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European Journal of Cardio-Thoracic Surgery, Vol 12, 228-235, Copyright © 1997 by European Association for Cardio-thoracic Surgery
SS Tsui, PM Kirshbom, MJ Davies, MT Jacobs, FH Kern, JW Gaynor, WJ Greeley and RM Ungerleider
OBJECTIVE: Following the use of deep hypothermic circulatory arrest in
cardiac surgery, cerebral blood flow and cerebral oxygen metabolism are
impaired. These may result from abnormal cerebral vasospasm. Powerful
vasoconstrictors including endothelins and thromboxane A2 could mediate
these processes. We investigated possible involvement of these two factors
by assessing the effects of (a) phosphoramidon-an inhibitor of endothelin
converting enzyme, and (b) vapiprost (GR32191B)-a specific thromboxane
A2-receptor antagonist, on the recovery of cerebral blood flow and cerebral
oxygen metabolism following deep hypothermic circulatory arrest. METHODS: A
total of 18 1-week-old piglets were randomised into three groups (n = 6 per
group). At induction, the control group received saline; group PHOS
received phosphoramidon 30 mg kg-1 intravenously. Group VAP received
vapiprost 2 mg kg-1 at induction and at 30 min intervals thereafter. All
groups underwent cardiopulmonary bypass cooling to 18 degrees C, exposed to
60 min of deep hypothermic circulatory arrest, rewarmed and reperfused for
1 h. Cerebral blood flow was measured with radio-labeled microspheres:
cerebral oxygen metabolism was calculated at baseline before deep
hypothermic circulatory arrest and at 1 h of reperfusion and rewarming.
RESULTS: In the control group, cerebral blood flow decreased to 40.2 +/-
2.0% of baseline after deep hypothermic circulatory arrest and cerebral
oxygen metabolism decreased to 50.0 +/- 5.5% (P < 0.0005). The responses
in group PHOS were similar. In group VAP, cerebral blood flow and cerebral
oxygen metabolism were 64.3 +/- 10.6 and 80.1 +/- 9.8% of baseline,
respectively, after deep hypothermic circulatory arrest. Thus, treatment
with vapiprost significantly improved recovery of cerebral blood flow (P =
0.046) and cerebral oxygen metabolism (P = 0.020) following deep
hypothermic circulatory arrest. No such improvement was seen after
treatment with phosphoramidon. CONCLUSIONS: Thromboxane A2 mediates
impairments in cerebral perfusion and metabolism following deep hypothermic
circulatory arrest. These changes were attenuated by blockade of
thromboxane A2-receptors using vapiprost. Endothelins are not shown to be
involved. Better knowledge of injury mechanisms will enable development of
more effective cerebral protection strategies and allow safer application
of deep hypothermic circulatory arrest.
ARTICLES
Thromboxane A2-receptor blockade improves cerebral protection for deep hypothermic circulatory arrest
Department of Surgery, Duke University Medical Center, Durham, NC, USA.
This article has been cited by other articles:
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S. M. Langley, P. J. Chai, S. E. Miller, J. R. Mault, J. J. Jaggers, S. S. Tsui, A. J. Lodge, A. Lefurgey, and R. M. Ungerleider Intermittent perfusion protects the brain during deep hypothermic circulatory arrest Ann. Thorac. Surg., July 1, 1999; 68(1): 4 - 12. [Abstract] [Full Text] [PDF]
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