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All rats were anesthesized and ventilated mechanically with FiO2 0.5, BR 100·min-1, VT12ml·kg-1 and I/E 1/1.5. The blood was withdrawed to induce hemorrhagic shock via the carotid until blood pressure reached 45±5mmHg and lasted for 1 hour, and the shed blood and Ringers lactate in volume equal to the shed blood were reinfused for resuscitation in two hours in groups B~F . Afterwards, LPS was given via the trachea(200μg·kg-1,in 500μl normal saline) to establish the ARDS model.

所有动物均行机械通气,吸入氧浓度(FiO2 )0.5,B~F动物在20min内自颈动脉放血至平均动脉压为45±5mmHg,休克1h后开始液体复苏,在2h内回输全部采集血液及等量平衡液,然后气管内给予内毒素200μg·kg-1。

Also, the OR of carotid atherosclerosis across quartiles of CRI was 1.51 (95% CI: 1.10–2.09) after multivariate adjustment.

而且,经过多变量调整后,变时反应指数所有四分位数对颈动脉粥样硬化的优势比为1.51(95%的可信区间:1.10-2.09)。

Objective: To explore the clinical association between blood lipids and the formation of carotid plaques.

目的:研究血脂与颈动脉斑块形成之间的临床关联。

CEUS can be used to evaluate the effect of atorvastatin in treatment of soft carotid plaques.

超声造影可以作为阿托伐他汀对颈动脉斑块疗效的评价手段。

Xanthelasma is not associated with increased risk of carotid atherosclerosis in normolipidaemia.

在正常脂质血液中,黄斑瘤并不增加颈动脉粥样硬化的危险性

This article introduces the effect of high central nervous system,changes of cerebral blood flow after hypoxia,damage of hypoxia to neurons in the respiratory center,neurotransmitters and neuromodulators in hypoxic respiratory depression.

Barnard等[2]在成年动物也发现了类似的情况,并且指出,缺氧2h内,颈动脉窦传入神经放电一直加强。以上研究结果提示,不论在新生动物还是成年动物,缺氧性呼吸抑制的发生都有其中枢来源。

Abstract] Objective To explore the effects of statin on carotid atherosclerosis and the preventive role in recurrence cerebral infarction.

目的 探讨辛伐他汀对颈动脉粥样硬化的影响,以及其在预防脑梗死患者复发中的作用。

Overall 34% of the asthmatics evidenced carotid atherosclerosis, compared with 46% of control subjects, Dr.

大阪大学医学研究生院的 Michio Otsuki 博士及其同事表示,总体而言,哮喘组和对照组的颈动脉粥样硬化发生率分别为34%和46%。

Objective To determine the clinical value of acoustic densitometry in evaluation of carotid plaque in patients with coronary artery diseases.

目的:探讨声学密度定量技术在冠心病患者颈动脉粥样斑块性质评价中的临床价值。

Hypoxia inhibits a variety of K+ channels in the type Ⅰ cells of the carotid body, in a seemingly species-dependent manner, and the resultant membrane depolarisation is sufficient to activate voltage-gated Ca2+ entry leading to neurosecretion and afferent discharge.

低氧可抑制颈动脉体Ⅰ型细胞中的多种K+通道,这种作用可能有种属差异;K+通道的抑制使膜电位去极化,启动电压依赖性Ca2+内流,最后导致神经分泌和传入放电。

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