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The Mechanisms of Propofol-induced Relaxation on Isolated Thoracic Aorta Rings in Rats

Author: WenXiangYu
Tutor: WangLi
School: Suzhou University
Course: Anesthesiology
Keywords: Propofol Thoracic aorta Vasodilation Nitric oxide KATP channel Protein kinase C
CLC: R614
Type: Master's thesis
Year: 2011
Downloads: 16
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Abstract


Objective: To investigate propofol on isolated rat aortic rings of rats and its mechanism. Method 1: Insert the prepared SD rats were randomly divided into the thoracic aorta endothelium intact group (n = 36) and endothelium-denuded group (swab endothelium) (n = 30). Each group includes: ① 1 × 10 -6 mol / L noradrenaline (NA) treatment group (n = 6); ② 1 × 10 -6 mol / L NA propofol treatment group (n = 6); ③ 1 × 10 -6 mol / L NA 0.18% fat emulsion (corresponding to 1 × 10 -4 mol / L propofol emulsion contained in the amount of) treatment group (n = 6) and 1 × 10 -6 mol / L NA 1 × 10 -4 mol / L propofol treatment group (n = 6); ④ 1 × 10 -4 mol / L L-NAME 1 × 10 -6 mol / L NA treated propofol (n = 6) (endothelium group without the group); ⑤ 1 × 10 -5 mol / L Gliben 1 × 10 -6 mol / L NA propofol treatment group (n = 6). 1 × 10 -6 mol / L NA-induced contraction of rat aortic rings reached its peak after every 15min plus increasing concentrations (1 × 10 -6 mol / L, 5 × 10 -6 mol / L, 1 × 10 -5 mol / L, 5 × 10 -5 mol / L, 1 × 10 < sup> -4 mol / L) of propofol to observe changes in vascular tone determines propofol and endothelial vasodilator effect relationship. (2) The prepared SD rats were randomly divided into thoracic aorta endothelium intact group (n = 36) and endothelium-denuded group (swab endothelium) (n = 36), each group of six sub-groups: ① 10nmol / L Go6976 1 × 10 -6 mol / L NA propofol treatment group (n = 6); ② 10μmol / L Rottlerin 1 × 10 -6 mol / L NA Propofol phenol treatment group (n = 6); ③ 2μmol / L PKCε-Pseudo 1 × 10 -6 mol / L NA propofol treatment group (n = 6); ④ 2μmol / L PKCθ-Pseudo 1 × 10 -6 mol / L NA propofol treatment group (n = 6); ⑤ 2μmol / L PKCζ-Pseudo 1 × 10 -6 mol / L NA propofol treatment group (n = 6); ⑥ group: 1 × 10 -6 mol / L NA propofol treatment group (n = 6). PKCα inhibitor Go6976, PKCδ inhibitor Rottlerin, PKCζ, θ and ε false substrate incubation vascular ring after 30min, add 1 × 10 -6 mol / L NA vascular ring contraction reached its peak every 15min plus increasing concentrations of propofol (1 × 10 -6 mol / L, 5 × 10 -6 mol / L, 10 -5 mol / L, 5 × 10 -5 mol / L, 10 -4 mol / L), observed changes in vascular tone determine whether PKC isoforms mediated propofol phenol-induced vasodilation. Results: 1. Propofol caused concentration-dependent vasodilation in amplitude, more pronounced in endothelium-intact group, diastolic rate were (11.28 ± 1.51)%, (25.23 ± 4.03)%, (44.08 ± 4.49)%, ( 66.28 ± 4.83)% and (74.59 ± 4.78)%, with the same concentration of drug-treated group compared to the endothelium difference was statistically significant (p lt; 0.01). Endothelium intact group, nitric oxide synthase inhibitor L-NAME (1 × 10 -4 mol / L) was significantly lower propofol pretreatment vasodilation effect, and 1 × 10 -6 mol / L NA propofol treatment group difference was significant (p lt; 0.01). In addition, the specificity of the KATP channel inhibitor Gliben pretreatment also significantly inhibited vascular ring propofol endothelium-dependent vasodilation amplitude (p lt; 0.05, and 1 × 10 -6 mol / L NA C treatment group compared to propofol), and the low concentration (1 × 10 -6 mol / L, 5 × 10 -6 mol / L) of blood propofol relaxation effects into contraction, compared with baseline values, significant difference. (2) In endothelium intact group, Go6976, PKCε and PKCθ false false substrates substrates were reduced propofol induced vasodilation magnitude, and endothelium-intact control group, the difference was statistically significant (p lt; 0.05); PKCδ inhibitor Rottlerin completely inhibited propofol vasodilation effect, and the 1 × 10 -6 mol / L and 1 × 10 -5 mol / L propofol vasodilation effect flip to contraction, compared with baseline difference was statistically significant (p lt; 0.05). In endothelium group, inhibition above PKCs isoforms can enhance vasodilation propofol effect: Rottlerin, PKCε and PKCθ false false substrate substrate treatments were so propofol (1 × 10 -6 mol / L, 5 × 10 -6 mol / L, 1 × 10 -5 mol / L, 5 × 10 -5 mol / L, 1 × 10 -4 mol / L) significantly increased the amplitude of vasodilation, compared with the control group without endothelium difference was statistically significant (p lt; 0.05); Go6976 and PKCζ false Substrate processing, respectively, the 1 × 10 -5 mol / L and 1 × 10 -4 mol / L concentration range of propofol rate significantly increased vasodilation, endothelium compared with the control group difference was statistically significant (p lt; 0.05). Conclusions: 1. Propofol vasodilation in a concentration-dependent and endothelium. Nitric oxide and KATP channel mediated endothelium-dependent vasodilation drugs. 2. PKC isoforms, such as α, δ, ε and θ propofol mediated vasodilation effect. When endothelial integrity and endothelium, PKCs are of a different mechanism to regulate vasodilation propofol effect.

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