supplied

Venous pressures in the alert rat: effects of activity and single injections of catecholamines.

Short bursts of activity are accompanied by a sharp rise, then a sharp drop, followed facultatively by a tonic rise of pressure in the portal and mesenteric vein. Caval vein and abdominal pressure show only a monophasic rise during activity. The drop of portal pressure immediately after the activity peak can be shown to be passive, due to a fall in portal flow rate. The tonic rise after activity can be reproduced by single injections of catecholamines, noradrenalin being more effective than adrenalin. Systemic injections as against intramesenteric injections show, on the other hand, that adrenalin more effectively produces the postactivity pressure drop in the V. portae than noradrenalin. Raising venous pressures in the abdominal cavity by 15-40 mm H2O through acute introduction of air into the abdomen produces no change of venous hematocrit values. The results are discussed in connection with transvascular fluid shifts caused by activity and catecholamines. Portal vein pressure fluctuates with the same frequency, but with a phase displacement of 180 degrees, as Mayer waves.

Abdomen↗
PubMedDate not supplied

Transvascular fluid shifts following single injections of catecholamines in the alert rat: comparison of the effects of adrenaline, noradrenaline and stimulated activity.

Single injections of noradenaline and adrenalineeeee were made into the v. cava of conscious rats during continuous registration of arterial blood pressure and conductivity (reciprocal hematocrit) in blood from different circulatory areas. The resulting hct and B.P. changes were compared with similar changes elicited by a 3-sec tactile stimulus. Two phases of hct response--the first due to local vascular reactions, the second due to a general vasodilatory reaction--can be distinguished. Whereas adrenalin and noradrenaline show differential effectivity in producing the local reactions (the former more potent as a precapillary vasoconstrictor, promoting hct drop due to fluid inflow in the portal and hepatic vein, the latter more so in the renal vein and the aorta), adrenalin is invariably more effective in producing the second phase dilatory reaction with fluid outflow (hct rise). In the v. cava close to the iliac bifurcation a greater hemoconcentrative potency of adrenalin can be demonstrated, but only by close injections into the aorta. Close injections into the portal vein make postcapillary hepatic reactions more sensitive to adrenalin manifest. The catecholamine dose equivalent to a 3-sec tactile stimulus in the rat is 80-120 ng.

Animals↗
PubMedDate not supplied

Volume control during periodic changes of blood volume in the alert rat.

Blood (3.4-13.5% of blood volume) was pumped in and out of the circulation of rats at different rates and period lengths during continuous measurements of blood conductivity (reciprocally related to hematocrit) and arterial pressure. Hct followed the same zig-zag course as the induced changes of blood volume in every case, indicating that fluid shifts (delta v) between interstitium and intravascular space closely follow blood volume changes. As the hct increase during reinfusion was not as great as the preceding decrease, hct dropped continuously during the 20-90 minutes of experimentation, so that a final volume increase (delta v) by about 4% was calculated, which was confirmed by a corresponding decrease of plasma protein concentration. Both final delta v and delta v during periodic volume change (delta % B.V.) were greater when arterial pressure dropped. delta v was directly related to delta % B.V. but not to its rate of change. Heart rate dropped slightly at the end of the reinfusion periods, whereas it rose to control at the end of the withdrawal periods. The results were regarded as evidence of blood volume regulation proportional to the absolute volume of blood lost in non-hypotensive hemorrhage.

Animals↗