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fang zhi xue xi chong bing yao wu de yan jiu . tu jiu shi dui tu nao xue liu de ying xiang
Pages: 29-36
Year: Issue:  1
Journal: Acta Physiologica Sinica

Keyword:  吐酒石脑血流量血吸虫病心律紊乱动脉注射静脉注射脑血管阻力平均血压毫米汞柱椎动脉;
Abstract: The intoxication from tartar emetic is presumed to be concerned with certain disorders of the central nervous system, but the study of the cerebral circulation in this aspect is still lacking. We used unanesthetized male rabbits, ligated the vertebral arteries and all the branches of the common carotid arteries except the internal carotid. Both common carotid arteries were connected to the bubble flow meter for measuring the intracranial blood flow. The averages and the standard deviations of 84 normal rabbits: the mean arterial blood pressure (BP) was 107±17 mm Hg, the cerebral blood flow (CBF) 142±35 ml/100 g brain/minute, and the cerebral vascular resistance (CVR) 0.80±0.24 mm Hg/ml blood/100 g brain/minute. Intravenous injection of a dose of tartar emetic 4-6 mg/kg or three-day's intensive treatment (4 mg/kg b. i. d.) had no measurable influence on the cerebral circulation. Intravenous drip of 15-20 mg/kg produced a slowing of CBF, but no action on CVR. Intraperitoneal administration of 20 mg/kg gave only slight alterations; with increasing doses up to 80 mg/kg, the decrease of CBF and the increase of CVR became remarkable. So the therapeutic doses of tartar emetic rendered little change in the cerebral circalation, while the toxic doses yielded a reduction of CBF and a constriction of the intracranial vessels. Before the cardiac arrhythmias occurred, the CBF had been diminishing and the CVR enhancing. At the time that the cerebral circulation was in a state of very low BP, very slow CBF and very high CVR, the electro cardiogram also revealed arrhythmias. Intracarotid injections of small doses (below 4μg) of tartar emetic did not modify the cerebral circulation, whereas a large dose (0:8 mg) induced a striking rise of CBF and a precipitous drop of CVR, lasting a few minutes. Intravenous administration of sodium dimercaptosuccinate 0.25 g/kg conferred no marked action, but a dose twice the amount brought about cardiac arrhythmia together with a dwindling CBF and an augmenting CVR. Intravenous injection of atropine sulfate 1 mg/kg yielded a tendency to decreasing CBF and increasing CVR, while 2 mg/kg produced an evidently high CBF accompanied by a low CVR. Intracarotid injections of either sodium dimercaptosuccinate or atropine elicited a prompt rise of CBF and a fall Of CVR.
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