Paul A.H. HollowaySanjeev KrishnaNicholas J. WhiteJohn Radcliffe HospitalMahidol University2018-08-102018-08-101991-01-01Experimental Parasitology. Vol.72, No.2 (1991), 123-13310902449001448942-s2.0-0026113849https://repository.li.mahidol.ac.th/handle/20.500.14594/22058Fulminant malaria infections are characterised by hypoglycaemia and potentially lethal lactic acidosis. In young adult Wistar rats (n = 26) infected with Plasmodium berghei (ANKA strain), hyperparasitaemia (>50%), anaemia (PCV 19.6 ± 5.3%; mean ± SD) hypoglycaemia (1.04 ± 0.74 mmol/litre), hyperlactataemia (13.2 ± 2.20 mmol/litre), hyperpyruvicaemia (0.51 ± 0.12 mmol/litre) and metabolic acidosis (arterial pH 6.96 ± 0.11) developed after approximately 14 days of infection. Hypoglycaemia was associated with appropriate suppression of plasma insulin concentrations. In a second series of experiments the metabolic effects of treatment with glucose (500 mg/kg/hr), quinine (5 mg/kg bolus followed by 10 mg/kg over 1 hr) and a potent activator of pyruvate dehydrogenase, dichloroacetate (300 mg/kg) were studied over a 1-hr period. In control animals quinine had no measurable effects, but dichloroacetate significantly reduced arterial blood lactate (74%) and pyruvate (80%). In infected animals, glucose infusion attenuated the rise in lactate (38% compared with 82%; P < 0.01) but quinine had no additional metabolic effects. Dichloroacetate further attenuated the rise in lactate (14%; P < 0.01). © 1991.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1016/0014-4894(91)90130-O