EFFECTS OF HYPOTENSIVE TREATMENT WITH ALPHA(2)-AGONIST AND BETA(1)-ANTAGONIST ON CEREBRAL HEMODYNAMICS IN SEVERELY HEAD-INJURED PATIENTS
EFFECTS OF HYPOTENSIVE TREATMENT WITH ALPHA(2)-AGONIST AND BETA(1)-ANTAGONIST ON CEREBRAL HEMODYNAMICS IN SEVERELY HEAD-INJURED PATIENTS
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DOI：
10.1111/j.1399-6576.1995.tb04075.x
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发表时间：
1995-04-01
影响因子：
2.1
通讯作者：
RYDING, E
中科院分区：
文献类型：
--
作者：
ASGEIRSSON, B;GRANDE, PO;RYDING, E
创伤后脑水肿的治疗通常包括保持高动脉血压以避免对脑的继发性缺血性损伤。这种做法可能会受到质疑，因为高动脉血压可能会通过毛细血管静水压力升高而加剧脑水肿，导致液体过滤穿过受损的血脑屏障。后一种观点与我们的临床经验一致，因此使用α（2）-肾上腺素能激动剂进行过度治疗（可乐定）和β（1）-肾上腺素能拮抗剂美托洛尔（metoprolol）已成为我们治疗重型颅脑损伤患者以减轻创伤后脑水肿的方案的一部分，本研究试图分析所使用的膨胀剂是否有任何直接的局部脑血管效应，也可能影响颅内压对严重颅脑损伤患者进行了调查。在可乐定（6例）和美托洛尔（9例）推注剂量前后，测量心率、平均动脉血压、颅内压、脑血流量和动静脉氧含量差。可乐定降低平均动脉血压和脑血管阻力，而不影响其他测量参数。美托洛尔降低心率和平均动脉压，但对脑血管参数无影响，结果表明可乐定和美托洛尔对严重脑损伤患者局部脑血流动力学无或仅有轻微的直接影响。这意味着，如果这些药物具有降低颅内压的作用（如所建议的），则这一定是由于其他机制，即继发于动脉血压和心率降低的毛细血管静水压力降低。
Therapy of post-traumatic brain oedema often includes preservation of high arterial blood pressure to avoid secondary ischaemic injuries to the brain. This practice can be questioned since high arterial blood pressure may aggravate brain oedema through raised hydrostatic capillary pressure, causing fluid filtration across the damaged blood-brain barrier. This latter view is in agreement with our clinical experience and therefore hypotensive therapy with an alpha(2)-adrenergic agonist (clonidine) and a beta(1)-adrenergic antagonist (metoprolol) has become part of our treatment protocol for severely head injured patients to decrease the post-traumatic brain oedema.The present study is an attempt to analyse whether there are any direct local cerebrovascular effects of the hypotensive agents used, which also might influence intracranial pressure. Severely head injured patients were investigated. Heart rate, mean arterial blood pressure, intracranial pressure, cerebral blood flow and arteriovenous difference in oxygen content were measured before and after a bolus dose of clonidine (six patients) and metoprolol (nine patients).Clonidine decreased mean arterial blood pressure and cerebrovascular resistance without affecting other parameters measured. Metoprolol decreased heart rate and mean arterial pressure, but had no effect on the cerebrovascular parameters.The results show that clonidine and metoprolol have no, or only minor, direct influence on local cerebral haemodynamics in severely brain injured patients. This implies that if there is an intracranial pressure reducing effect of these drugs, as suggested, this must be due to other mechanisms, namely a reduction in capillary hydrostatic pressure secondary to decreased arterial blood pressure and heart rate.