✓ The microgravimetric technique and the drying-weighing method for the determination of brain water content are analyzed and compared. A new method has been devised for the automatic production of the gradient column. For gravimetry, tissue samples weighing more than 30 mg have proven adequate for measurement. Specific gravity (SG) should be determined as early as 1 minute after tissue is inserted into the gradient column. Calculations of cerebral blood volume (CBV) from changes in SG of both brain tissue and intravascular perfusate have shown that the SG of brain tissue is considerably influenced by changes in CBV. This is because the SG of blood is higher than that of brain tissue, and may lead to a decrease of SG of about 0.002 in anemic cortex and of 0.001 in anemic white matter, which will simulate a false increase in tissue volume as water of 4% and 2%, respectively. This methodological error may be relevant when the early stages of ischemic brain edema development are studied. Water content of brain tissue can also be determined with acceptable accuracy by vacuum freeze-drying samples of brain tissue weighing about 100 mg. In contrast to cortex, white matter shows a wide range of individual and regional differences in water content. Thus, conclusions on the presence of brain edema drawn from tissue water determinations should always be subjected to cautious analysis and criticism.

The development of cerebral edema after experimental subarachnoid hemorrhage (SAH) was studied in cats by determining regional brain tissue water content with the microgravimetric technique as well as the drying-weighing method. SAH was induced by withdrawing needles previously pierced into one or both infraclinoid internal carotid arteries through a unilateral transorbital approach. Serial determinations of regional cerebral blood flow (rCBF) by labelled microspheres, and monitorings of vital signs such as intracranial pressure (ICP), blood pressure and EEG were carried out up to 24 h after SAH. Animals could be classified into three grades according to the severity of SAH. In grade I, the increase of ICP was transient and minor. In grade II, ICP increased up to 200 mm Hg with a marked reduction of rCBF below 20% of control in cerebral hemispheres. Following subsequent reduction of ICP, rCBF increased over control, indicating reactive hyperemia. Thereafter, a great reduction of rCBF was again observed. In grade III, rCBF was sustained at essentially zero flow with the presence of continuously increased ICP above 100 mm Hg. Cerebral edema was observed particularly in the parasagittal water-shed areas of all grade II animals. It is concluded that cerebral edema complicating SAH is caused by the combination of an initially induced global cerebral ischemia and the subsequent recovery of cerebral circulation. Post SAH hypertension is another factor to exacerbate the development of cerebral edema.

SUMMARY The effect of indomethacin on rCBF was studied in cats anesthetized with Nembutal either under resting conditions or with temporary middle cerebral artery (MCA) occlusion. RCBF was measured by the microsphere method. In control animals (n = 3), indomethacin (4 mg/kg, i.v.) significantly reduced rCBF by about 25% in both cortex (from 44 ± 6 to 32 ± 3 ml/100 g/min, p < 0.001) and white matter (from 36 ± 4 to 26 ± 2 ml/100 g/min, p < 0.001). After MCA occlusion rCBF was markedly decreased in the sylvian region ipsilateral to occlusion (ischemic core) (from 38 ± 4 to 14 ± 2 ml/100 g/min in cortex, 4 animals). Although pretreatment with indomethacin (4 mg/kg) (4 animals) 30 min prior to occhision did not alter rCBF during ischemia, a marked enhancement of reactive hyperemia was observed in the ischemic core immediately upon reperfusion following 2 h occlusion (54 ± 1 1 untreated vs 95 ± 13 treated, p < 0.05). In the delayed postischemic period, namely 2 h after ^circulation, rCBF still remained to be higher in the animals treated with indomethacin (40 ± 6 untreated vs 96 ± 9 treated, p < 0.001). Such an effect of indomethacin for ameliorating postischemic blood flow in both the immediate and delayed period was less prominent in the adjacent area (penumbra) ipsilateral to occlusion. In the contralateral hemisphere, indomethacin caused slight reduction in rCBF during ischemia. An altered relationship between the actions of PGI 2 and TXA 2 has been proposed to occur at the blood-endothelium interface during reperfusion after ischemia in which a disproportionate synthesis of TXA 2 might be suppressed by indomethacin, whereas indomethacin dominantly suppresses PGI 2 synthesis under normal conditions. Stroke Vol 16, No 2, 1985AN ALTERED RELATIONSHIP between the actions of several prostaglandins (PGs) such as prostacyclin (PGIj) and thromboxane A 2 (TXA 2 ) may occur in pathological situations, whereas a balanced interaction is maintained under normal conditions. In addition to the general agreement that PGI 2 is produced in vascular endothelia, and TXA 2 in platelets, 1 there is increasing evidence that TXA 2 synthesis can also occur in the vascular endothelium, 2 " 9 where a dominant but opposing role of PGI 2 with respect to TXA 2 has been documented. Thus previous results which have shown a decrease in basal cerebral blood flow with indomethacin treatment 10 "18 might be indicative of preferential suppression of PGI 2 synthesis at the vascular endothelia, although indomethacin is thought to inhibit more or less all the products of cyclooxygenase. 19In cerebral ischemia, a significant accumulation of cyclooxygenase products is known to occur, particularly when the ischemia is either transient 20 "22 or incomplete.22 " 24 Although the pathogenetic role of accumulation of PGs in cerebral ischemia remains unclear, the improvement shown in cerebral microcirculation with indomethacin treatment following global cerebral ischemia suggests a reversal of roles: a relative dominance in TXA 2 level during this pathological ...

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