Effects of cerebroplegic solutions during hypothermic circulatory arrest and short-term recovery
Autor: | David Holtzman, Paul R. Hickey, Mitsuru Aoki, Fumikazu Nomura, Richard A. Jonas, Michael E. Stromski, Miles Tsuji |
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Rok vydání: | 1994 |
Předmět: |
Pulmonary and Respiratory Medicine
Resuscitation business.industry medicine.medical_treatment Hemodynamics Hypothermia medicine.anatomical_structure Cerebral blood flow Anesthesia Circulatory system medicine Vascular resistance Surgery Viaspan medicine.symptom Cardiology and Cardiovascular Medicine business Saline |
Zdroj: | The Journal of Thoracic and Cardiovascular Surgery. 108:291-301 |
ISSN: | 0022-5223 |
DOI: | 10.1016/s0022-5223(94)70011-7 |
Popis: | Previous studies have suggested that a simple crystalloid "cerebroplegic" solution may prolong the safe duration of hypothermic circulatory arrest. We tested the hypothesis that pharmacologic modification of the cerebroplegic solution would further enhance cerebral protection. Forty-six 4-week-old miniature piglets underwent core cooling to 15° C nasopharyngeal temperature and 2 hours of hypothermic circulatory arrest. Twelve animals had a 50 ml/kg dose of saline infused into the carotid artery system at the onset of hypothermic circulatory arrest and repeat doses of 10 ml/kg every 30 minutes during arrest. Eleven animals received the same initial and repeat doses of University of Wisconsin organ preservation solution and 10 received University of Wisconsin solution with 7.5 mg/L of MK-801, an excitatory neurotransmitter antagonist. In 13 control animals blood was partially drained from the piglet before 2 hours of circulatory arrest at 15° C and no cerebroplegic solution was infused. All solutions were delivered at 4° C. Brain temperature ( n = 24) at the onset of hypothermic circulatory arrest was 15.0° ± 0.1° C (mean ± standard error). Brain temperature after cerebroplegic infusion dropped to 13.0° ± 0.3° C and stayed lower than brain temperature in the control group throughout the hypothermic circulatory arrest period. Recovery of cerebral adenosine triphosphate and intracellular pH determined by phosphorus 31 magnetic resonance spectroscopy ( n = 22) was significantly improved by saline infusion and was further improved with University of Wisconsin solution and University of Wisconsin solution plus MK-801 ( p n = 24) also was augmented by University of Wisconsin solution ( p n = 24) was increased by University of Wisconsin solution and University of Wisconsin solution with MK-801 ( p = 0.002). Brain water content ( n = 46) was significantly lower in all cerebroplegia-treated groups than in controls ( p Conclusion : Cerebroplegia improves short-term recovery after 2 hours of circulatory arrest in hypothermic piglets. Pharmacologic modification with University of Wisconsin solution further improves the recovery of cerebral blood flow and metabolism. MK-801 does not augment the protective effects of University of Wisconsin solution and reduces the recovery of cerebral blood flow by a direct vascular action. Modified cerebroplegia may provide a novel approach to improved cerebral protection when prolonged hypothermic circulatory arrest is necessary. (J T HORAC CARDIOVASC SURG 1994;108:291-301) |
Databáze: | OpenAIRE |
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