Experimental Study On Cellular Apoptosis Of Basilar Artery In Cerebral Vasospasm

Cerebral vasospasm (CVS) is a major cause of mortality and neurological morbidity following aneurysmal and traumatic subarachnoid hemorrhage (SAH) and it still remains to be a hard nut to crack. Because in vivo experiment using human vessels is not possible, and postmortem pathological examination of human arteries in vasospasm provides only limited amount of information, a number of animal models of vasospasm have been developed. Most models, however, are asymptomatic ones and only a few focus on symptom. The former is more frequently used for morphologic study of spastic arteries and for the CVS-reverting study, not for studying the secondary changes of cerebral function and morphology. But clinically, the symptomatic CVS after SAH causes more injuries and half of cases developed delayed neurological deficits. So the establishment andstudy of symptomatic CVS models are very important.Objective With the recent development of clinical and experimental studies on CVS, people come to realize that SAH-induced CVS is a complicated pathophysiological process, not just the cerebral arterial constriction and resultant decrease of regional cerebral blood flow (rCBF). So more and more attention is being paid to symptomatic CVS models. But during the establishment of these models, blood is usually injected through the needle inserted into the cisterna magna, which is not simple and often injuries the brain stem. So the goal of this study was to establish an experimental model of symptomatic cerebral vasospasm after SAH in rabbits, which cost less and was easy to establish and repeat. Furthermore, the spastic arteries' cells were to be studied under transmission electron microscope (TEM).Methods New Zealand rabbits were used for this study. (1)10 rabbits received cerebral angiography and common carotid arteries' (CCA) ligation. 2 weeks later, the remaining rabbits again received cerebral angiography. (2) 24 rabbits underwent CCA's ligation. 2 weeks later, the rest animals were randomly divided into 2 groups: SAH group(injected with arterial blood) and Control group(injected with physiological saline). Then we induced CVS by injecting arterial blood twice via a cranial hole (3 X 3mm). After that, neurological symptoms ,regional cerebral blood flow (rCBF) and food intake were evaluated. Some rabbits again underwent cerebral angiography on SAH Day 5. (3) On SAH Day 5 , some animals were sacrificed and basilar arteries were removed for electron microscopic study.Results (1) After the ligation of bilateral CCAs, the basilar arteriesbecame longer, tortuous and more dilated. (2) After SAH, all rabbits showed the decrease of food intake and rCBF. Neurological diorders were observed, worst on the fourth day or fifth day. Cerebral angiography demonstrated basilar arteries' spasm on SAH Day 5. (3)TEM demonstrated desquamation of endothelial cells, chromatin condensation, vacuolated cytoplasm and other morphological changes similar to atypical apoptosis.Conclusions (l) After the ligation of bilateral CCAs, the basilar arteries became longer, tortuous and more dilated, which makes it more convenient to perform cerebral angiography and easy to observe and measure arteries' diameters. (2) An experimental rabbit model of symptomatic CVS can be established by injecting blood via a cranial hole after bilateral common carotid arteries' ligation. (3) The cells of spastic arteries showed apoptosis-like changes, which suggests apoptosis may be involved hi the pathogenesis of CVS and may open a new chapter in the study and treatment of CVS.