The effect of dopamine hydrochloride (DA : Inovan ^(R) ) on the local cerebral blood flow (lCBF) of the cat brain following occlusion of the middle cerebral artery (MCA) was studied using the hydrogen clearance method. The administration of DA (10μg/kg/min) prior to MCA occlusion caused no change in the lCBF. In the contralateral hemisphere following MCA occlusion, DA in the employed doses (5, 10, and 15, μg/kg/min) caused no change in the lCBF. DA administration was not associated with any overt changes in the systemic arterial pressure except in the intermediate dose (10μg/kg/min) after MCA was occluded.
In the affected hemisphere, the low dose of DA (5μg/kg/min) caused a significant increase in the lCBF (+ 16.3%) in the moderately reduced area where the lCBF became above 20 ml/100 g/min following MCA occlusion.
The intermediate dose of DA (10μg/kg/min) showed no significant effect on the lCBF. Whereas the high dose of DA (15μg/kg/min) caused a significant decrease (-21.3%) of thelCBF in the severely reduced area where the lCBF became less than 20 ml/100 g/min following MCA occlusion.
Thus, DA showed a biphasic effect on the lCBF only in the ischemic hemisphre. The vosodilatative and vasoconstrictive effect of DA may be attributed to the stimulation of the DA and alpha-adrenergic receptors of the cerebral artery, respectively. Nevertheless, the fact that the lCBF in the contralateral hemisphere was not at all affected by DA would indicate that the sensitivity of the cerebral artery to this compound may be changed by the ischemic insult.

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In the present study, 35 cases with cerebrovascular diseases were examined with PaO₂, PaCO₂, AaDO₂ (alveolararterial oxygen difference), physiologic dead space, intrapulmonary shunt, and urinary catecholamine excretion.
The value of PaO₂ was negatively correlated to the ones of AaDO₂, that means that the hypoxemia which was occasionally seen in the acute stage of cerebrovascular diseases, was not caused by pulmonary hypoventilation.
Catecholamine, particularly noradrenaline had a positive correlation with AaDO₂.And there existed an increase in intrapulmonary shunt in patients with widened AaDO₂.Moreover, the increase in intrapulmonary shunt under room air was brought by the increase in the ones under pure oxygen inhalation. Phentolamine, an alpha blocker, and trimethaphan camsilate, a ganglionic blocking agent bought a decrease in AaDO₂ and intrapulmonary shunt.
From above mentioned facts, we can speculate that there exists an overactivity of sympathetic nervous system in the acute stage of cerebrovascular diseases, and this overactivity plays an important role in pulmonary insufficiency by stimulating alpha receptors in lungs, and increasing intrapulmonary shunt.

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In our previous report, it was suggested that sympathetic hypertonic state is probably the cause for hypoxemia in the patients with acute stage of cerebrovascular disease. In the present study, 43 cases with cerebrovascular accident were studied with PaO₂, PaCO₂, AaDO₂ (alveolar-arterial PO₂ difference), physiologic dead space, and urinary catecholamine excretion.
Increase in AaDO₂ is positively correlated to increase in urinary catecholamine excretion. In the cases with cerebral infarction, increases in AaDO₂ and in urinary catecholamine excretion are higher in cases with occlusion of the internal carotid artery than in cases with infarction of the perforaters. In 3 cases with internal carotid occlusion or middle cerebral arterial occlusion, increase in AaDO₂ is observed during period of marked cerebral edema. In the cases with supratentorial hemorrhage, maximal diameter of the lesion in CAT scan, urinary adrenalin excretion and AaDO₂are all positively correlated. In 5 cases with increased AaDO₂, reductions of AaDO2 and of Qs/Qt were ovserved with administration of phenotolamine and/or trimetaphan.
It is considered that the present authors further accumulated evidences of symphathetic overflow that plays an important role, if any, in hypoxemia of acute stage of cerbrovascular accidents and that is probably due to elevated intracranial pressure or hypothalamic dysfunction.

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Two cases with aphasia and one case with visuospatial neglect caused by putaminal damage were presented.
The first aphasic patiet was a 52-year-old right handed male with left putaminal infarction and showed Broca 's type of aphasia with non-fluent output and remarkable verbal apraxia. The second was a 55-year-old right handed female with left putaminal hemorrhage and showed on the contrary, fluent output with a long circuit, resembling amnestic aphasia. In both, speech output was more disturbed than input and without conduction aphasia.
The third case, a 55-year-old right handed female with right putaminal hemorrhage, showed visuospatial neglect. The visuospatial neglect was confirmed by our quantitative visuo-perceptive test, though ADL was not disturbed except for mild dressing apraxia.
Aphasia and visuospatial neglect found in the contralateral lesions of the cerebral hemisphere suggest, symptomatologically the lateralization of language function in the left cerebral hemisphere, and of visuospatial perceptive performance in the right. From the results of our three cases, this functional dyssymmetry of right and left putamens was suggested.

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