沙鼠运动活动对脑缺血的保护作用。潜在机制。

Cerebral protection against ischemia by locomotor activity in gerbils. Underlying mechanisms.

作者信息

Stummer W, Baethmann A, Murr R, Schürer L, Kempski O S

机构信息

Institute for Surgical Research, Ludwig-Maximilians-University Munich, Germany.

出版信息

Stroke. 1995 Aug;26(8):1423-9; discussion 1430. doi: 10.1161/01.str.26.8.1423.

DOI:10.1161/01.str.26.8.1423

PMID:7631348

Abstract

BACKGROUND AND PURPOSE

A previous communication of this laboratory demonstrated reduced mortality and neuronal damage by spontaneous locomotor activity preceding forebrain ischemia in Mongolian gerbils. The present experiments seek to elucidate potential mechanisms of protection by measurement of cerebral blood flow, cerebral tissue conductance as an indicator of ischemic cell swelling, and the cerebral release of eicosanoids.

METHODS

Gerbils were maintained either in conventional cages (nonrunners) or with free access to running wheels (runners) for 2 weeks preceding 15 minutes of forebrain ischemia. During ischemia and 2.5 hours of reperfusion, cerebral tissue conductance was determined with a two-electrode system. Simultaneously, prostaglandin D2, prostaglandin F2 alpha, and thromboxane B2 were measured in ventriculocisternal perfusate. In additional animals cerebral blood flow was assessed by hydrogen clearance.

RESULTS

Decreases in tissue conductance during ischemia were similar in nonrunners (56 +/- 3%) and runners (62 +/- 3%) but normalized more rapidly in runners during reperfusion. In both groups reperfusion was accompanied by marked increases of perfusate prostaglandin D2, prostaglandin F2 alpha, and thromboxane B2. In nonrunners, however, thromboxane B2 was already elevated during ischemia (147 +/- 9%, P < .01) and remained elevated longer during recirculation (P < .05). Postischemic perfusion maxima were higher in runners (70.8 +/- 7.4 versus 47.0 +/- 5.0 mL/100 g per minute, P < .05) and were observed sooner (27.4 +/- 6.9 versus 62.2 +/- 12.3 minutes, P < .05). Both groups displayed delayed hypoperfusion of a similar magnitude (runners, 29.0 +/- 2.4 mL/100 g per minute; nonrunners, 30.1 +/- 2.4 mL/100 g per minute).

CONCLUSIONS

Protection by preischemic locomotor activity may involve enhanced postischemic reperfusion, leading to more rapid normalization of conductance and thus of cell volume. Enhanced reperfusion may be the consequence of attenuated thromboxane liberation during and after ischemia.

摘要

背景与目的

本实验室之前的一份报告表明，蒙古沙鼠在发生前脑缺血之前进行自发运动可降低死亡率并减轻神经元损伤。本实验旨在通过测量脑血流量、作为缺血性细胞肿胀指标的脑组织电导率以及类花生酸的脑释放量，来阐明潜在的保护机制。

方法

在进行15分钟前脑缺血之前，将沙鼠饲养在传统笼子里（不运动组）或可自由使用跑轮的环境中（运动组）两周。在缺血期间和再灌注2.5小时期间，用双电极系统测定脑组织电导率。同时，在脑室池灌注液中测量前列腺素D2、前列腺素F2α和血栓素B2。在另外的动物中，通过氢清除法评估脑血流量。

结果

缺血期间不运动组（56±3%）和运动组（62±3%）的组织电导率下降情况相似，但运动组在再灌注期间电导率恢复正常的速度更快。两组再灌注时均伴有灌注液中前列腺素D2、前列腺素F2α和血栓素B2显著增加。然而，在不运动组中，血栓素B2在缺血期间就已升高（147±9%，P<.01），并且在再循环期间保持升高的时间更长（P<.05）。运动组缺血后灌注最大值更高（70.8±7.4对47.0±5.0 mL/100 g每分钟，P<.05），且出现时间更早（27.4±6.9对62.2±12.3分钟，P<.05）。两组均表现出相似程度的延迟性灌注不足（运动组，29.0±2.4 mL/100 g每分钟；不运动组，30.1±2.4 mL/100 g每分钟）。