| Purpose: To investigate the developing course of cerebral vasospasm and the change of brain temperature following subaracbnoid hemorrhage (SAH) in rabbits. To study the mechanism of mild hypothermia effects on vasospasm. Methods: Thirty-six of New Zealand rabbits were divided randomly into three groups including Group A (blood-injection), B (mild hypothermia-treatment after blood-injection) and C (normal control ). A rabbit model of the "double subarachnoid hemorrhage"was selected. One flexible micro-catheter for monitoring brain temperature was inserted into the forehead frontal pole, the blood flow velocity and the diameter of the basilar artery were measured by transcranial dopple (TCD) and digital subtraction angiography (DSA). Mild hypothermia was experiimenty performed at 30 minute after injection of blood into occipital cistema and lasted for S hours.The vital sign also were monitored simutaneously. 4 of rabbits in each group were sacrified at 7 day following the different experimental condictions.The basilar artery was preserved for the pathological examination by the light and electronic microscopes. Results: In Group A one rabbit died, and four rabbits were symptomic. All of them showed a reducement in the activity, diet amount, and self- cleaning ability. They recovered to the normal 4-5 days later. Vital signs were stably kept in all of the experiments. The brain temperature began to increased at 150 minute .It reached the tiptop(38.0C) at 2-4 hour and recovered to the normal at 8 hour after SAH. The speed of basilar artery ftow accelerated(29.Ocmls) on the same day of SAH.It reached the peak(43 ? 4.7cni/s) on the fouth day, and began to be slow on the seventh day(30? 1.lcm/s) after SAH.The basilar arterial(BA) diameter narrowed continuously,and reducded most obviously on the seventh day after SAH, which showed only 56.4 14.7% of the original BA diameter. By the pathological examination,it was found that the endothelium of artery to be damaged and swollen severely. In the Group B, the mild hypothermia- treatment group no any rabbits suffered from the dieth . The speed of BA flow( on the 4th day) and the BA diameter (on the 7th day) were 25 .6cm/s and 76.61.0% of original reprectively. The Pathological damage was also reduced obviously. No thrombosis and endothelium death appeared . In the Group C, the normal control , no abnormal results were found. Conclusion: 1.The vital signs of the"double hemorrhage"rabbit model established by injectings of blood into the occipital ciseterna twicely were stable. The frequency and strength of vasospasm in it were ideal. The model suited the study of single factor during CVS. 2.The vasospasm after SAM displayed a pathologial change process from funtion to struction. The artery wall was damaged severely following a serious of functional changes. 3.If the mild hypothermia was performed as soon as possible, the CVS and the pothological damage in the blood vessels following SHA can be lightened obviously. 4.Brain temperature after SHA showed a temperal increase , which was becauses of the blood diffuseing into the subarachnoid cavity and the increased activity of brain function. 5.33-35 of mild hypothermia has a signficant effect on preventing the CVS after SHA. On the other hand, it has no any effect on vital signs either. 6.The protective mechanisms of mild hypothermia are not clear yet... |
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