rutin and Brain-Edema

The changes in the terminal blood stream appeared with and without protection by 0-(beta-hydroxyethyl)-rutoside (HR) were studied in irradiated rat brains by means of the electron and light microscope. Thirty minutes before irradiating the animals with doses of 1, 5, 10, and 20 Gy, they were given simultaneous i.p. and s.c. doses of 250 mg each of HR per kg of body weight or, as a control, of physiologic NaCl solution. 2, 6, 9, and 14 days after the irradiation, small tissue specimens from the parasagittal parietal cortex were examined according to the following criteria: 1. number of widely open, i.e. well perfused capillaries and small vessels, 2. number and size of perivascular, optically unstructured "light haloes" which are signs of intracellular oedemas of the perivascular astrocyte processes, 3. incidence of hyperchromic, partly shrunken neurons. The control animals not pretreated with HR showed a collapse of most capillaries and an increase in number and size of "light haloes" around capillaries, arterioles and venules. In the electron microscope, these haloes corresponded to the strongly swollen parts of the perivascular neuropile consisting mainly of oedematous astrocyte processes. These severe perivascular cell alterations were prevented for all dose ranges by the pretreatment with HR. Thus our findings do not only demonstrate a clear antiedematous effect of HR on the radiogenic cell oedema of the perivascular neuropile, they support moreover the working hypotheses with regard to the mode of action of this substance as a "membrane protector".

Topics: Animals; Blood-Brain Barrier; Brain; Brain Edema; Cerebrovascular Circulation; Female; Hydroxyethylrutoside; Male; Parietal Lobe; Radiation Dosage; Radiation-Protective Agents; Rats; Rutin

The disturbances of the carbohydrate metabolism and the activation of acid phosphatases with and without protection by O-(beta-hydroxyethyl)-rutoside (HR) were studied in irradiated rat brains by means of the light microscope. The histochemically demonstrable deposition of glycogen and acid mucopolysaccharides serves as a criterion for a reversible lesion of the irradiated cerebral tissue. The extent of local activation of repair processes following to irradiation can be determined by the quantity of acid phosphatases in the lysosomes. For the dose range of 1 to 5 Gy, HR seems to exert a protective effect on the cellular metabolism of the irradiated cerebral tissue shown by a slight decrease of glycogen and mucopolysaccharide deposits compared to the untreated animals. However, when exceeding a threshold dose of 10 Gy, the deposition of carbohydrates in the HR group is strongly increased. A slightly increased activity of acid phosphatases induced by HR can be supposed at best for the dose range of 5 to 7.5 Gy. If the dose is even more increased, the reverse effect found in the carbohydrate metabolism, too, and an increased activation of acid phosphatases in the control group will be observed. This unexpected reversion of the protective effect could be related to the assumed inhibitory effect of HR on the ATPases and thus on the anaerobic part of glycolysis or to a breakdown of the cell interaction system of endothelial cells, glia cells, and neurons.

Topics: Acid Phosphatase; Animals; Brain; Brain Edema; Carbohydrate Metabolism; Enzyme Activation; Histocytochemistry; Hydroxyethylrutoside; Radiation Dosage; Radiation-Protective Agents; Rats; Rutin

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Animals; Brain Edema; Cats; Drug Combinations; Drug Evaluation, Preclinical; Drug Synergism; Drug Therapy, Combination; Female; Glycerol; Hydroxyethylrutoside; Male; Rutin