COUPLING BETWEEN LOCAL CEREBRAL BLOOD-FLOW AND METABOLISM AFTER HYPERTONIC HYPERONCOTIC FLUID RESUSCITATION FROM HEMORRHAGE IN CONSCIOUS RATS

The effects of small volume hypertonic/hyperoncotic fluid resuscitatio n from hemorrhage on brain metabolism and blood flow were evaluated by autoradiographic techniques with high spatial resolution. The data we re compared to fluid resuscitation with a volume equal to shed blood o f isotonic 6% hydroxyethyl starch solution (HES) and a control group w ithout hemorrhage and fluid resuscitation (n = 6 in each group). In co nscious rats, volume-controlled hemorrhage for 30 min (30 mL/kg body w eight, resulting in a blood loss of approximately 50% of the circulati ng blood volume) was followed by intravenous infusion of a hypertonic/ hyperoncotic saline hydroxyethyl starch solution (HTHO; 7.5% saline/10 % hydroxyethyl starch, 4.0 mL/kg body weight). Local cerebral blood fl ow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures 2 h after fluid resuscitation by means of the q uantitative autoradiographic iodo [C-14]antipyrine and 2-[C-14]-deoxy- D-glucose methods. Compared to the untreated control group, LCBF incre ased significantly in all brain regions analyzed after fluid resuscita tion with HTHO (mean, +63%) or HES (mean, +56%). The increases in LCBF after fluid resuscitation were sufficient to restore cerebral oxygen delivery to the level calculated for the untreated control group. LCGU was unchanged after fluid resuscitation. The close relationship betwe en LCGU and LCBF observed in the control group (r = 0.95) was preserve d after hemorrhage and fluid resuscitation with HTHO (r = 0.97) and HE S (r = 0.96), although the LCBF-to-LCGU ratio was reset to a higher le vel (1.5 mL/mu mol in the control group and 2.7 mL/mu mol after fluid resuscitation with HTHO and HES, P < 0.05). We conclude that the incre ase in LCBF compensates for the reduction of arterial oxygen content t o maintain cerebral oxygen delivery. Therefore, ''small volume resusci tation'' appears to be as effective as resuscitation with large volume s of isotonic HES in meeting the circulatory and metabolic demands of the brain tissue within the first 2 h after fluid resuscitation from h emorrhage.