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Arterial sympathetic innervation and cerebrovascular diseases in original rat models
The role of the arterial sympathetic innervation in cerebrovascular pathology was investigated in new experimental models using Brown Norway (BN) and Long–Evans (LE) rats. The BN rat is susceptible to intracerebral hemorrhage (ICH) within the cerebral cortex when rendered hypertensive whereas the LE...
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Published in: | Autonomic neuroscience 2003-03, Vol.104 (2), p.137-145 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The role of the arterial sympathetic innervation in cerebrovascular pathology was investigated in new experimental models using Brown Norway (BN) and Long–Evans (LE) rats. The BN rat is susceptible to intracerebral hemorrhage (ICH) within the cerebral cortex when rendered hypertensive whereas the LE rat is prone to cerebral aneurysms (CAs) in arteries of the circle of Willis with hypertension and carotid ligation. Noradrenaline (NA) content, determined by high performance liquid chromatography (HPLC), was lower both in the caudal and cerebral arteries in the BN than in the LE rat. Denervation of cerebral arteries by superior cervical ganglionectomy did not increase ICH lesion incidence in BN hypertensive rats. A possible link between the level of caudal artery NA content and the occurrence of ICH lesions and CAs was studied in rats from two distinct BNXLE crosses: back-cross (BC) rats (F1XBN) and F2 rats (F1XF1) which respectively display, with hypertension and carotid ligation, a high incidence of either ICH lesions or CAs. In BC rats, the level of caudal artery NA content was not related to ICH lesion occurrence. However, in F2 rats a low caudal artery NA content was associated with a high incidence of ruptured CAs. Thus, a low arterial sympathetic innervation may participate in mechanisms leading to rupture of CAs. |
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ISSN: | 1566-0702 1872-7484 |
DOI: | 10.1016/S1566-0702(03)00018-3 |