Submitted on March 3, 2004
Accepted on April 2, 2004
Role of Sensory Input from the Lungs in Control of Muscle Sympathetic Nerve Activity During and After Apnea in Humans
Rami N Khayat1, Tadeusz Przybylowski2, Keith C Meyer1, James B Skatrud1, and Barbara J Morgan3*
1 Department of Medicine, University of Wisconsin-Madision, Madison, Wisconsin, USA; Middleton Veterans Administration Hospital, Madison, Wisconsin, USA
2 Department of Population Health Sciences, University of Wisconsin-Madision, Madison, Wisconsin, USA; Middleton Veterans Administration Hospital, Madison, Wisconsin, USA
3 Department of Orthopedics and Rehabilitation, University of Wisconsin-Madision, Madison, Wisconsin, USA; Middleton Veterans Administration Hospital, Madison, Wisconsin, USA
* To whom correspondence should be addressed. E-mail: morgan{at}surgery.wisc.edu.
We reasoned that if the lung inflation reflex contributes importantly to apnea-induced sympathetic activation such activation would be attenuated in bilateral lung transplant recipients (LTX). We measured muscle sympathetic nerve activity (MSNA; intraneural electrodes), heart rate, mean arterial pressure, tidal volume, end-tidal CO2, and arterial oxygen saturation in 7 LTX and 7 healthy control subjects (CON) before, during, and after 20-sec end-expiratory breath holds. Our evidence for denervation in LTX was: 1) greatly attenuated respiratory sinus arrhythmia and 2) absence of cough reflex below the level of the carina. During apnea, the temporal pattern and the peak increase in MSNA were virtually identical in LTX and CON (347±99 and 359±46% of baseline, p>0.05). In contrast, the amount of MSNA present in the first 5 sec after resumption of breathing was greater in LTX vs. CON (101±4 vs. 38±7% of baseline, p<0.05). There were no between-group differences in apnea-induced hypoxemia or hypercapnia, hemodynamic or ventilatory responses. Thus, cessation of the rhythmic sympathoinhibitory feedback that normally accompanies eupneic breathing does not contribute importantly to sympathetic excitation during apnea. In contrast, vagal afferent input elicited by hyperventilation-induced lung stretch plays an important role in the profound, rapid sympathetic inhibition that occurs following resumption of breathing after apnea.
