相关实验视频

Updated: May 7, 2026

A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
07:03

A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage

Published on: January 17, 2013

14.4K

系统性炎症反应指数和系统性免疫-炎症指数的动态变化与动脉瘤下arachnoid 出血后的延迟大脑缺血有关

Ho Jun Yi1, Dong-Seong Shin2, Bum-Tae Kim2

  • 1Department of Neurosurgery, Soonchunhyang University Bucheon Hospital, Bucheon, South Korea; Department of Neurosurgery, St. Vincent's Hospital, College of Medicine, The Catholic University of Korea, Seoul, South Korea; Department of Neurosurgery, Hangang Sacred Heart Hospital, Hallym University, Seoul, South Korea.

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
|February 7, 2024
PubMed
概括

系统性免疫-炎症指数 (SII) 和系统性炎症反应指数 (SIRI) 的炎症标志物的动态变化,预测了动脉瘤下关节出血 (aSAH) 后的延迟脑缺血症 (DCI). 这些标记显示了DCI发生的显著预测价值.

关键词:
炎症 炎症是一种炎症.淋巴细胞 淋巴细胞单细胞 (Monocytes) 是一种单细胞.中性粒细胞中性粒细胞.血小板是血小板的组成部分.甲状腺下下垂体出血

更多相关视频

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage10:34

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

10.5K
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model09:14

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Published on: June 18, 2021

2.3K

相关概念视频

Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...