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Journal of Korean Neurosurgical Society 1994;23(8): 902-915.
Effect of Mannitol in Acute Cerebral Ischemia.
Kyoung Suck Cho, Yong Kil Hong, Min Woo Baik, Dal Soo Kim, Joon Ki Kang, Chang Rak Choi
Department of Neurosurgery, Catholic University Medical College, Seoul, Korea.
ABSTRACT
The development of postischemic irreversible brain damage depends upon the length of ischemia and its severity during arterial occlusion, although release of the occlusion always leads to restoration of normal or above noraml cerebral blood flow. The experiment was planned to determine the effects of mannitol on cerebral ischemia on subsequential regional cerebral blood flow(rCBF) and somatosensory evoked potential(SEP) following reperfusion after ischemia and also define the proper time of vascular occlusion without irreversible brain damage. Cerebral ischemia was induced in cat by transorbital occlusion of the left MCA with a Sugita clip for period of 30 minutes and the ischemic brain was reperfused for 180 minutes by removing the clip. Forty adult cats, weighing 2.5 to 4.0 Kg were divided into 5 group ; control(Group I, n=8), permanent MCA occlusion(Group II, n=8), permanent MCA occlusion with mannitol infusion(Group III, n=8), permanent MCA occlusion with mannitol infusion(Group III, n=8), 30 minutes MCA clipping followed by reperfusion(Group IV, n=8) and 30 minutes MCA clipping with mannitol infusion followed by reperfusion groups(Group V, n=8) respectively. The rCBF and SEP measurents were carried out in each animal immediately, after MCA occlusion, at 30 minutes, 60 minutes, 90 minutes, 120 minutes, 150 minutes and 180 minutes followed by perfusion. The rCBF was measured by the hydrogen clearance technique. Mannitol was given in bolus of lg/kg body weight as a 25% solution delivered via the femoral vein. The results were as follows : 1) Gradual elevation of intracranial pressure(ICP) and systolic blood pressure were observed after MCA occlusion. Treatment with mannitol in MCA occlusion animals(Group III & V) decreased ICP immediately after infusion of mannitol. 2) Normal control rCBF(ml/100 g/min) were 51.94+/-5.05 in the left temporal(LT) and 50.80+/-4.87 in the left perietal lobes(LP). 3) The MCA occlusion resulted in a reduction of the blood flows to 72% of the normal control ones(LT : 14.29+/-4.81 ml/100 g/min) at the left temporal area immediately after occlusion and also a reduction of flows to 80.4% of the normal control ones(LT : 10.24+/-3.69 ml/100 g/min) at 180 minutes after occlusion in Group II. 4) In the mannitol-treated group(group IV), reperfused animals, with removal of the clip on MCA had an improved postischemic recovery of blood flow and ipsilateral cerebral blood flows were restored to 42.5% of the normal control ones(LP : 21.2+/-4.13 ml/100 g/min) at 180 minutes after occlusion in Lt. parietal CBF. 5) In the reperfusion group(group IV), reperfused animals, with removal of the clip on MCA had an increase in rCBF to the level of 83.3% of the control value(LT : 45.78+/-6.80 ml/100 g/min) at 180 minutes after reperfusion and also reperfused animals, with treated mannitol had further increase the blood flow up to the level of 92.5% of the control value(LT : 49.04+/-43.6 ml/100 g/min) at 180 minutes after reperfusion. 6) After the MCA occlusion, the SEP was present but markedly altered in shape and particularly the early components of the SEP were suppressed in the ipsilateral occlusion hemisphere. 7) In the mannitol-treated reperfusion group(Group V) the amplitude of the SEP was restored to 80% of control value. The SEP was significantly suppressed if the rCBF fell below 10-14 ml/100 g/min. These result suggest that provided CBF can be restored to above the 40% threshold well within 30 minutes, prevention of ischemic brain damage can be expected and also the mannitol may of benefit in prolongation of the time threshold for the formation of the cerebral ischmia after vessel occlusion.
Key Words: Acute cerebral ischemia; Mannitol; CBF; Evoked potential; Time threshold
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