Cardiovascular effects of intracisternal 6-hydroxydopamine and of subsequent lesions of the ventrolateral medulla coinciding with the Al group of noradrenaline cells in the rabbit.

The acute cardiovascular effects of intracisternal injections of 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine and 5,7-dihydroxytryptamine and the degree of neurotransmitter depletion achieved by such injections were studied. The two different vehicles used--0.2% ascorbic acid in 0.9% NaCl, or 0.9% NaCl--had little effect on the cardiovascular response to 6-OHDA injections but had a striking effect on levels of noradrenaline (NA) subsequently measured in the thoracic spinal cord. 6-OHDA (600 micrograms kg-1 free base) dissolved in normal saline depleted spinal cord NA to less than 1% of control levels whereas the same dose of 6-OHDA dissolved in ascorbate saline only depleted spinal cord NA to 24% of control levels. The degree of depletion of NA in medulla, pons and hypothalamus was similar in the two groups. Ascorbic acid also appeared to contribute to the non-specific toxicity of intracisternal injections of 6-OHDA. The hypertension and bradycardia that followed lesions of the ventrolateral medulla coinciding with the A1 group of noradrenergic cells (Al lesions) were attenuated in animals in which spinal cord NA had been depleted to 2% of control using 6-OHDA in normal saline. However, pretreatment with 6-OHDA in ascorbate saline, which only reduced spinal cord NA to 23% of control, had no effect on the cardiovascular response to Al lesions. It seems likely that the effects of Al lesions are mediated, at least in part, by NA projections descending within the spinal cord.