Response of tumour red blood cell flux to hyperthermia and/or hyperglycaemia

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Abstract
Laser Doppler flowmetry has been applied to subepidermal rat tumours during localized ultrasound hyperthermia and/or moderate, short-term hyperglycaemia. Blood glucose levels were elevated 4-fold by continuous i.v. infusion of D-glucose (4.8 g/kg/60 min). To determine whether the effects of hyperglycaemia on tumour blood flow involved increased rates of glycolysis and lactic acid production, galactose, a sugar not metabolized by the tumour, was administered using the same dose schedule. Hyperglycaemia was accompanied by a 3-fold increase in blood lactate levels and a slight hypervolaemic haemodilution without any significant systematic changes of the arterial blood pressure or respiratory blood gas parameters. pH of the arterial blood decreased only slightly. Results suggest that neither i.v. glucose nor i.v. galactose alone can cause any statistically significant changes in the red blood cell flux within superficial tumour regions. Doses of hyperthermia which had no effect on tumour microcirculation (e.g. at 40°C), also had no impact on RBC flux when combined with moderate, short-term hyperglycaemia. However, hyperglycaemia (mean blood glucose levels 60 min after initiation of glucose loading: 21–25 mM) in conjunction with appropriate heating can decrease tumour blood flow to a greater extent than heat alone. This effect was more pronounced during 42°C hyperthermia than during heating at 44°C. Thus moderate short-term hyperglycaemia is recognized as a potentiator for hyperthermia at 42–44 °C. Intensified glycolysis and restricted venous drainage of lactic acid seem to play an important part in these pathogenetic events.

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