Tumour hyperacidulation through intravenous glucose infusion enhanced by amygdalin and beta-glucosidase application (author's transl)]

Tumour peracidity in otherwise moderately hyperacidulated tumours or tumour regions of DS carcinosarcoma-bearing Wistar rats attained by glucose infusion was substantially increased by simultaneous infusion of amygdalin and intratumoral i.m. or i.v. application of beta-glucosidase. Here the pH value of healthy tissue, measured at the sceletal muscle, remained unchanged. By means of the said process, tumour hyperacidulation has been raised to a level of deltapH =0.97; attaining a pH difference between tumourous and normal tissue of up to deltapH = 1.6. In one case, the slope of pH reduction in the tumour increased to 870%. Moreover, combined administration of glucose, amygdalin and beta-glucosidase evoked a significant cancerostatic effect hypogenesis, tumour regression) being comparable with the action of an Ifosfamid dosage of 150 mg-kg-1. However, i.m. and i.v. application of beta-glucosidase under narcosis results in an overall process that still remains somewhat too toxic. Hence optimizing studies are intended with the particular aim to further improve the comparability of this process.     

Electrophysiological studies in vincristin-polyneuropathy (author's transl)

21 Patients with malignant brain tumors were treated with vincristine (1,4 mg/m2) in the course of combination chemotherapie, given in 14 days series over 3 months up to 26 month. 18 patients developed clinical signs of a sensory and 4 patients of a sensomotoric polyneuropathy. Changes in nerve conduction velocity of the N. peronaeus and N. suralis and amplitude of the evoked muscle response (M. extensor digitorum brevis) and nerve action potential were studied in dependency of the total vincristine dosage. The following conclusions were drawn. 1. Clinical occurrence of vincristine polyneuropathy and decrease of nerve conduction velocity of peroneal and sural nerve and the amplitude of the muscle response and nerve action potential are dosage dependent. 2. Sensory fibres appear to be damaged earlier and more severe than motor fibers, but this difference was statistically not significant. 3. Nerve conduction velocity of peroneal and sural nerve is normal or slightly decreased in vincristine polyneuropathy, but the amplitude of the evoked response in extensor digitorum brevis muscle and of the nerve action potential of the suralis nerve are markedly diminished. This result indicates that vincristine polyneuropathy is of primary axonal orgin. 4. If vincristine dosage is reduced to half or vincristine is discontinued after a reduction of the potential amplitude in the extensor digitorum brevis muscle below 1 mV, severe, not reversible polyneuropathies may be avoided.