Key result
Sustained lung inflation reflexively increases systemic vascular capacitance up to ~4.3 ml/kg, lowering SVR and SENA.
Sustained lung inflation causes a reflex increase in systemic vascular capacitance and a decrease in systemic vascular resistance and cardiac sympathetic efferent nerve activity, primarily mediated by vagal afferent nerve fibers.
Animal data link lung inflation to vascular capacitance changes; leaves open human relevance and clinical translation.
The effects of sustained lung inflation on systemic vascular capacitance (SVC), systemic vascular resistance (SVR), and cardiac sympathetic efferent nerve activity (SENA) were investigated in anesthetized dogs. By use of a total cardiopulmonary bypass, the lungs were inflated to tracheal pressures of 10, 15, and 20 mmHg. Tracheal pressures of 10, 15, and 20 mmHg increased system vascular capacitance by 1.4, 3.1, and 4.3 ml/kg and decreased systemic vascular resistance by 0.11, 0.15, and 0.16 mmHg.kg.min-ml-1, respectively, at low carotid sinus pressure (CSP) of 41 mmHg. SENA showed a concomitant decrease. Bilateral vagotomy attenuated the change in SVR by 69%, SVC by 62%, and SENA by 97% when lungs were inflated to a tracheal pressure of 20 mmHg at a low CSP. These results indicate that lung inflation causes a reflex induced increase in SVC as well as a decrease in both SVR and SENA. The lung inflation reflex is mediated primarily through vagal afferent nerve fibers with a small contribution from other afferent nerve pathways.
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Cheng et al. (1989) studied this question. Sustained lung inflation vs. Baseline / bilateral vagotomy was evaluated on Systemic vascular capacitance (SVC), systemic vascular resistance (SVR), and cardiac sympathetic efferent nerve activity (SENA). Sustained lung inflation caused a reflex-induced increase in systemic vascular capacitance (up to 4.3 ml/kg) and a decrease in systemic vascular resistance and cardiac sympathetic efferent nerve activity.
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