Ar. Laptook et al., QUANTITATIVE RELATIONSHIP BETWEEN BRAIN TEMPERATURE AND ENERGY-UTILIZATION RATE MEASURED IN-VIVO USING P-31 AND H-1 MAGNETIC-RESONANCE SPECTROSCOPY, Pediatric research, 38(6), 1995, pp. 919-925
In neonatal and adult animals, modest reduction in brain temperature (
2-3 degrees C) during ischemia and hypoxia-ischemia provides partial o
r complete neuroprotection. One potential mechanism for this effect is
a decrease in brain energy utilization rate with consequent preservat
ion of brain ATP, as occurs with profound hypothermia, To determine th
e extent to which modest hypothermia is associated with a decrease in
brain energy utilization rate, in vivo P-31 and H-1 magnetic resonance
spectroscopy (MRS) was used to measure the rate of change in brain co
ncentration of phosphocreatine, nucleoside triphosphate, and lactate a
fter complete ischemia induced by cardiac arrest in 11 piglets (8-16 d
). Preischemia metabolite concentrations and MRS-determined rate const
ants were used to calculate the initial flux of high energy phosphate
equivalents (d[similar to P]/dt, brain energy utilization rate). Basel
ine physiologic and MRS measurements were obtained at 38.2 degrees C a
nd repeated after brain temperature was adjusted between 28 and 41 deg
rees C. This was followed by measurement of d[similar to P]/dt during
complete ischemia at 1-2 degrees C increments within this temperature
range, Adjusting brain temperature did not alter any systemic variable
except for heart rate which directly correlated with brain temperatur
e (r = 0.95, p < 0.001). Before ischemia brain temperature inversely c
orrelated with phosphocreatine (r = -0.89, p < 0.001), and reflected c
hanges in the phosphocreatine-ATP equilibrium, because brain temperatu
re inversely correlated with intracellular pH (r = -0.77, p = 0.005).
Brain temperature and d[similar to P]/dt were directly correlated and
described by a linear relationship (slope = 0.61, intercept = -12, r =
0.92, p < 0.001). A reduction in brain temperature from normothermic
values of 38.2 degrees C was associated with a decline in d[similar to
P]/dt of 5.3% per 1 degrees C, and therefore decreases in d[similar t
o P]/dt during modest hypothermia represent a potential mechanism cont
ributing to neuroprotection.