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Lisuride and bromocryptine in L-Dopa stable-responder parkinsonian patients: a comparative, double-blind evaluation of cardiopressor and neurochemical effects.

In this study, we compared the haemodynamic and biochemical effects of bromocryptine to those of lisuride, in L-Dopa stable responder parkinsonian (PD) patients. Nineteen PD patients were admitted to the study. A double-blind, parallel group, randomized study was performed. Patients were randomly chosen to receive lisuride or bromoryptine. Both drugs were administered in increasing dosages until a maximum of either 0.6 mg lisuride or 7.5 mg bromocryptine was reached. The following tests were carried out: periprandial study, tilt table test and cardiovascular tests (sustained handgrip test, deep-breathing, lying-to-standing and Valsalva manoeuvre). During the tests, systolic and diastolic blood pressure and heart rate were monitored with an automatic sphyngomanometer. Blood samples for catecholamine assay were taken during tilt table test. In basal conditions 70% of the randomly chosen men in the bromocryptine group showed significant orthostatic hypotension (OH), while only one subject in the lisuride group demonstrated comparable OH values. The deepest derangement of orthostatic regulation was observed in the lisuride group but it should not be attributed to the greater hypotensive effects of this drug. Infact, the cardiopressor effects of bromocryptine may well be "masked" by the alteration detected in baseline conditions. Only bromocryptine significantly reduced supine and orthostatic NE plasma levels on the 14th day of therapy. Neither bromocryptine nor lisuride significantly altered periprandial blood pressure values. In conclusion, this study demonstrates that lisuride and bromocryptine are well tolerated as far as the analysis of the development of hypotensive effects is concerned. Further, more sophisticated study, with other agents that block the peripheral and/or central effects of dopamine-agonists in PD patients should be conducted in order better to define the precise role of these types of agents and the potential cardiopressor risks in these subjects.