Does low-dose intravenous atropine affect cardiovascular reflexes in healthy volunteers?
Low doses of intravenous atropine increase cardiovascular responses to active standing in healthy volunteers, suggesting increased excitability of the medullary cardiovascular center.
Effects of exciting the central nervous system (CNS) with low doses of atropine on cardiovascular reflexes was investigated in 6 healthy volunteers. Cumulative doses of atropine sulfate (1.43-28.57 micrograms/kg intravenously, i.v.) were used. The ECG parameters used to quantify the nervous activities on the heart were ratios of the longest to the shortest R-R intervals recorded during forced expirations and deep inspirations (respiratory sinus arrhythmia), the ratio of the longest to the shortest R-R intervals which occur immediately after one rises from a low sitting position (30:15 ratio), and the SD of R-R intervals recorded in standing and supine positions. Very low doses of atropine (1-3 micrograms/kg) increased the 30:15 ratios from (means +/- SEM) 1.21 +/- 0.07 to 1.34 +/- 0.04 (60% increase, p less than 0.01) and SD recorded in standing positions from 32.4 +/- 3.5 to 56.0 +/- 11.0 ms (71% increase, p less than 0.01). Respiratory sinus arrhythmia was not affected in either the standing or supine position, nor was SD recorded in supine positions significantly affected by these low doses of atropine. The only indexes increased by low doses of atropine were those that measure cardiovascular responses to active standing, consistent with an increased excitability of the medullary cardiovascular (vasomotor) centre. There was no evidence of central vagal excitation caused by low doses of atropine in the conscious, spontaneously breathing volunteers. The increased excitability of the medullary cardiovascular centre in response to a low dose of atropine may suggest that normal responses of this centre to arterial baroreceptor stimulation is restrained by a cholinergic inhibitory pathway.
Peter O.O. Julu (1992) studied this question.