Reduction in cardiac contractility during upper respiratory stimulation with cigarette smoke

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Abstract
Lightly anesthetized rabbits were instrumented to measure arterial pressure, peak left ventricular pressure (LVP) and its 1st derivative (LV dP/dt), ECG, heart rate (HR) and respiratory movements. Through a midtracheal incision 2 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, apnea was seen (33.3 s), increased mean arterial pressure (MAP) (31.9 mmHg) and LVP (38.3 mmHg) and decreased HR (-125 beats/min) and LV dP/dtmax [maximum 1st derivative of peak left ventricular pressure] (-45%). After bilateral vagotomy, the responses of MAP and LVP to smoke exposure were not different from those in intact animals. Decreased LV dP/dtmax (-27%) was significantly less than in intact animals. HR responses were not as pronounced after vagotomy. .beta.-Blockade after vagotomy abolished LV dP/dt response to smoke and the HR response was nearly abolished. MAP and LVP still underwent significant increases due to smoke. After total sinoaortic denervation plus vagotomy in a 2nd 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. Sympathetic outflow to the heart decreased while there was a net increase in sympathetic activity to the peripheral vasculature. The dramatic vagal bradycardia observed contributed part of the change in LV dP/dtmax. Reflexes originating in the circulation (vagal or sinoaortic) also contributed to the fall in LV dP/dtmax but a significant response persisted in their absence.