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CEREBROVASCULAR PROTECTION BY SEQUENTIAL BILATERAL CAROTID ARTERY LIGATION IN AGED SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Horie R.,
Mano M.,
Omura K.
Publication year - 1993
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1993.tb00577.x
Subject(s) - medicine , ligation , ischemia , spontaneously hypertensive rat , cardiology , common carotid artery , carotid arteries , stroke (engine) , infarction , internal carotid artery , anesthesia , cerebral infarction , blood pressure , myocardial infarction , mechanical engineering , engineering
SUMMARY 1. Sequential bilateral carotid artery ligation (BCL) separated by a 1 week interval was performed on 5 month spontaneously hypertensive rats (SHR) (i.e. SHRSR‐B 1 /Izm) and the developmental course of hypertension and cerebrovascular lesions in advanced age were analysed as compared with those in age‐matched sham‐operated controls. 2. Behavioural activity and behavioural reaction to light were also investigated in the above‐mentioned SHR, young and adult stroke‐prone SHR (i.e. SHRSP‐A 3 /Izm), SHR (i.e. B 1 /Izm) and Wistar‐Kyoto rats (i.e. WKY/Izm). 3. All of the control SHR developed severe hypertension resulting in cerebral stroke with focal oedema due to cerebral haemorrhage and infarction as a result of arterionecrosis 18 months after birth. 4. SHR usually die within a few days of BCL. In the present study, however, they successfully survived without cerebrovascular damage for a long time, although they developed a similar severe hypertension in a significantly shorter period of time ( P < 0.05) and showed behavioural abnormalities that were probably due to severe cerebral ischaemia. 5. These experimental results suggest an ischaemic tolerance phenomenon in a hypertensive model that was exposed to mild ischaemic stress by unilateral carotid artery ligation (UCL) before the subsequent induction of severe ischaemia by BCL. The results also suggest that an aggravation of hypertensive cerebrovascular changes due to long‐lasting ischaemia after BCL was prevented through a possible cumulative effect of ischaemic stress.