Evaluation of the direct myocardial efects of dexmedetomidine in the transplanted infant heart

Abstract

Background The denervated state of the transplanted heart excludes it from central autonomic control. Dexmedetomidine (dex) is an imidazole with selective α2 adrenoceptor (α2AR) agonist properties. The α2AAR isoreceptor mediates central analgesic and sedative effects via the locus ceruleus. The central antihypertensive and antiarrhymic effect of dex is mediated via medullary imidazoline-1 receptors (I1R). While the desired effects of dex are centrally mediated, it has recently been determined that both α2AAR and I1R are present in the human heart. The hemodynamic significance of this is not understood. The denervated cardiac physiology of an infant cardiac transplant presents a unique opportunity to examine the direct myocardial effects of dex. Methods This report details the hemodynamic impact of dex on a 6 month old infant 4 weeks post transplant. Dex was administered at a rate of 0.8–1 μg/kg/hr with q6–8h loading doses of 1 μg/kg (on days 1–5) for 18 days in the PICU to facilitate withdrawal from a 3-mos. exposure to opioids. HR and BP assessments were made with an arterial line. Results Neither bradycardia nor hypotension occurred throughout the dex administration. The only evidence of opioid withdrawal was retching on days 4–6 accompanied by sinus tachycardia (200–220). Conclusions There was no hemodynamic impact of dex administered either by bolus or infusion technique. It may be that any effect was obscured by the catecholamines elaborated during opioid withdrawal. Clinical Pharmacology & Therapeutics (2005) 77, P70–P70; doi: 10.1016/j.clpt.2004.12.159