Subarachnoid haemorrhage produces differential effects on transmitter kinetics at cerebral periarterial noradrenergic...

The functional states of cerebral perivascular noradrenergic terminals were investigated following experimental 'closed-space' subarachnoid haemorrhage (SAH) in cat. The left middle cerebral artery (L-MCA) was compared to the ruptured right (R-MCA) one. Permeability kinetics of 3H-NA (noradrenaline) were measured simultaneously in isolated segments of paired R- and L-MCAs, testing responses to electrical field stimulation and the presence of the alpha-adrenoceptor antagonist, phentolamine, at different concentrations and times post-SAH. Fractional 3H-NA efflux from ruptured R-MCAs was reduced to undetectable levels at 18 h to at least 3 d post-SAH. Response to electrical stimulation partially recovered at 10 d and approached the controls by 16 to 30 d. In the L-MCAs, 3H-NA efflux was decreased up to 90% at 18 h, but recovered to control level by 3 d, unless it too became involved by encroachment of blood from the SAH side. The fractional 3H-NA efflux in the controls was typically augmented by phentolamine, reaching a peak at 0.3 microM of the drug. This overflow response was completely lost between 0.03 and 3.0 microM phentolamine in the R-MCAs for at least 30 d post-SAH, whereas uninvolved L-MCAs regained drug-induced overflow at 10 to 16 d post-SAH. Uptake of 3H-NA after SAH was also decreased 30 to 50% for both MCAs at 18 h and 3 d post-SAH. Control 3H-NA uptake was regained by 10 d post-SAH in the L-MCA but not until 16 d in the R-MCA.(ABSTRACT TRUNCATED AT 250 WORDS)