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Reduction in cardiac contractility during upper respiratory stimulation with cigarette smoke
The American Journal of Physiology
|April 1, 1981
Summary
Cigarette smoke exposure in rabbits causes apnea and increases blood pressure, while decreasing heart rate and cardiac contractility. Vagal and sinoaortic denervation reveal complex autonomic responses to smoke, indicating reduced cardiac sympathetic outflow.
Area of Science:
- Cardiovascular Physiology
- Autonomic Nervous System Research
- Respiratory Physiology
Background:
- Cigarette smoke inhalation is known to affect cardiovascular function.
- The precise autonomic mechanisms underlying these effects are not fully elucidated.
Purpose of the Study:
- To investigate the autonomic nervous system's role in mediating cardiovascular and respiratory responses to cigarette smoke exposure in rabbits.
Main Methods:
- Rabbits were instrumented to monitor arterial pressure, left ventricular pressure (LVP), its derivative (LV dP/dt), ECG, heart rate (HR), and respiration.
- Upper airways were perfused with cigarette smoke following tracheal incision.
- Experiments involved sequential interventions: vagotomy, beta-blockade, and sinoaortic denervation.
Main Results:
- Smoke exposure induced apnea, increased mean arterial pressure (MAP) and LVP, and decreased HR and LV dP/dtmax.
- Vagotomy reduced the decrease in LV dP/dtmax and attenuated HR responses.
- Beta-blockade abolished LV dP/dtmax and HR responses to smoke.
- Sinoaortic denervation plus vagotomy still resulted in a significant fall in LV dP/dtmax and a small HR decrease.
Conclusions:
- Cigarette smoke decreases sympathetic outflow to the heart but increases peripheral sympathetic activity.
- Vagal bradycardia contributes to the reduction in LV dP/dtmax.
- Circulatory reflexes (vagal, sinoaortic) influence smoke-induced cardiovascular changes, but a residual response suggests other mechanisms are involved.