AUTONOMIC CARDIOVASCULAR-RESPONSES TO SMOKE EXPOSURE IN CONSCIOUS RATS

Autonomic cardiovascular responses and the change in renal sympathetic nerve activity (RSNA) in response to smoke exposure were investigated in unrestrained conscious rats. Smoke exposure caused a prominent increase in RSNA (to 557.3 +/- 221.9% of the control level) and plasma norepinephrine [from 0.18 +/- 0.08 (control) to 0.66 +/- 0.22 ng/ml (at peak response of smoke exposure)], a slight increase in arterial blood pressure (from 89.6 +/- 3.3 to 103.6 +/- 3.8 mmHg), and marked bradycardia (from 386.6 +/- 12.8 to 231.3 +/- 20.6 beats/min). Respiratory rate in conscious rats was initially increased (from 1.6 +/- 0.1 to 6.1 +/- 0.3 breaths/s) but was decreased (to 0.9 +/- 0.1 breaths/s) at the peak phase of the cardiovascular responses to smoke inhalation. Blood gases and pH reflected these changes in respiratory rate to some extent. Sinoaortic denervation did not attenuate the bradycardia (from 402 +/- 17.5 to 255.8 +/- 16.2 beats/min) or increase in RSNA (to 413.4 +/- 74.9%) that occurred during smoke inhalation. Atropine sulfate abolished the bradycardic response (from 440.4 +/- 13.8 to 485.4 +/- 8.6 beats/min). Initial tachypnea was also observed in both sinoaortic denervated rats and atropine-treated rats. Anesthesia, induced by pentobarbital sodium (30 mg/kg iv) or alpha-chloralose (65 mg/kg iv), abolished the bradycardia, the increase in RSNA, and the change in respiratory rate caused by smoke exposure. Ablation of the olfactory lobes also greatly attenuated the smoke-induced increase in RSNA (to 150.9 +/- 22.9%), bradycardia (from 372.9 +/- 19.6 to 376.3 +/- 24.1 beats/min), and the respiratory change. The results indicate that smoke exposure caused sympathetic and parasympathetic nerve activation via the olfactory pathway and that these responses were integrated at a site in the central nervous system that could be suppressed by anesthetics.