Regional cerebral blood flow (rCBF), regional cerebral glucose metabolic rate (rCMR), and regional pH (r-pH) were measured simultaneously in fulminant acute experimental allergic encephalomyelitis (EAE) by the use of triple-label autoradiography. No changes were found in the absence of lesions (lymphocytic accumulations). In the lesions, rCBF was 79% increased and rCRM was 13% increased, whereas r-pH was unaltered compared to normal values. The reported changes result in a CBF/CMR ratio of almost 3 in the lesions compared to the normal value of 1.5. The changes may be interpreted as primary disturbances in glucose metabolism, resulting in a secondary increase in CBF. This theory is supported by quoted observations on abnormal morphology and abnormal enzyme content in brain mitochondria in EAE.
AlvordECKiesMWSucklingAJ, (eds) (1984) Experimental allergic encephalomyelitis. A useful model for multiple sclerosis. In: Progress in Clinical and Biological Research, vol 146. New York, Alan R Liss
2.
BlasbergRGGroothuisDMolnarP, (1981) Application of quantitative autoradiographic measurements in experimental brain tumor models. Semin Neurol1:203–221.
3.
BlasbergRGFenstermacherJDPatlakCS, (1983) Transport of alpha-amino isobutyric acid across brain capillary and cellular membranes. J Cereb Blood Flow Metabol3:8–32.
4.
BrosnanCFTraugottURaineCS, (1983) Analysis of humoral and cellular events and the role of lipid haptens during CNS demyelination. Acta Neuropathol (Berl)Suppl 9:59–71.
5.
di RoccoRJHashimGA, (1983) Increased glucose utilization associated with inflammatory brain lesions of experimental allergic encephalomyelitis. Neurosci Lett37:105–110.
6.
DiemerNHRosenørnJ, (1981) Determination of local cerebral blood flow and glucose metabolism or transfer by means of a double autoradiographic method. J Cereb Blood Flow Metab1(suppl 1):72–73.
7.
GjeddeA, (1982) Calculation of cerebral glucose phosphorylation from brain uptake of glucose analogues in vivo: A reexamination. Brain Res Rev4:237–274.
8.
HakimAMArrietaM, (1986) Cerebral acidosis in focal ischemia: I. A method for the simultaneous measurement of local cerebral pH with cerebral glucose utilization or cerebral blood flow in the rat. J Cereb Blood Flow Metabol6:667–675.
9.
HinkeJAMMenardMR, (1978) Evaluation of the DMO method for measuring intracellular pH. Respir Physiol33:31–40.
10.
IngvarMSiesjøBK, (1983) Local blood flow and glucose consumption in the rat brain during sustained bicuculine-induced seizures. Acta Neurol Scand68:129–144.
JuhlerMDiemerNH, (1987) A method for 14C and 3H double label autoradiography. J Cereb Blood Flow Metabol1:572–577.
13.
JuhlerMBarryDIOffnerHKonatGKlinkenLPaulsonOB, (1984) Blood–brain and blood–spinal cord barrier permeability during the course of experimental allergic encephalomyelitis in the rat. Brain Res302:347–355.
14.
JuhlerMBlasbergRGFenstermacherJDPatlakCSPaulsonOB, (1985) A spatial analysis of the blood–brain barrier damage in experimental allergic encephalomyelitis. J Cereb Blood Flow Metabol5:545–553.
15.
KiesMW, (1965) Chemical studies on an encephalitogenic protein from guinea pig brain. Ann NY Acad Sci122:161–169.
16.
KuschinskyW, (1983) Coupling between functional activity, metabolism and blood flow in the brain: State of the art. Microcirculation2:357–378.
17.
KuschinskyWSudaSSokoloffL, (1981) Local cerebral glucose utilization and blood, flow during metabolic acidosis. Am J Physiol241:H772–H777.
18.
LampertPW, (1982) Pathological implications of immunological disease in the central nervous system. In: Clinics in Immunology and Allergy, vol 2: Immunoneuropathology (WaksmanBH, ed), London, WB Saunders, pp 347–371.
19.
LampertPWCarpenterS, (1965) Electron microscopic studies on the vascular permeability and the mechanism of demyelination in experimental allergic encephalomyelitis. J Neuropathol Exp Neurol24:11–24.
20.
LassenNAGjeddeA, (1983) Kinetic analysis of the uptake of glucose and some of its analogues in the brain using the single capillary model: Comments on some points of controversy. In: Tracer Kinetics and Physiologic Modelling. Lecture Notes in Biomathematics, vol 48 (LambrechtRMResignoA, eds), Berlin, Springer, pp 384–407.
21.
LassmannH, (1983) Comparative neuropathology of chronic experimental allergic encephalomyelitis and multiple sclerosis. In: Schriftenreihe Neurologie, vol 25. Berlin, Springer
22.
LearJLJonesSCGreenbergJMFedoraTJReivichM, (1981) Use of 123-I and 14-C in a double radionuclide autoradiographic technique for simultaneous measurement of LCBF and LCMR gl. Theory and method. Stroke12:589–597.
23.
MiesGNiebuhrIHossmannK-A, (1981) Simultaneous measurement of blood flow and glucose metabolism by autoradiographic techniques. Stroke12:581–588.
24.
MohamedAAMendelowADTeasdaleGMHarperAMMcCullochJ, (1985) Effect of calcium antagonist nimodipine on local cerebral blood flow and metabolic coupling. J Cereb Blood Flow Metabol5:26–34.
25.
MutchWACHansenAJ, (1984) Extracellular pH changes during spreading depression and cerebral ischaemia: Mechanisms of brain pH regulation. J Cereb Blood Flow Metabol4:17–27.
26.
PattersonPYDrobishDGHansenMAJacobsAR, (1970) Induction of experimental allergic encephalomyelitis in Lewis rats. Int Arch Allergy37:26–40.
27.
PickardJD, (1981) Role of prostaglandins and arachidonic derivatives in the coupling of cerebral blood flow to cerebral metabolism. J Cereb Blood Flow Metabol1:361–384.
28.
PulsinelliWALevyDEDuffyTE, (1982) Regional cerebral blood flow and glucose metabolism following transient forebrain ischaemia. Ann Neurol11:499–509.
29.
RoizinL, (1964) Some basic principles of molecular pathology. J Neuropathol Exp Neurol23:209–252.
30.
RottenbergDAGinozJZKearfottKJHJunckLRContiJDhawanV, (1982) Feasibility of measuring regional brain tissue pH 11-C dimethyloxazolidindione and positron emission tomography: Preliminary observations in animal and man. In: Workshop on Time-of-Flight Tomography. New York, IEEE
31.
SakuradaOKennedyCJehleJBrownJDCarbinGLSokoloffL, (1978) Measurement of local cerebral blood flow with iodo-14-C-antipyrine. Am J Physiol234:H59–H66.
32.
SarageaMClopotarvMSicaMVladutiuANegruTRotaruN, (1965) Biochemical changes occurring in animals with EAE. Med Pharmacol Exp13:74–80.
33.
SiesjøBK, (1978) Brain Energy Metabolism. New York, John Wiley and Sons
34.
SiesjøBKvon HanwehrRNergeliusGNevanderGIngvarM, (1985) Extra- and intracellular pH in the brain during seizures and in the recovery period following the arrest of seizure activity. J Cereb Blood Flow Metabol5:47–57.
35.
SimmonsRDBernardCCASingerGCarnegiePR, (1982) Experimental autoimmune encephalomyelitis. An anatomically based explanation of clinical progression in rodents. J Neuroimmunol3:307–318.
36.
SmithME, (1966) Glucose metabolism of central nervous tissues in rats with experimental allergic encephalomyelitis. Nature209:1,031–1,032.
37.
SokoloffL, (1979) The 14-C deoxyglucose method: Four years later. In: Cerebral Blood Flow and Metabolism (GotohFNagaiHTazakiY, eds), Copenhagen, Munksgaard, pp 640–649.
38.
SokoloffL, (1981) Localization of functional activity in the central nervous system by measurement of glucose utilization with radioactive deoxyglucose. J Cereb Blood Flow Metabol1:7–36.
39.
SokoloffLReivichMKennedyCdes RosiersMHPatlakCSPettigrewKDSakuradaOShinoharaM, (1977) The 14-C deoxyglucose method for measurement of local cerebral glucose utilization: Theory, procedure and normal values in the conscious and anaesthetized albino rat. J Neurochem28:897–916.
40.
WajdaIJ, (1972) Changes in metabolic processes during pathogenesis of experimental allergic encephalomyelitis. In: Handbook of Neurochemistry, vol 7 (LajthaA, ed), New York, Plenum Press, pp 221–234.
41.
WaksmanBH, (ed) (1982) Immunoneuropathology. Clinics in Immunology and Allergy, vol 2. London, WB Saunders
