This study investigates directly the possibility that sympathetic discharge to the heart is decreased while it is increased to other organs during upper respiratory perfusion with cigarette smoke. Blood pressure (BP), heart rate, ECG, and respiratory movements were monitored in urethane-anesthetized rabbits. Insertion of two cannulas allowed respiration of room air while passing smoke across the upper respiratory irritant receptors and out through the nares. Through a retroplural incision, the left stellate ganglion was exposed and a cardiac branch isolated. Similarly, a left renal nerve was isolated. Multiunit nerve recordings were obtained from both nerves. In four control animals, cigarette smoke (50 ml) caused apnea, bradycardia (-116 beats/min) and increased BP (33 mmHg). Activity in the renal nerve increased (248% of control [C]) and activity in the cardiac nerve was reduced (62% C). In these animals after Flaxedil and artificial respiration, nerve activity responses were still pronounced (renal, 178% C; cardiac, 66% C). In four other barodenervated animals neural responses to smoke were similar to those observed with baroreceptors intact (renal, 211% C; cardiac, 51% C). In these animals after artificial ventilation and Flaxedil, responses were not significantly changed. These results indicate that smoke stimulation causes a differential pattern of sympathetic discharge. The responses observed cannot be accounted for by secondary adjustments through arterial baroreceptors, chemoreceptors, or pulmonary stretch receptors.

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Depression found in Parkinson disease (PD) usually responds to selective serotonin reuptake inhibitors (SSRIs). Drugs that modify experimental neuroleptic catalepsy (NC) might affect extrapyramidal symptoms in PD. Therefore, the effects of SSRIs on NC were tested in mice, 26-36 g, separated by sex. Catalepsy was induced with haloperidol (H; 1 mg/kg, ip) and measured at 30-min intervals using a bar test. An SSRI (sertraline, ST; paroxetine, PX; fluoxetine) or vehicle (C) was injected ip 30 min before H. Dunnett's test was used for comparison of means. ST (1-5 mg/kg) or PX (1-5 mg/kg) attenuated NC, with a similar inhibition found in both sexes (5 mg/kg, 180 min: ST -males: 124 ± 10 vs 714 ± 15 s in C; females: 116 ± 10 vs 718 ± 6 s in C; PX -males: 106 ± 10 vs 714 ± 14 s in C; females: 102 ± 10 vs 715 ± 14 s in C). At 0.3 mg/kg, neither of these drugs affected NC. Fluoxetine (1-25 mg/kg) also inhibited catalepsy, although the effect was not dosedependent; no differences were observed between males and females (5 mg/kg, 180 min: males, 185 ± 14 vs 712 ± 14 s in C; females, 169 ± 10 vs 710 ± 19 s in C). For these SSRIs, maximal inhibition of NC was obtained with 5 mg/kg, 180 min after H. These results are consistent with the hypothesis that serotonergic mechanisms modulate nigrostriatal transmission, and suggest that SSRIs are possibly safe in depressive PD patients.