七氟醚对肺动脉高压大鼠模型血流动力学和诱导型一氧化氮合酶/可溶性鸟苷酸环化酶信号通路的影响
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Effects of Sevoflurane on Hemodynamics and Inducible Nitric Oxide Synthase/Soluble Guanylate Cyclase Signaling Pathway in a Rat Model of Pulmonary Arterial Hypertension
背景与目的
七氟醚对右心室功能的作用尚未完全了解。在实验诱导的肺动脉高压（PAH）大鼠模型中，我们研究了七氟醚对右心室功能和诱导型一氧化氮合酶/可溶性鸟苷酸环化酶（iNOS / sGC）信号通路表达的影响。我们假设七氟烷通过iNOS / sGC通路改善肺动脉高压大鼠的右心室功能。
方 法
将SD大鼠随机用野百合碱或生理盐水处理，诱导PAH。四周后，将大鼠随机分为对照组和七氟醚组。大鼠麻醉后置入肺动脉或右心室导管，吸入3个不同剂量的七氟醚（90分钟）。记录血流动力学变化并检测iNOS和sGC的表达。
结 果
七氟烷均抑制了正常大鼠和PAH大鼠的右心室功能。然而，与对照组大鼠相比，PAH大鼠右心室 dP / dtmax降低程度较小，七氟烷增加了iNOS表达，降低了sGC表达。
结 论
七氟醚对肺动脉高压大鼠右心室收缩功能的抑制程度较正常大鼠低。七氟烷上调了肺动脉高压大鼠iNOS表达，并下调了sGC表达，而对照组大鼠sGC并未下调。这些发现可以解释七氟醚对有无肺动脉高压的大鼠右心室功能的不同影响。
原始文献摘要
Qin G, Luo H, Yin X, et al. Effects of Sevoflurane on Hemodynamics and Inducible Nitric Oxide Synthase/Soluble Guanylate Cyclase Signaling Pathway in a Rat Model of Pulmonary Arterial Hypertension[J]. Anesth Analg,2017 ,125(1):184-189.
doi: 10.1213/ANE.0000000000001937.
BACKGROUND:
The effects of sevoflurane on right ventricular (RV) function are incompletely understood. In a rat model of experimentally induced pulmonary arterial hypertension (PAH), we studied effects of sevoflurane on RV function and the expression of inducible nitric oxide synthase/soluble guanylate cyclase (iNOS/sGC) signaling pathway. We hypothesized that sevoflurane would improve RV function in rats with PAH via a iNOS/sGC pathway.
METHODS:
To induce PAH, Sprague-Dawley rats were randomly assigned to treatment with monocrotaline or normal saline. Four weeks later, rats were then randomly assigned to either control or sevoflurane inhalation. After rats were anesthetized and instrumented with a pulmonary artery or RV conductance catheter, they were treated with inhaled sevoflurane at 3 doses for 90 minutes each. Hemodynamic changes and expression of iNOS and sGC were recorded.
RESULTS:
Sevoflurane inhalation depressed RV function in both normal and PAH rats. However, RV dP/dtmax fell to a lesser degree in rats with PAH than normal rats. Sevoflurane inhalation increased iNOS expression, but decreased sGC expression.
CONCLUSIONS:
Sevoflurane depressed RV contractility to a lesser degree in PAH than in normal rats. Sevoflurane also upregulated iNOS expression and downregulated sGC expression in PAH, but not control rats. This observation may explain the differential effects of sevoflurane on RV function in rats with and without PAH.
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