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Cerebral blood flow and metabolism during adenosine–induced hypotension in patients undergoing cerebral aneurysm surgery

 

作者: M. LAGERKRANSER,   G. BERGSTRAND,   E. GORDON,   L. IRESTEDT,   C. LINDQUIST,   K. STANGE,   A. SOLLEVI,  

 

期刊: Acta Anaesthesiologica Scandinavica  (WILEY Available online 1989)
卷期: Volume 33, issue 1  

页码: 15-20

 

ISSN:0001-5172

 

年代: 1989

 

DOI:10.1111/j.1399-6576.1989.tb02852.x

 

出版商: Blackwell Publishing Ltd

 

关键词: Adenosine;cerebral aneurysm;cerebral blood flow;cerebral metabolism;controlled hypotension;subarachnoid hemorrhage;thermodilution

 

数据来源: WILEY

 

摘要:

The effects of adenosine–induced hypotension on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRo2), and cerebral lactate production, together with systemic haemodynamics, were studied in 10 patients undergoing cerebral aneurysm surgery in neurolept anaesthesia with controlled hyperventilation. CBF changes were determined in six of the patients with a retrograde thermodilution technique in the jugular vein. Hypotension was induced with a continuous infusion of adenosine in the superior vena cava. The dose range was 0.06–0.35 mg/kg/min, and this caused a 42% reduction in mean arterial blood pressure (MABP) from 79 × 4 to 46 × 1 raraHg (10.5 × 0.5 to 6.1 × 0.1 kPa) through a profound reduction in systemic vascular resistance (SVR), which amounted to 61%. No significant change occurred in CBF. Whole body AV–difference of oxygen was decreased by 37%, and cerebral AV–difference by 28%, corresponding to reductions in whole body oxygen uptake and CMR02 of 16 and 17%, respectively. Cerebral AV–difference of lactate did not change. In the posthypotensive period MABP was increased by 10%, together with a minor increase in CBF (15%). It is concluded, that adenosine–induced hypotension at MABP levels between 40–50 mmHg (5.3–6.7 kPa) does not affect cerebral oxygenation unfavourably, and may even offer a protective effect by reducing cerebral oxygen demand. The slight CBF increase in the posthypotensive period was probably secondary to an increase in MABP together with a blunted autoregulation, but in no case was this effect considered to be harm

 

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