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吡啶甲酸铬对自发性高血压大鼠血管反应性和心肌缺血再灌注损伤的影响。

Effects of chromium picolinate on vascular reactivity and cardiac ischemia-reperfusion injury in spontaneously hypertensive rats.

机构信息

Department of Oral Biology, CL 2136, School of Dentistry, Medical College of Georgia, Augusta, Georgia 30912-1128, USA.

出版信息

Pharmacol Rep. 2010 Jul-Aug;62(4):674-82. doi: 10.1016/s1734-1140(10)70324-8.

Abstract

Chromium picolinate [Cr(pic)(3)] is a nutritional supplement widely promoted to exert beneficial metabolic effects in patients with type 2 diabetes/impaired glucose tolerance. Frequent comorbidities in these individuals include systemic hypertension, abnormal vascular function and ischemic heart disease, but information on the effects of the supplement on these aspects is sparse. Utilizing male spontaneously hypertensive rats (SHR), we examined the potential impact of Cr(pic)(3) on blood pressure, vascular reactivity and myocardial ischemia-reperfusion injury (IRI). Dietary Cr(pic)(3) supplementation (as 10 mg chromium/kg diet for six weeks) did not affect blood pressure of the SHR. Also, neither norepinephrine (NE) and potassium chloride (KCl)-induced contractility nor sodium nitroprusside (SNP)-induced relaxation of aortic smooth muscle from the SHR was altered by Cr(pic)(3) treatment. However, Cr(pic)(3) augmented endothelium-dependent relaxation of aortas, produced by acetylcholine (ACh), and this effect was abolished by N-nitro-L-arginine methyl ester (L-NAME), suggesting induction of nitric oxide (NO) production/release. Treatment with Cr(pic)(3) did not affect baseline coronary flow rate and rate-pressure-product (RPP) or infarct size following regional IRI. Nonetheless, Cr(pic)(3) treatment was associated with improved coronary flow and recovery of myocardial contractility and relaxation following ischemia-reperfusion insult. In conclusion, dietary Cr(pic)(3) treatment of SHR alters neither blood pressure nor vascular smooth muscle reactivity but causes enhancement of endothelium-dependent vasorelaxation associated with NO production/release. Additionally, while the treatment does not affect infarct size, it improves functional recovery of the viable portion of the myocardium following IRI.

摘要

吡啶羧酸铬[Cr(pic)(3)]是一种营养补充剂,广泛用于改善 2 型糖尿病/糖耐量受损患者的代谢。这些患者常合并有系统性高血压、血管功能异常和缺血性心脏病,但关于该补充剂对这些方面影响的信息却很少。利用雄性自发性高血压大鼠(SHR),我们检测了 Cr(pic)(3)对血压、血管反应性和心肌缺血再灌注损伤(IRI)的潜在影响。6 周的饮食补充 Cr(pic)(3)(以 10mg 铬/kg 饮食的形式)对 SHR 的血压没有影响。此外,Cr(pic)(3)处理也没有改变 SHR 主动脉平滑肌对去甲肾上腺素(NE)和氯化钾(KCl)的收缩反应性,或对硝普钠(SNP)的舒张反应性。然而,Cr(pic)(3)增强了乙酰胆碱(ACh)诱导的主动脉内皮依赖性舒张作用,而这种作用被 N-硝基-L-精氨酸甲酯(L-NAME)所消除,提示诱导了一氧化氮(NO)的产生/释放。Cr(pic)(3)处理并不影响基线冠状动脉血流速度和心率-血压乘积(RPP),也不影响区域 IRI 后的梗塞面积。尽管如此,Cr(pic)(3)处理与缺血再灌注损伤后冠状动脉血流的增加以及心肌收缩和舒张功能的恢复有关。总之,饮食补充 Cr(pic)(3)既不改变 SHR 的血压也不改变血管平滑肌的反应性,但会导致与 NO 产生/释放相关的内皮依赖性血管舒张增强。此外,虽然该处理不影响梗塞面积,但能改善 IRI 后存活心肌部分的功能恢复。

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