[Laws of substrate supply, of cell kinetics and of therapy mechanisms in the intercapillary region of cancer tissue].
Up to now, the microtopography of glucose and O2 concentration in the intercapillary region of tumour tissue has been determined under the simplifying assumption that substrate consumption is constant up to the periphery of the envisaged cylindrical space around a capillary. The general diffusion field equation presented in this paper takes into account that substrate consumption is constant up to the periphery of the envisaged cylindrical space around a capillary. The general diffusion field equation presented in this paper takes into account that substrate consumption decreases in the unsaturated region of cancer cell glycolysis and respiration so that - compared to former computations - the critical supply radii needed for maintained proliferation increase by a factor of almost 1.8. With the aid of its general solution and the discussed parameters, the laws governing substrate supply, cell kinetics and therapy mechanisms in the intercapillary region of intact and treated tumour tissue are presented and discussed. The essential results there are as follows: - Even in case of hyperglycemia it is glucose supply (and not the O2 supply) which determines proliferation and proliferation rate. - Under the conditions of longtime-hyperglycemia (400 mg%), the tumour volume being accessible to the attack of cancerostatica or radiation, is almost three times as high as under standard conditions. - For glucose (and cancerostatica) the time constant for interactions between circulation and tumour tissue near the necrotic region is equal to or greater than 400 min. This is why stimulation of cancer cell glycolysis in the most therapy-resistant cancer cell portions (i. e., increased proliferation rate and tumour hyperacidification) can only be achieved if hyperglycemia is maintained for 24 hours or more. - Therapeutically treated cancer tissue is characterized by the discussed changes in the diffusion field of glucose and O2 as well as a drop in the interaction time constant for glucose.
D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002196:Capillaries / Q000254:growth & development / Q000503:physiopathology; D002465:Cell Movement; D003238:Connective Tissue / Q000473:pathology*; D005947:Glucose / Q000502:physiology; D006019:Glycolysis; D006943:Hyperglycemia / Q000503:physiopathology; D009369:Neoplasms / Q000188:drug therapy / Q000473:pathology / Q000532:radiotherapy / Q000628:therapy*; D009360:Neoplastic Cells, Circulating; D010100:Oxygen / Q000502:physiology; D011827:Radiation; D051381:Rats; D012119:Respiration
D000970:Antineoplastic Agents; D005947:Glucose; D010100:Oxygen
Gesetzmäbetaigkeiten der Substratversorgung, der Zellkinetik und der Therapiemechanismen im Interkapillarraum der Krebsgewebe