- Author:
Yong Seok OH
1
Author Information
- Publication Type:Original Article
- Keywords: Brain; Ischemia; Middle cerebral artery occlusion; Induced hypertension; Phenylephrine; Brain edema; Focal brain ischemia
- MeSH: Animals; Arterial Pressure; Brain Edema*; Brain Ischemia*; Brain*; Edema; Hypertension*; Infarction, Middle Cerebral Artery; Ischemia; Neurons; Phenylephrine*; Rats; Specific Gravity
- From:Korean Journal of Anesthesiology 1990;23(1):1-6
- CountryRepublic of Korea
- Language:Korean
- Abstract: The author investigated the effect of phenylephrine-induced hypertension on the development of cerebral edema and neuronal dysfunction during focal cerebral ischemia. Middle cerebral artery occlusion (MCAO) was performed in isoflurane-anesthetized rats. In the induced hypertension group (n=14), immediately after MCAO, mean arterial pressure (MAP) was increased gradually by 30-35 mmHg above the pre-MCAO level by infusion of phenylephrine. In control animals (n=14), there was no manipulation of MAP. The MAP increase was maintained for three hours at which time the brains were decapitated and sectioned along coronal planes spanning the distribution of the MCA. Specific gravity (SG) was determined in specimens of cortex and sub-cortex. Brain sections adjacent to those used for SG measurement were incubated in 2, 3, 5-triphenyltetrazolium (TTC) and photographed. In both groups, in a coronal section near the center of the MCA distribution, SG was lower (i. e., more edema) in cortex and subcortex ipsilateral to MCAO than in the normal contralateral hemisphere. However, edema accumulation was less (SG was greater) in the induced hypertension group than in control animals (subcortex; 1.046+/-.002 vs 1.042+/-.003, p< 0.05;cortex 1.043+/-.004 vs 1.040+/-.005, p= 0.16). On the brain surface adjacent to the same coronal plane, the area of reduced or absent TTC staining was significantly (p<0.05) less in the induced hypertension group. The data indicate that, in this model, indueed hypertension established soon after the onset of ischemia can serve to reduce the area of neuronal dysfunction, and that not only is edema formation not aggravated, but it is actually reduced.

