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 resuscitation from hemorrhage on brain metabolism and blood flow were evaluated by autoradiographic techniques with high spatial resolution. The data were compared to fluid resuscitation with a volume equal to shed blood of isotonic 6% hydroxyethyl starch solution (HES) and a control group without hemorrhage and fluid resuscitation (n = 6 in each group). In conscious rats, volume-controlled hemorrhage for 30 min (30 mL/kg body weight, resulting in a blood loss of approximately 50% of the circulating 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 flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures 2 h after fluid resuscitation by means of the quantitative autoradiographic iodo [14C]antipyrine and 2-[14C]-deoxy-D-glucose methods. Compared to the untreated control group, LCBF increased significantly in all brain regions analyzed after fluid resuscitation 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 between LCGU and LCBF observed in the control group (r = 0.95) was preserved after hemorrhage and fluid resuscitation with HTHO (r = 0.97) and HES (r = 0.96), although the LCBF-to-LCGU ratio was reset to a higher level (1.5 mL/mumol in the control group and 2.7 mL/mumol after fluid resuscitation with HTHO and HES, P < 0.05). We conclude that the increase in LCBF compensates for the reduction of arterial oxygen content to maintain cerebral oxygen delivery. Therefore, "small volume resuscitation" appears to be as effective as resuscitation with large volumes of isotonic HES in meeting the circulatory and metabolic demands of the brain tissue within the first 2 h after fluid resuscitation from hemorrhage.
Waschke
K F
KF
Institut für Anästhesiologie und Operative Intensivmedizin, Fakultät für Klinische Medizin Mannheim der Universität Heidelberg, Mannheim, Germany.
Albrecht
D M
DM
van Ackern
K
K
Kuschinsky
W
W
D000818:Animals; D000983:Antipyrine / Q000378:metabolism; D001345:Autoradiography; D001921:Brain / Q000098:blood supply* / Q000378:metabolism*; D002250:Carbon Radioisotopes; D002560:Cerebrovascular Circulation / Q000502:physiology*; D003847:Deoxyglucose / Q000378:metabolism; D005440:Fluid Therapy / Q000379:methods*; D005947:Glucose / Q000378:metabolism; D006470:Hemorrhage / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*; D006895:Hydroxyethyl Starch Derivatives / Q000627:therapeutic use; D006982:Hypertonic Solutions; D007552:Isotonic Solutions; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012151:Resuscitation
D002250:Carbon Radioisotopes; D006895:Hydroxyethyl Starch Derivatives; D006982:Hypertonic Solutions; D007552:Isotonic Solutions; D003847:Deoxyglucose; D005947:Glucose; D000983:Antipyrine