Reduction in cardiac contractility during upper respiratory stimulation with cigarette smoke.

Lightly anesthetized rabbits were instrumented to measure arterial pressure, peak left ventricular pressure (LVP) and its first derivative (LV dP/dt), electrocardiogram (ECG), heart rate (HR), and respiratory movements. Through a midtracheal incision two cannulas were inserted, one to allow spontaneous respiration of room air and the other to permit perfusion of the upper airways with unfiltered cigarette smoke. When 50 ml of smoke were passed out of the nostrils, we observed apnea (33.3 s), increases in mean arterial pressure (MAP) (31.9 mmHg) and LVP (38.3 mmHg), as well as decreases in HR (-125 beats/min) and LV dP/dtmax (-45%). After bilateral vagotomy, the responses of MAP and LVP to smoke exposure were not different from those in intact animals. The decrease in LV dP/dtmax (-27%) was, however, significantly less than in intact animals. Also, HR responses were not as pronounced after vagotomy. beta-Blockade after vagotomy abolished the LV dP/dt response to smoke, and the HR response was nearly abolished. MAP and LVP still underwent significant increases due to the smoke. After total sinoaortic denervation plus vagotomy in a second group of animals, a significant fall in LV dP/dtmax (-25%) persisted, and a small HR decrease was observed even when MAP was not allowed to change significantly. The results demonstrate that sympathetic outflow to the heart decreases while there is a net increase in sympathetic activity to the peripheral vasculature. The dramatic vagal bradycardia observed contributes part of the change in LV dP/dtmax. Reflexes originating in the circulation (vagal or sinoaortic) may also contribute to the fall in LV dP/dtmax, but a significant response persists in their absence.