The prechiasmatic SAH model seems to be the most suitable for study of the sequelae after SAH; it produces a significant decrease in CBF, an acceptable mortality rate, and substantial pathological lesions, with high reproducibility. The CBF reduction is predominantly dependent on the amount of subarachnoid blood.

SUMMARY A subarachnoid haemorrhage (SAH) in the rat was produced by the injection of blood via a previously implanted catheter connected to the cisterna magna. Repeated angiographical examinations of the vertebro-basilar arteries revealed a biphasic vasospasm with a maximal acute spasm at ten minutes and a maximal late spasm at two days after cisternal blood injection. Fluorescence microscopical examination of the major cerebral arteries at day two after the SAH revealed a reduction in the fluorescence intensity and in the number of histochemically visible sympathetic nerve terminals. Stroke Vol 16, No 4, 1985 CEREBRAL VASOSPASM is an angiographically demonstrable, variable arterial constriction that can be clinically asymptomatic or give rise to increasing neurological deficits or death. Vasospasm frequently occurs following a subarachnoid haemorrhage (SAH) secondary to rupture of an intracranial aneurysm. The mechanism underlying the development of spasm is not known.Research has focused on the discovery of a spasmogenic factor. Monoamines'~6 and prostaglandins 7 " 9 have been proposed as spasm inducing factors. Breakdown products of erythrocytes'°~1 2 and free radicals 13 -M have also been suggested. Correspondingly, monoamine antagonists or inhibitors have been used to prevent or treat vasospasm. l5~19 The effect of thromboxane synthetase inhibitors and prostacyclin on spasm has also been investigated. 2021 However, there is still no definitive treatment for spasm.In our opinion, there is a need for a simple and inexpensive SAH model giving a reproducible vasospasm in the investigation of the mechanism underlying the spasm syndrome. Therefore, we have developed a SAH model in the rat. This communication presents the angiographical data, and the results of the fluorescence microscopical examinations of the major cerebral arteries following a SAH. Materials and MethodsEighty-seven Sprague-Dawley rats weighing between 300 and 425 g were used. Animal PreparationsStage I. The animals were anaesthetized with chloral hydrate (250 mg/kg i.p.). An opaque x-ray catheter was inserted into the cisterna magna for subsequent injection of blood. The proximal part of the catheter was blunted and attached to the atlanto-occipital membrane with a purse string suture. The distal tip of the catheter was sealed and sutured subcutaneously to an external skull muscle. Stage II. Three to seven days after the implantation of the cisternal catheter, the animals were prepared for angiography. The anaesthesia was initiated with 4% halothane. The trachea was exposed and a tube (premature Infant feeding tube size 8 -CR Bard International Ltd., England) was inserted orally and observed entering the trachea. Respiration was controlled in a semiopen circuit using a servoventilator (manufactured at the University Hospital, Lund, Sweden). Anaesthesia was maintained with 70% nitrous-oxide and 30% oxygen.Catheters were inserted into a femoral artery and vein for continuous blood pressure monitoring and for infusion of drugs, respectiv...

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A new experimental model of subarachnoid hemorrhage (SAH) in rats is described. A needle was stereotaxically placed in the prechiasmatic cistern and 300, 250 or 200 microl of blood was injected manually, keeping the intracranial pressure (ICP) at the mean arterial blood pressure (MABP) level. An acceptable mortality was observed only after injection of 200 microl of blood. In this group, MABP and ICP increased immediately after SAH, but soon approached baseline levels. The subarachnoid blood was mainly distributed in the basal cisternal system and its estimated volume was about 95% of the amount injected. This new model resembles clinical SAH, is very reproducible, easy to use and seems to be a suitable model for studies of the pathophysiology of SAH.

Subarachnoid hemorrhage resulted in delayed cell death in a large proportion, but not all, of the surviving animals. The acute CBF decrease was related to the degree of subsequent cell death. These findings indicated the relevance of apoptotic-like pathways. There appears to be a temporal therapeutic window during which adequate treatment might reduce the final damage following SAH.