Fitch W, Pickard J D, Tamura A, Graham D I
Wellcome Surgical Institute, University of Glasgow.
J Neurol Neurosurg Psychiatry. 1988 Jan;51(1):88-93. doi: 10.1136/jnnp.51.1.88.
Cerebral blood flow (CBF) and mean arterial pressure (MAP) were monitored in six normal baboons and six further animals in which an artificial subarachnoid haemorrhage (SAH) had been induced one week previously. MAP was reduced by the infusion of sodium nitroprusside. In the normal animals with administration of sodium nitroprusside, CBF increased initially but started to decrease as MAP was reduced below 65 mm Hg and fell below its baseline value when MAP was less than 50 mm Hg. In the SAH group, there was no initial hyperaemic response and CBF fell below baseline values when MAP was reduced below 50 mm Hg. When, during the infusion of the sodium nitroprusside, MAP was returned to normal using angiotensin, CBF increased above its baseline value. These results suggest that the cerebrovascular effects of sodium nitroprusside are the net result of competition between direct cerebral vasodilatation, falling arterial blood pressure and the degree of impairment of the "autoregulatory" mechanism. Evidence of ischaemic brain damage was found in the arterial boundary zones of both groups of animals.
对6只正常狒狒以及另外6只一周前诱发人工蛛网膜下腔出血（SAH）的动物进行脑血流量（CBF）和平均动脉压（MAP）监测。通过输注硝普钠降低MAP。在给予硝普钠的正常动物中，CBF最初增加，但当MAP降至65 mmHg以下时开始下降，当MAP低于50 mmHg时降至基线值以下。在SAH组中，没有最初的充血反应，当MAP降至50 mmHg以下时，CBF降至基线值以下。在输注硝普钠期间，当使用血管紧张素使MAP恢复正常时，CBF增加至基线值以上。这些结果表明，硝普钠对脑血管的影响是直接脑动脉扩张、动脉血压下降和“自动调节”机制受损程度之间竞争的净结果。在两组动物的动脉边缘区均发现了缺血性脑损伤的证据。
