Role of nitric oxide following cardiac transplantation

Chester, AH; Birks, E.J.; Mh, Yacoub

doi:10.1038/sj.jhh.1000735

Cited by 10 publications

(2 citation statements)

References 63 publications

(82 reference statements)

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“…Alternatively, an impaired nitric oxide (NO) pathway after heart transplantation might play a role (15) since a reduced exercise capacity was associated with a reduced NO production after heart transplantation (16). Accordingly, heart failure patients – also characterized by an impaired NO pathway and an increase in plasmatic ET‐demonstrated no ET changes after an 8‐wk training program (17).…”

Section: Discussionmentioning

confidence: 90%

Improving exercise capacity, 6 wk training tends to reduce circulating endothelin after heart transplantation

Doutreleau

Piquard

Lonsdorfer

et al. 2004

Clinical Transplantation

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Short-term survival is no longer the pivotal issue after heart transplantation but, most heart-transplant (Htx) patients still present with increased circulating endothelin-1 (ET) and reduced exercise capacity. ET-1 limits both exercise-induced vasodilation and blood flow redistribution toward acting muscles and might be accessible to training. This study was performed to investigate the effect of training on ET-1 and whether an eventual training-induced improvement in exercise capacity may be related to reduced baseline or exercise circulating ET-1 in Htx patients. Five Htx patients performed a maximal bicycle exercise test and an endurance exercise test before and after a training program of 18 exercises sessions during 6 wk. ET-1 was determined by radioimmunoassay at rest, end endurance exercise and 30 min recovery, before and after training. Training improved significantly Htx's maximal oxygen uptake (+13.1 +/- 4.8%; p < 0.05) and also reduced significantly the endurance exercise-induced heart rate increase. Resting ET-1 was increased in Htx (5.98 +/- 1.88 vs. 1.61 +/- 0.25 pmol/L in controls; p < 0.01) but although ET-1 modulation might participate in training-induced beneficial effects, training failed to modulate either resting or exercise ET-1 plasma level. Training-induced improvement in exercise capacity might not mainly due to decreased ET-1 after heart transplantation. Further supporting the usefulness of training, these preliminary data suggest that improved exercise capacity may not be mainly due to decreased ET-1 in Htx patients. Further, larger scale studies will be needed to investigate whether an impaired nitric oxide pathway stimulation might explain such results and whether a longer training program can reduce local ET-1, arising from working muscles after heart transplantation.

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