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55 Adverse Events Following the Combination of Dexmedetomidine with Therapeutic Hypothermia in a Piglet Asphyxia Model
  1. M Ezzati1,
  2. K Broad1,
  3. G Kawano1,
  4. I Fiorens1,
  5. K Kawano1,
  6. J Rostami1,
  7. E Cady2,
  8. P Gressens3,
  9. R Sanders4,
  10. X Golay5,
  11. NJ Robertson1
  1. 1Institute for Women’s Health, University College London
  2. 2Medical Physics and Bioengineering, University College Hospitals, London, UK
  3. 3Inserm, Paris, France
  4. 4Anesthetics, Imperial College London
  5. 5Brain Repair and Rehabilitation, Institute of Neurology, London, UK


Background Dexmedetomidine (DXM) is a potent, selective a2 adrenoceptor agonist which exerts sedative, neuroprotective, analgesic and anti-inflammatory properties that may be beneficial for neonatal asphyxia. The safety of DXM combined with therapeutic hypothermia is unknown.

Aim To assess safety of low (0.6–1.5mcg/kg/h) and high dose (10mcg/kg/h) DXM with hypothermia as part of a larger study investigating neuroprotection with DXM-augmented cooling.

Methods Following a quantified hypoxic-ischaemic insult, 16 male piglets were randomized to either hypothermia alone (33.5oC from 4–22h, n=7) or DXM plus hypothermia (n=9). Mean arterial blood pressure (MABP) was measured continuously; when MABP was < 40mmHg, a saline bolus was given followed by inotropes. At 48 h the experiment was terminated.

Results There was no difference in baseline variables. Compared to hypothermia only, the DXM hypothermia group required more saline, adrenaline and cardiac arrests (all p<0.05). These adverse events occurred at both high and low dose DXM.

Abstract 55 Table 1

Volume replacement, adrenaline and cardiac arrests

Conclusion Adverse cardiovascular events with low and high dose DXM combined with cooling occurred mainly after 16 h and could be due to perturbed central autonomic function, vasoconstriction via peripheral alpha adrenoceptor stimulation or effects on the imidazoline receptor.

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