The effects of dexmedetomidine on human internal mammary artery and saphenous vein grafts under hypothermia and normothermia.

OBJECTIVES: The purpose of this study was to determine the effects of hypothermia and normothermia on the isolated human saphenous vein (SV) and internal mammary artery (IMA) responses to dexmedetomidine. METHODS: The response of human IMA and SV strips with (E+) and without (E-) endothelium subjected to cumulative concentrations of (10-9, 0-6 M) dexmedetomidine were recorded at 37 °C and at 28 °C. OnE-way ANOVA was used for analysis. A p < 0.05 was considered significant. RESULTS: At 37˚C dexmedetomidine resulted in similar significant concentration-dependent contractions in both E+ and E- SV strips (p < 0.05). At 37 °C dexmedetomidine resulted in significant concentration-dependent contractions in E+ IMA strips, these contractions were significantly lower at all concentrations of dexmedetomidine in E- compared to E+ IMA strips (p < 0.05). When results between similar groups of SV and IMA strips were compared, the contractions were significantly higher in the IMA strips in E+ and E- at 37 °C and also E- 28 °C groups compared to SV (p < 0.05). CONCLUSION: In conclusion, dexmedetomidine causes in vitro vasoconstriction in human IMA and SV grafts. These contractions are greater in IMA compared to SV grafts. Endothelium-derived pathways are possibly involved in the contractile responses of IMA. Moderate hypothermia augments vasoconstriction in SV grafts (Fig. 3, Ref. 27).

In vitro vasoactive effects of dexmedetomidine on isolated human umbilical arteries.

OBJECTIVE: We aimed to investigate the vasoactive effects of dexmedetomidine on isolated human umbilical arteries and possible mechanisms involved. METHODS: Human umbilical artery strips were suspended in Krebs-Henseleit solution and dose-response curves were obtained for cumulative dexmedetomidine before and after incubation with different agents; propranolol, atropine, yohimbine, prazosin, indomethacin, verapamil. Effects of calcium on cumulative dexmedetomidine-induced contractions were also studied. RESULTS: Cumulative dexmedetomidine resulted in dose dependent contraction responses. Incubation with propranolol (Emax: 93.3 ± 3.26 %), atropine (Emax: 92.0 ± 6.54 %), or indomethacin (Emax: 94.25 ± 2.62 %), did not attenuate dexmedetomidine-elicited contractions (p > 0.05). There were significant decreases in the contraction responses of cumulative dexmedetomidine with yohimbine (Emax: 12.1 ± 11.9 %), prazosin (Emax: 28.8 ± 4.6 %) and verapamil (Emax: 11.2 ± 13.6 %) (p < 0.05). In Ca+2 free medium contraction responses to cumulative dexmedetomidine was insignificant (Emax: 5.20 ± 3.42 %). Addition of cumulative calcium to the Ca+2 free medium resulted in concentration dependent increase in contractions (Emax: 64.83 ± 37.7 %) (p < 0.05). CONCLUSION: Dexmedetomidine induces vasoconstriction in endothelial-free umbilical arteries via both, α1- and α2-adrenergic receptors and also extracellular Ca+2 concentrations play a major role. ß-adrenergic receptors, muscarinic cholinergic receptors, and inhibition of cyclooxygenase enzyme are not involved in this vasoconstriction (Fig. 3, Ref. 36).