Induced hypertension treatment to improve cerebral ischemic injury after transient forebrain ischemia

被引:24
作者
Hosomi, N [1 ]
Mizushige, K [1 ]
Kitadai, M [1 ]
Ohyama, H [1 ]
Ichihara, SI [1 ]
Takahashi, T [1 ]
Matsuo, H [1 ]
机构
[1] Kagawa Med Sch, Dept Internal Med 2, Kagawa 7610793, Japan
关键词
cerebral ischemia; brain edema; cerebral blood flow; energy metabolism; induced hypertension;
D O I
10.1016/S0006-8993(99)01577-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The effect of induced hypertension treatment on cerebral ischemia is still controversial. We investigated the preferred blood pressure manipulation level and presser agent required to reduce cerebral ischemic injury following transient forebrain ischemia induced by bilateral occlusion of the common carotid arteries in anesthetized gerbils. Following 60-min cerebral ischemia, we evaluated the preferred blood pressure manipulation level and presser agent required to treat cerebral ischemic injury after reperfusion by examining the effects of different levels of mean arterial blood pressure (MABP), increased with phenylephrine or angiotensin Ii or decreased by blood withdrawal, on cerebral blood flow (CBF), survival ratio, cerebral edema, and brain energy metabolism following transient forebrain ischemia in gerbils. Mild phenylephrine-induced hypertension treatment (21 +/- 4 mmHg) during post-cerebral ischemia-reperfusion improved the survival ratio and reduced cerebral edema, which was also associated with an increase in local CBF and a recovery of brain energy metabolism. However, intense phenylephrine-induced hypertension, angiotensin II-induced hypertension, or hypotension worsen the survival rate and produced extra cerebral edema, that were also associated with deterioration of brain energy metabolism. These results demonstrate that a mild induced hypertension with phenylephrine (21 +/- 4 mmHg above the baseline level) results in reduction of the cerebral edema and improves the survival ratio and brain energy metabolism, Furthermore, angiotensin II may have neurotoxic effect to use as the presser agent for induced hypertension after cerebral ischemia. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:188 / 196
页数:9
相关论文
共 39 条
[31]   Pharmacological elevation of blood pressure in acute stroke - Clinical effects and safety [J].
Rordorf, G ;
Cramer, SC ;
Efird, JT ;
Schwamm, LH ;
Buonanno, F ;
Koroshetz, WJ .
STROKE, 1997, 28 (11) :2133-2138
[32]   ANGIOTENSIN-CONVERTING ENZYME-INHIBITORS ATTENUATE ISCHEMIC BRAIN METABOLISM IN HYPERTENSIVE RATS [J].
SADOSHIMA, S ;
FUJII, K ;
OOBOSHI, H ;
IBAYASHI, S ;
FUJISHIMA, M .
STROKE, 1993, 24 (10) :1561-1566
[33]  
SASAKI M, 1989, ARZNEIMITTEL-FORSCH, V39-2, P886
[34]   EFFECT OF ENHANCED CAPILLARY ACTIVITY ON THE BLOOD-BRAIN BARRIER DURING FOCAL CEREBRAL-ISCHEMIA IN CATS [J].
SHIGENO, T ;
ASANO, T ;
MIMA, T ;
TAKAKURA, K .
STROKE, 1989, 20 (09) :1260-1266
[35]   PATHOPHYSIOLOGY AND TREATMENT OF FOCAL CEREBRAL-ISCHEMIA .1. PATHOPHYSIOLOGY [J].
SIESJO, BK .
JOURNAL OF NEUROSURGERY, 1992, 77 (02) :169-184
[36]   CAPTOPRIL IMPROVES NEUROLOGIC OUTCOME FROM INCOMPLETE CEREBRAL-ISCHEMIA IN RATS [J].
WERNER, C ;
HOFFMAN, WE ;
KOCHS, E ;
RABITO, SF ;
MILETICH, DJ .
STROKE, 1991, 22 (07) :910-914
[37]   The Treatment of Brain Ischemia With Vasopressor Drugs [J].
Wise, Gary ;
Sutter, Robert ;
Burkholder, James .
STROKE, 1972, 3 (02) :135-140
[38]   PATHOPHYSIOLOGY OF BRAIN-SWELLING AFTER ACUTE EXPERIMENTAL BRAIN COMPRESSION AND DECOMPRESSION [J].
XU, BN ;
YABUKI, A ;
MISHINA, H ;
MIYAZAKI, M ;
MAEDA, M ;
ISHII, S .
NEUROSURGERY, 1993, 32 (02) :289-296
[39]   PIAL ARTERIAL-PRESSURE CONTRIBUTION TO EARLY ISCHEMIC BRAIN EDEMA [J].
YAMAGUCHI, S ;
KOBAYASHI, S ;
YAMASHITA, K ;
KITANI, M .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1989, 9 (05) :597-602