PHENYLEPHRINE-INDUCED HYPERTENSION REDUCES ISCHEMIA FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION IN RATS
PHENYLEPHRINE-INDUCED HYPERTENSION REDUCES ISCHEMIA FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION IN RATS
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DOI：
10.1161/01.str.20.11.1538
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发表时间：
1989-11-01
期刊：
影响因子：
8.3
通讯作者：
SHAPIRO, HM
中科院分区：
文献类型：
--
作者：
DRUMMOND, JC;OH, YS;SHAPIRO, HM
我们研究了苯肾上腺素诱导的高血压对大脑中动脉短暂闭塞时缺血面积的影响。用1.2最小肺泡浓度（MAC）异氟烷麻醉大鼠，并通过颞下颅骨切除术闭塞大脑中动脉。此后，立即在一组（n = 9）动脉血压增加30 - 35毫米汞柱以上的preocclusion水平静脉输注苯丙氨酸。在第二个对照组（n = 10）中，没有血压操纵。局部脑血流测定放射自显影15分钟后闭塞。测量局部脑血流量降至三个范围（0 - 6 ml/100 g/min [可能的快速神经元死亡]、6 - 15 ml/100 g/min [可能的延迟神经元死亡]和15 - 23 ml/100 g/min [可能的电生理功能障碍伴延长存活]）的面积（表示为总角膜横截面积的百分比）。局部脑血流量下降到两个更严重的缺血范围的区域在苯乙醯胺组比对照组小。例如，在大脑中动脉分布的中心的冠状截面中，在6.7 ± 1.5 μ g/min中局部脑血流量为0 - 6 ml/100 g/min。正常血压大鼠切片的1.4%，但仅1.7 ± 1.4%的大鼠在该范围内。苯肾上腺素性高血压组为0.6%（p <0.05）。对于6 - 15 ml/100 g/min范围，面积为6.8 ± 1.5。0.8%和3.8 ±。0.7%（p <0.05）。对于15 - 23 ml/100 g/min范围，组间无差异。在非缺血半球，皮质和皮质下区域的局部脑血流在组间没有差异。这些数据表明，苯肾上腺素诱导的高血压可以急性改善局部脑血流量局灶性缺血的区域，此外，表明苯肾上腺素是不是一种脑血管收缩剂在异氟烷麻醉大鼠。
We studied the influence of phenylephrine-induced hypertension on the area of ischemia during brief middle cerebral artery occlusion. Rats were anesthetized with 1.2 minimal alveolar concentration (MAC) isoflurane, and the middle cerebral artery was occluded via a subtemporal craniectomy. Immediately thereafter, in one group (n = 9) arterial blood pressure was increased 30-35 mm Hg above preocclusion level by intravenous infusion of phenylphrine. In a second, control, group (n = 10) there was no manipulation of blood pressure. Local cerebral blood flow was determined autoradiographically 15 minutes after occlusion. The areas (expressed as a percentage of the total corneal cross-sectional area) in which local cerebral blood flow decreased to three ranges (0-6 ml/100 g/min [rapid neuronal death probable], 6-15 ml/100 g/min [delayed neuronal death probable], and 15-23 ml/100 g/min [electrophysiologic dysfunction with prolonged survival probable]) were measured. The areas in which local cerebral blood flow decreased to the two more severely ischemic ranges were smaller in the phenylephrine group than in the control group. For example, in the coronal section in the center of the middle cerebral artery distribution, local cerebral blood flow was 0-6 ml/100 g/min in 6.7 .+-. 1.4% of the section in normotensive rats but was in that range in only 1.7 .+-. 0.6% of the section during phenyleprine-induced hypertension (p < 0.05). For the 6-15 ml/100 g/min range, the areas were 6.8 .+-. 0.8% and 3.8 .+-. 0.7%, respectively (p < 0.05). For the 15-23 ml/100 g/min range, there were no differences between groups. In the nonischemic hemisphere, local cerebral blood flow in cortical and subcortical regions did not differ between groups. The data suggest that phenylephrine-induced hypertension can acutely improve local cerebral blood flow in an area of focal ischemia and, in addition, suggest that phenylephrine is not a cerebral vasoconstrictor in isoflurane-anesthetized rats.