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Eur J Cardiothorac Surg 2002;21:753-759
© 2002 Elsevier Science NL

The effect of chronic L-arginine administration on vascular recovery following cold cardioplegic arrest in rats

^a National Heart and Lung Institute Heart Science Centre, Harefield Hospital, Harefield, Middlesex UB9 6JH, UK
^b Electron Microscopy Unit, Brompton Hospital, London, UK
^c Cell Biology Department, Brompton Hospital, London, UK

Received 26 June 2001; received in revised form 8 January 2002; accepted 10 January 2002.

* Corresponding author. Tel.: +44-1895-828-550; fax: +44-1895-828-992
e-mail: mr.amrani{at}rbh.nthames.nhs.uk

Objective: Acute administration of L-arginine (LA), the physiological substrate of nitric oxide, has been used as a strategy for myocardial protection during ischemia-reperfusion. The aim of this study was to assess the effects of chronic oral LA administration on vascular functions and morphology after prolonged cold cardioplegic arrest. Methods: Adult male Sprague–Dawley rats (600–650 g) were divided into control and LA groups, which received LA (4 mg/ml) for 6 weeks. Two experimental protocols were carried out. (1) Isolated rat heart perfusion was performed and hearts were subjected to ischemia for 4 h at 4°C using cold crystalloid cardioplegia (n=8 in LA, n=7 in control). Endothelial and vascular smooth muscle functions were assessed through observations of pre- and post-ischemic coronary flow response to 5-hydroxytryptamine (5-HT) and glyceryl trinitrate (GTN) (%5-HT and %GTN, respectively). (2) Semi-quantitative assessment of tissue morphology was conducted after the same ischemia-reperfusion protocol (n=4 in each group). Results: The LA group showed significantly better recovery (post-/pre-ischemic value) of %5-HT (97.0±65.6 versus 21.5±25.7%, P=0.015) and %GTN (124.5±117.6 versus 47.7±16.6%, P=0.021). The histological assessment showed no significant differences between the two groups. Conclusions: Chronic oral administration of LA significantly ameliorated the postischemic recovery of endothelial and vascular smooth muscle functions after cold cardioplegic arrest in rats.

Key Words: Endothelial function • Ischemia • Nitric oxide • Reperfusion • Vasoconstriction/dilation

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