ISOLATED CEREBRAL HYPOTHERMIA BY SINGLE CAROTID-ARTERY PERFUSION OF EXTRACORPOREALLY COOLED BLOOD IN BABOONS

Citation
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
Citations number
22
Categorie Soggetti
Surgery,"Clinical Neurology
Journal title
ISSN journal
0148396X
Volume
39
Issue
3
Year of publication
1996
Pages
577 - 581
Database
ISI
SICI code
0148-396X(1996)39:3<577:ICHBSC>2.0.ZU;2-L
Abstract
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 In a closed-circuit system, blood was continually withdrawn from the femoral artery, cooled by water bath, and infused through the common carotid artery with its external branch es occluded.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.