Site of hematoma and clinical outcome in cerebral hemorrhage were analyzed in 25 maintenance hemodialysis (HD) patients and compared with those in 27 non-HD patients. Ganglionic-thalamic hemorrhage was found in 56% of HD and 74% of non-HD patients, lobar hemorrhage in 36% and 11 %, respectively. Size of hematoma, expressed as a ratio (%) of hematoma area to entire brain on CT slice, was 6.5 ± 4.2% (mean ± SD) in HD, being significantly larger than that of 4.7 ± 3.5% in non-HD patients (p < 0.05). Mortality rate was 60% in HD patients, nearly twice as much as the 33% in non-HD patients. The hematomas were significantly larger in the death cases (8.4 ± 3.7%) than the survivors on HD (3.6 ± 3.1%, p < 0.005). Likewise, the fatal cases in the non-HD group had bigger hematomas (6.9 ± 4.3%) than the non-fatal ones (3.6 ± 2.4%, p < 0.05). Intraventricular hemorrhage (IVH) was found in 40% of HD and 44% of non-HD patients. Hematomas were significantly larger in HD patients with IVH (9.3 ± 3.3%) than in those without IVH (4.6 ± 3.7, p < 0.005). Ninety percent of the HD patients with IVH but only 42% of non-HD patients died of hemorrhage. Hypertension was equally seen in HD (76%) and non-HD patients (74%).It is concluded that in HD patients cerebral hemorrhage is more severe in terms of hematoma size, association of IVH and clinical outcome. Chronic systemic heparinization might be responsible to the severity in HD patients.

SUMMARY Autoregulation of cerebral (CBF) and cerebellar blood flow (CeBF) was studied before, during and after acutely induced cerebral ischemia in spontaneously hypertensive rats. Cerebral ischemia of the supratentorial portion was induced for one hour by bilateral carotid artery ligation (BCL). The animals were artificially ventilated and the blood flow was measured with a hydrogen clearance technique. To test the autoregulation, the blood pressure was stepwise lowered by bleeding and maintained at a new level, i.e. 15% or 30% lower than the baseline values before, during and after cerebral ischemia. At the preischemic state, CBF and CeBF were 52.1 ± 6.2 and 58.9 ± 4.6 ml/100 g/min (mean ± SEM), of which autoregulations were normally preserved. Following BCL, CBF was markedly decreased to about 10% of control value while CeBF was minimally reduced to 46.9 ± 8.6 ml/100 g/min (80%). At the ischemic state, CBF became almost zero flow during hypotension. CeBF was also reduced to 74 % and further to 58 % of the resting value by 15% and 30% decrease in the blood pressure, respectively, indicating impaired CeBF autoregulation. At the 30 min post-ischemic state, CBF was recovered to 48.0 ± 4.9 and CeBF to 53.9 ± 5.4 ml/100 g/min. Autoregulation of CBF was still abolished, whereas CeBF was kept constant by 15% fall of blood pressure and slightly reduced to 84% by 30% hypotension, indicating almost recovery of CeBF autoregulation. The present results suggest that autoregulatory function of the cerebellum may be modulated to some degree by the supratentorial brain but a more likely explanation for the results in the present work is the loss of perfusion pressure in cerebellar vessels.

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To provide a tool for studying regeneration in planarians, we have produced monoclonal antibodies against a variety of cells and tissues of the freshwater planarian Phagocata vivida (Ijima et Kaburaki). We obtained five kinds of monoclonal antibodies specific, respectively, to 1) the excretory system, 2) nerve cells, 3) rhabdoid-forming cells and body-surface mucus, 4) gastrodermal and epidermal cells, and 5) male germ cells and epidermis.