An exaggerated vasoconstriction response to dexmedetomidine, an α-2 adrenergic agonist, has been associated with 2 genotypes: a deletion in the α-2B adrenoreceptor gene ( ADRA2B deletion) and SNP rs9922316 in the gene for protein kinase C type β ( PRKCB). We hypothesized that children with a marked systemic vascular resistance index (SVRI) increase following intravenous dexmedetomidine bolus would carry these genotypes. Following institutional review board approval, DNA samples from 16 children with transplanted hearts who participated in a study in the cardiac catheterization laboratory of hemodynamic responses to dexmedetomidine boluses underwent genotyping by polymerase chain reaction (PCR) amplification and PCR Sanger sequencing for the ADRA2B deletion and for PRKCB rs9922316. A wide range of SVRI (-12% to +76%, median 33%) and mean arterial blood pressure (MAP; -7% to +50%, median 26%) responses to dexmedetomidine was observed. The responses were not significantly different among genotype groups. An association between exaggerated SVRI or MAP responses and either ADRA2B deletion or PRKCB rs9922316 was not observed.
Keywords: adrenoreceptor; dexmedetomidine; genotype; vasoconstriction.