We have developed a stroke model involving middle cerebral artery occl
usion in the rat which elicits changes in cardiac and autonomic variab
les that are similar to those observed clinically. It is likely that t
hese neurogenic autonomic responses are mediated by changes in neurotr
ansmitter systems subsequent to the stroke. This possibility was inves
tigated by examining changes in immunohistochemical staining for tyros
ine hydroxylase, neuropeptide Y, leu-enkephalin, neurotensin and dynor
phin following middle cerebral artery occlusion in the rat. Computeriz
ed image analysis was used to provide semi-quantitative measurements o
f the changes. The ischemic region was centered primarily in the insul
ar cortex. The results indicate that there are significant increases i
n immunostaining for tyrosine hydroxylase and neuropeptide Y in the in
sular cortex within the peri-infarct region. Neuropeptide Y staining w
as also significantly increased in the basolateral nucleus of the amyg
dala, ipsilateral to the middle cerebral artery occlusion, which did n
ot appear to be included in the infarct. Leu-enkephalin, neurotensin a
nd dynorphin staining was significantly elevated in the central nucleu
s of the amygdala ipsilateral to the occlusion of the middle cerebral
artery. These neurochemical changes are discussed as possible mechanis
ms mediating the cardiac and autonomic consequences of stroke or as pa
rt of a process to provide neuro-protection following focal cerebral i
schemia.