Published Online
on March 28, 2005

A more recent version of this article appeared on May 1, 2005

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Submitted on January 9, 2005
Revised on February 28, 2005

Effects of Peripheral Chemoreceptors Deactivation on Sympathetic Activity in Heart Transplant Recipients

Agnieszka Ciarka^*; Boutaïna Najem; Nicolas Cuylits; Marc Leeman; Olivier Xhaet; Krzysztof Narkiewicz; Martine Antoine; Jean-Paul Degaute; and Philippe van de Borne

From the Department of Cardiology (A.C., B.N., N.C., M.L., O.X., J.-P.D., P.v.d.B.) and the Department of Cardiac Surgery (M.A.), Erasme University Hospital, Brussels, Belgium; and the Department of Hypertension and Diabetology (K.N.), Medical University of Gdansk, Poland.

^* To whom correspondence should be addressed. E-mail: Agnieszka.Ciarka{at}ulb.ac.be.

Abstract--Heart transplantation initially normalizes sympathetic hyperactivity directed at the muscle circulation. However, sympathetic activity increases with time after transplantation and the exact mechanisms responsible for sympathetic control in heart transplant recipients remain unclear. We examined the effects of peripheral chemoreflex deactivation caused by breathing 100% oxygen on muscle sympathetic nerve activity (expressed as number of burst per minute and mean burst amplitude), heart rate, and mean blood pressure in 13 heart transplant recipients, 13 patients with essential hypertension, and 10 controls. Heart transplant recipients disclosed the highest sympathetic activity, whereas it did not differ between controls and patients with essential hypertension (51±16 versus 37±14 versus 39±12 burst/min, respectively; P<0.05). Breathing 100% oxygen, in comparison with 21% oxygen, reduced sympathetic activity (-4±4 versus -1±2 burst/min, P<0.01; 85±9 versus101±8% of amplitude at baseline, P<0.001) and mean blood pressure (-4±5 versus +3±6 mm Hg; P<0.05) in heart transplant recipients, decreased sympathetic activity (-4±4 versus 0±3 burst/min, P<0.05; 90±16 versus101±9% of amplitude at baseline, P<0.05) in patients with essential hypertension, but did not reduce sympathetic activity (2±4 versus 3±3 burst/min, P=NS; 95±11 versus 95±13% of amplitude at baseline, P=NS) in control subjects. The sympathetic response to hyperoxia was more marked in heart transplant recipients than in controls (85±9 versus 95±11% of baseline amplitude; P<0.05). The decrease in sympathetic activity was most evident in patients with the longest time after heart transplantation (r=-0.75, P<0.01). In conclusion, tonic chemoreflex activation increases resting muscle sympathetic nerve activity and favors blood pressure elevation after heart transplantation.

Key words: chemoreceptors • sympathetic nervous system • transplantation

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