Bidirectional Regulatory Effects of Dexmedetomidine on Porcine Coronary Tone In Vitro

Abstract

BackgroundStudies in vivo have shown that dexmedetomidine (DEX) could protect the myocardium and modulate the coronary blood flow. This study aimed to investigate the direct and concentration-dependent effects of DEX on the tone of porcine coronary artery in vitro and the underlying mechanisms.Material/MethodsDistal branches of the porcine anterior descending coronary arteries were dissected and cut into 3–5 mm rings. The tones of coronary rings in response to cumulative DEX were measured using the PowerLab system. Coronary rings were divided into three groups: 1) endothelium-intact coronary rings without drug pretreatment (control); 2) endothelium-intact coronary rings pretreated with either yohimbine, tetraethylamine (TEA) or NG-nitro-L-arginine methyl ester (L-NAME); and 3) endothelium-denuded coronary rings pretreated with either yohimbine or TEA.ResultsDEX induced coronary ring relaxation at lower concentrations (10−9 to 10−7 M) followed by constriction at higher concentrations (10−6 to 10−5 M). The coronary constrictive effect of higher DEX (10−5 M) was greater in the endothelium-denuded rings than in the endothelium-intact rings. Yohimbine reduced the coronary constrictive effect of DEX at higher concentrations (10−6 to 10−5 M). TEA and L-NAME significantly reduced the coronary relaxing effect of DEX at lower concentrations (10−9 to 10−7 M) in endothelium-intact rings. TEA attenuated the coronary relaxation induced by DEX in endothelium-denuded rings.ConclusionsDEX exerts bidirectional effects on porcine coronary tone. The coronary relaxing effect of DEX at lower concentrations is likely associated with endothelium integrity, NO synthesis and BKCa channel activation, while the coronary constrictive effect of DEX at higher concentrations is mediated by α2 adrenoceptors in the coronary smooth muscle cells.

Dexmedetomidine Combined with Low-Dose Norepinephrine Continuous Pumping to Prevent Hypotension after Cesaresan Section: A Randomized Controlled Trial

“…Although dexmedetomidine is a highly selective α 2 -adrenoceptor agonist, it can bind to diferent α 2adrenoceptors and α 1 -adrenoceptors at a certain plasma concentration. Sedation and antisympathetic action on α 2A receptors can lead to a decrease in blood pressure and heart rate, vasoconstriction on α 2B receptors can lead to an increase in blood pressure, and the activation efect of α 1adrenoceptors can also cause an increase in blood pressure [18,19]. In this study, the incidence of maternal hypotension in group S was 52.5%, while that in group D was 30%, which was signifcantly lower than that in group S. Tis may be due to the high plasma concentration of dexmedetomidine within a few minutes after spinal anesthesia, and the vasoconstriction caused by α 2B and α 1 receptors on peripheral vascular smooth muscle alleviated the vasodilation efect after spinal anesthesia to some extent.…”

Dexmedetomidine suppresses the development of abdominal aortic aneurysm by downregulating the mircoRNA‑21/PDCD 4 axis

“…As a prevalent neuroprotectant applied in anesthetic surgeries, dexmedetomidine (Dex) is able to suppress the activities of neuroendocrine hormones and inflammatory mediators ( 7 ). In addition, Dex helps to maintain a balanced and steady myocardial function and coronary blood flow ( 8 ). The administration of Dex during aortic vascular treatment can protect patients by reducing the incidence of myocardial ischemia as it effectively suppresses alterations in blood pressure and heart rate ( 9 ).…”