van Loon J, Shivalkar B, Plets C, Goffin J, Tjandra-Maga T B, Flameng W
Department of Neurosurgery, University Hospital Gasthuisberg, Catholic University, Leuven, Belgium.
J Neurosurg. 1993 Nov;79(5):705-9. doi: 10.3171/jns.1993.79.5.0705.
To determine the catecholamine response to progressive intracranial hypertension, intracranial pressure (ICP) was raised gradually by continuous expansion of an epidural balloon in seven dogs. Hemodynamic parameters, ICP, and cerebral perfusion pressure (CPP) were monitored continuously and serum catecholamine levels began to rise when CPP was in the low-positive range (20 to 30 mm Hg), reaching a peak just after brain death (CPP < or = o mm Hg). There was no correlation between ICP and the catecholamine peak. Compared to control values, the mean increase was 286-fold for epinephrine and 78-fold for norepinephrine. Temporally, the catecholamine peak corresponded well with the observed hemodynamic changes. These results suggest that ischemia in certain parts of the brain stem is responsible for the hemodynamic changes observed in intracranial hypertension (such as the Cushing response), and they show that catecholamines play an important role in these hemodynamic changes.
为了确定儿茶酚胺对进行性颅内高压的反应，通过在七只狗中持续扩张硬膜外球囊来逐渐升高颅内压（ICP）。连续监测血流动力学参数、ICP和脑灌注压（CPP），当CPP处于低正值范围（20至30毫米汞柱）时，血清儿茶酚胺水平开始升高，在脑死亡后即刻达到峰值（CPP≤0毫米汞柱）。ICP与儿茶酚胺峰值之间无相关性。与对照值相比，肾上腺素的平均增加倍数为286倍，去甲肾上腺素为78倍。从时间上看，儿茶酚胺峰值与观察到的血流动力学变化非常吻合。这些结果表明，脑干某些部位的缺血是颅内高压中观察到的血流动力学变化（如库欣反应）的原因，并且表明儿茶酚胺在这些血流动力学变化中起重要作用。
