The effect of cerebral perfusion pressure on the brain tissue after cerebral arterial occlusion was investigated. The cerebral perfusion pressure was changed by lowering the mean arterial blood pressure (MABP) by an exsanguination. Mongrel dogs were used as the experimental animal and they were divided into three groups (Group A, B and C). Group A had normal MABP, Group B 60 mmHg, and Group C 40 mmHg, respectively. Measurements of middle cerebral arterial blood pressure (MCAP), EEG and cerebral blood flow (CBF), and cerebral perfusion with carbon black solution (carbon perfusion) were performed on each group prior to, following occlusion of the right middle cerebral artery (MCA), and after de-occlusion.
Group A: MCAP was 98 mmHg when MABP was 128 mmHg. MCAP fell to 28 mmHg immediately following occlusion of MCA, however, 74% spontaneous recovery of MCAP was accomplished at 1 hour after occlusion. No ischemic change was recognized on EEG and carbon perfusion which were performed after occlusion of MCA.
Group B: MCAP was 50 mmHg when MABP was 60 mmHg. MCAP fell to 20-25 mmHg following MCA occlusion without recovery thereafter. EEG change appeared, continued and cerebral ischemia was recognized by carbon perfusion on the cerebral tissue of occluded side.
Group C: MCAP was 33 mmHg when MABP was 40 mmHg. MCAP fell to 5-10 mmHg following MCA occlusion without recovery. More severe EEG changes and cerebral ischemia than Group B were observed in the cerebral tissue on the occluded side. Group A had enough cerebral perfusion pressure to maintain the collateral circulation following MCA occlusion. On the contrary, Groups B and C did not have enough cerebral perfusion pressure to maintain the collateral circulation following MCA occlusion. Therefore, ischemic change appeared in the brain on the affected side after the occlusion of MCA. In another experiment, the reversibility of cerebral ischemia was investigated by the same method. It was found that irreversible damage on the occluded cerebral tissue might be caused by one hour occlusion of MCA under 60 mmHg of MABP. We think that low cerebral perfusion pressure may be responsible for the cerebral ischemia following main cerebral arterial occlusion.