@article{oai:niigata-u.repo.nii.ac.jp:00023192, author = {高橋, 壮一郎}, issue = {1}, journal = {新潟医学会雑誌, 新潟医学会雑誌}, month = {Jan}, note = {The central nervous system is a major target organ for the expression of hypertensive disease. Sustained increases in systemic blood pressure (BP) may produce pathological alteration in the intracranial vasculature. The major arterial changes found in hypertensive brains are large-vessel atherosclerosis and small-vessel fibrinoid necrosis as well as arteriolosclerosis. The results of these vascular derangements appear to be parenchymal infarction, commonly encountered in hyper beta-cholesterolemic patients, and intracranial hemorrhage and small lacunar infarcts, which are almost exclusively confined to hypertensive patients. The arteries in the ischemic area lose their normal autoregulatory control, and so any reduction in BP may reduce blood flow to an already compromised part of the brain. On the other hand, a very high BP may directly cause further ischemia, as in hypertensive encephalopathy, or hemorrhage. The wisest course would seem to be that the BP should only be reduced in the acute stage when the stroke is known to be due to a hemorrhage, or when encephalopathy is suspected, and then cautiously. In the chronic stage, there is little doubt that, in the long term, active control of hypertension after a first stroke is effective in reducing the risk of stroke. Accordingly, high BP should be lowered gently to a normal level with anti-hypertensive agents such as calcium antagonists, ACE inhibitors, beta-adrenoceptor antagonists with ISA and hydralazine delivatives.}, pages = {13--18}, title = {4) 脳卒中に伴う高血圧(シンポジウム 高血圧の病態と治療, 第437回新潟医学会)}, volume = {103}, year = {1989} }