Ae. Schwartz et al., ISOLATED CEREBRAL HYPOTHERMIA BY SINGLE CAROTID-ARTERY PERFUSION OF EXTRACORPOREALLY COOLED BLOOD IN BABOONS, Neurosurgery, 39(3), 1996, pp. 577-581
OBJECTIVE: Hypothermia has been demonstrated to protect the brain from
ischemic or traumatic injury. Previous efforts to induce cerebral hyp
othermia have relied on techniques requiring total body cooling that h
ave resulted in serious cardiovascular derangements. A technique to se
lectively cool the brain, without systemic hypothermia, may have appli
cations for the treatment of neurological disease. METHODS: After indu
ction of general anesthesia in 12 baboons, the right common carotid ar
tery and ipsilateral femoral artery were each occlusively cannulated a
nd joined to a centrifugal pump. In a closed-circuit system, blood was
continually withdrawn from the femoral artery, cooled by water bath,
and infused through the common carotid artery with its external branch
es occluded. Pump flow was varied so that right carotid pressure appro
ximated systemic blood pressure. In six animals, perfusate was cooled
to decrease right cerebral temperature to <19 degrees C for 30 minutes
. In six animals, right cerebral temperature was decreased to <25 degr
ees C for 3 hours. In those six animals, Xe-133 was injected into the
right carotid artery before, during, and after hypothermia. Peak radio
activity and washout curves were recorded from bilateral cranial detec
tors. Systemic warming was accomplished by convective air and warm wat
er blankets. Esophageal, rectal, and bilateral cerebral temperatures w
ere continuously recorded. RESULTS: In animals cooled to <19 degrees C
, right cerebral temperature decreased from 34 degrees C to 18.5 +/- 1
.1 degrees C (mean +/- standard deviation), P < 0.01, in 26 +/- 13 min
utes. Simultaneously, left cerebral temperature decreased to 20.7 +/-
1.6 degrees C. During 30 minutes of stable cerebral hypothermia, esoph
ageal temperature decreased from 35.1 +/- 2.3 degrees C to 34.2 +/- 2.
2 degrees C, P < 0.05. In animals cooled to <25 degrees C, right cereb
ral temperature decreased from 34 degrees C to 24.5 +/- 0.6 degrees C
in 12.0 +/- 6.0 minutes, P < 0.01. Simultaneously, left cerebral tempe
rature decreased to 26.3 +/- 4.8 degrees C. After 3 hours of stable ce
rebral hypothermia, esophageal temperature was 34.4 +/- 0.5 degrees C,
P < 0.05. Right hemispheric cerebral blood flow decreased during hypo
thermia (26 +/- 16 ml/min/100 g) compared to values before and after h
ypothermia (63 +/- 29 and 51 +/- 34 ml/min/100 g, respectively; P < 0.
05). Furthermore, hypothermic perfusion resulted in a proportionally i
ncreased radioactivity peak detected in the left cerebral hemisphere a
fter right carotid artery injection of Xe-133 (0.8 +/- 0.2:1, left:rig
ht) compared to normothermia before and after hypothermia (0.3 +/- 2 a
nd 0.3 +/- 1, respectively; P < 0.05). Normal heart rhythm, systemic a
rterial blood pressure, and arterial blood gas values were preserved d
uring hypothermia in all animals. CONCLUSION: Bilateral cerebral deep
or moderate hypothermia can be induced by selective perfusion of a sin
gle internal carotid artery, with minimal systemic cooling and without
cardiovascular instability. This global brain hypothermia results fro
m profoundly altered collateral cerebral circulation during artificial
hypothermic perfusion. This technique may have clinical applications
for neurosurgery, stroke, or traumatic brain injury.