Periodic acceleration (pGz) acutely increases endothelial and neuronal nitric oxide synthase expression in endomyocardium of normal swine
详细信息 查看全文
- 作者：Jose A. Adams ; Heng Wu ; Jorge A. Bassuk ; Jaqueline Arias ; Arkady Uryash ; Paul Kurlansky
- 关键词：Periodic acceleration ; Nitric oxide ; Endothelial nitric oxide synthase ; Neuronal nitric oxide synthase ; Inducible nitric oxide synthase ; Akt ; Pulsatile shear stress
- 刊名：Peptides
- 出版年：2009
- 出版时间：February 2009
- 年：2009
- 卷：30
- 期：2
- 页码：373-377
- 全文大小：324 K
文摘
Introduction: Periodic acceleration (pGz) is a non-invasive method of increasing pulsatile shear stress to the endothelium. pGz is achieved by the sinusoidal head to foot motion to the supine body. pGz increases endogenous production of nitric oxide in whole animal models and isolated perfused vessel preparations, and is cardioprotective when applied prior to, during and after ischemia reperfusion. In part, the protective effects of pGz are attributable to nitric oxide (NO). The purpose of this investigation was to determine whether pGz up-regulates NOS isoforms in the endomyocardium. Methods and results: Fifteen swine weight 15–20 kg, were anesthetized, instrumented to measure hemodynamics and randomized. Ten animals received 1 h of pGz at 180 cycles/min and Gz ± 3.9 m/s2 [pGz] in addition to conventional ventilatory support and five served as time controls. Results: pGz produced a 2.3 ± 0.4 and a 6.6 ± 0.1 fold significant increase in eNOS and phosphorylated eNOS, 3.6 ± 1.1 fold increase in nNOS, and no significant change in iNOS. pGz also produced a 2.4 ± 0.3 and 3.9 ± 0.2 folds significant increase in both total(t-Akt) and phosphorylated (p-Akt) Akt. Conclusions: pGz is associated with an increase in both total and phosphorylated eNOS and nNOS protein expression in endomyocardium, and induced significant increase in total and phosphorylated-Akt. The data indicates that pGz is a novel method to induce eNOS and nNOS production in the endomyocardium. Therefore, pGz may serve as a powerful non-invasive intervention to activate the beneficial cardiac effects of endothelial and neuronal NOS.