The mechanism of this anomalous vascular response is unknown . 此种不规则的血管反应的机制尚不清楚。
Effects of tetrandrine on phenotypic modulation of vascular smooth muscle cells and expression of p38 after intimal injury 粉防己碱对肾血管性高血压大鼠阻力血管反应性的影响
Ephedrine and phenylephrine can treat the hypotension , howeer an amplified asoconstrictie response may be obsered due to an alpha 2 agonist induced enhancement of baroreceptor reflexes ( 7 ) and potentiation of alpha 1 - adrenoceptor - mediated asoconstriction 麻黄素和苯肾上腺素可治疗低血压,然而可以观察到存在过度缩血管反应,因为- 2受体激动剂导致压力感受器反射[ 7 ]和- 1肾上腺素受体介导的血管收缩作用增强[ 8 ] 。
Ephedrine and phenylephrine can treat the hypotension , however an amplified vasoconstrictive response may be observed due to an alpha 2 agonist induced enhancement of baroreceptor reflexes ( 7 ) and potentiation of alpha 1 - adrenoceptor - mediated vasoconstriction 麻黄素和苯肾上腺素可治疗低血压,然而可以观察到存在过度缩血管反应,因为- 2受体激动剂导致压力感受器反射[ 7 ]和- 1肾上腺素受体介导的血管收缩作用增强[ 8 ] 。
The disorders of vascular regulations is characteristic of endotoxin shock with the manifestations of marked reduction in systemic mean arterial pressure whereas pulmonary arterial hypertension , as well as abnormal changes of vascular reactivities of systemic and pulmonary arteries at its initial stage 血管调节机制紊乱是内毒素休克特征性病理改变之一,主要表现为内毒素休克发生早期主动脉压下降、肺动脉压升高以及离体肺动脉及主动脉血管反应异常变化。
No , a first gas information molecule discovered in human being , is a typical endothelial - derived relaxant and mediates endothelium - dependent relaxation of blood vessels . in the pathogesis of endotoxin shock vec is one of the major target cells of lps and lps - induced proinflammatory cytokine such as tumor necrosis factor and interlukin 1 and activated . in vec inducible nitric oxide synthase ( inos ) is induced and lead to an increase in production of no , the while endothelial nitric oxide synthase ( enos ) is inhibited and elicit decrease in no formation , both of which are demonstrated to induce the 在内毒素休克过程中vec是lps及其诱导机体产生的多种促炎细胞因子如tnf 、 il - 1作用的主要靶细胞, vec诱导型一氧化氮合酶( induciblenitricoxidesynthase , inos )激活、 no大量诱生而内皮型一氧化氮合酶( endothelialnitricoxidesynthase , enos )活性被抑制、 no生成障碍,是血管反应性异常变化、血管调节机制紊乱的重要发病环节。
It has been well known that vascular endothelial cells ( vec ) are not only a mechanical and biological barrier of blood vessels , but also an endocrine organ , which maintain vascular normal tension and reactivities througth synthesis and release vasoactive substances such as nitric oxide ( no ) 研究发现,血管内皮细胞( vascularendothelialcells , vec )能合成多种血管活性物质,是维持血管正常张力状态和血管反应性的关键因素。其中vec释放的一氧化氮( nitricoxide , no )是人们发现的机体第一种气体信使分子,具有明显的血管活性、介导了血管内皮依赖性舒张反应。