Schrader H, Zwetnow N N, Mørkrid L
Acta Neurol Scand. 1985 Jun;71(6):453-63. doi: 10.1111/j.1600-0404.1985.tb03228.x.
In order to delineate the critical blood flow pattern during the Cushing response in intracranial hypertension, regional cerebral blood flow was measured with radioactive microspheres in 12 anesthetized dogs at respiratory arrest caused either by expansion of an epidural supratentorial balloon or by cisternal infusion. Regional cerebrospinal fluid pressures were recorded and the local cerebral perfusion pressure calculated in various cerebrospinal compartments. In the 8 dogs of the balloon expansion group, the systemic arterial pressure was unmanipulated in 4, while it was kept at a constant low level (48 and 70 mm Hg) in 2 dogs and, in another 2 dogs, at a constant high level (150 and 160 mm Hg) induced by infusion of Aramine. At respiratory arrest, regional cerebral blood flow had a stereotyped pattern and was largely independent of the blood pressure level. In contrast, concomitant pressure gradients between the various cerebrospinal compartments varied markedly in the 3 animal groups, increasing with higher arterial pressure. Flow decreased by 85-100% supratentorially and by 70-100% in the upper brain stem down to the level of the upper pons, while changes in the lower brain stem were minor, on the average 25%. When intracranial pressure was raised by cisternal infusion in 4 dogs, the supratentorial blood flow pattern at respiratory arrest was approximately similar to the flow pattern in the balloon inflation group. However, blood flow decreased markedly (74-85%) also in the lower brain stem. The results constitute another argument in favour of the Cushing response in supratentorial expansion being caused by ischemia in the brain stem. The critical ischemic region seems to be located rostrally to the oblongate medulla, probably in the pons.
为了描绘颅内高压库欣反应期间的关键血流模式,在12只麻醉犬中,通过放射性微球测量了局部脑血流量,这些犬处于呼吸停止状态,呼吸停止是由硬膜外幕上球囊扩张或脑池内输注引起的。记录了局部脑脊液压力,并计算了各个脑脊液腔室的局部脑灌注压。在球囊扩张组的8只犬中,4只犬的全身动脉压未进行控制,2只犬的全身动脉压保持在恒定的低水平(48和70 mmHg),另外2只犬通过输注阿拉明将全身动脉压维持在恒定的高水平(150和160 mmHg)。在呼吸停止时,局部脑血流量呈现出一种固定模式,并且在很大程度上与血压水平无关。相比之下,在3个动物组中,各个脑脊液腔室之间的伴随压力梯度变化显著,随着动脉压升高而增加。幕上血流量减少了85% - 100%,上脑干直至脑桥上缘水平的血流量减少了70% - 100%,而下脑干的变化较小,平均为25%。当通过脑池内输注使4只犬的颅内压升高时,呼吸停止时幕上的血流模式与球囊扩张组的血流模式大致相似。然而,下脑干的血流量也显著减少(74% - 85%)。这些结果构成了另一个证据,支持幕上扩张时的库欣反应是由脑干缺血引起的。关键的缺血区域似乎位于延髓上方,可能在脑桥。