Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing.

https://www.ahajournals.org/doi/pdf/10.1161/01.STR.16.4.562

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Toward the quiescent coronary plaque

Most studies on the natural course of coronary artery spasm in patients with normal or nearly normal coronary arteries are based on medium-term follow-up in small populations. The present series includes 277 successive patients with a median follow-up of 89 months (range: 1 to 198 months). There were 206 men and 71 women whose mean age was 53.6 +/- 9.3 years. They were all assessed with coronary arteriography which revealed no stenoses greater than 50%. Spasm was confirmed during the coronary arteriography in 157 patients (56.7%), by a positive provocation test following the arteriography in 113 patients (40.8%), and by an electrocardiogram which showed Prinzmetal's variant angina in seven patients (2.5%). The majority of patients, 264 (95.3%) were treated with calcium channel blockers. At the end of this study: 35 patients (12.6%) were lost to follow-up; 20 patients (7.2% died) including 10 (3.6%) from cardiac causes; 18 patients (6.5%) experienced myocardial infarction in 11 of whom repeat coronary arteriography consistently demonstrated one or more significant stenoses (greater than 70%); 109 patients (39%) had persistent angina, in 52 of whom the severity (more than one episode per month) warranted repeat coronary arteriography which detected significant stenosis in 19 cases; 95 patients (34.3%) were asymptomatic. Multivariate statistical analyses showed that only predictors of major coronary events (death, myocardial infarction or angina requiring repeat coronary arteriography) were systemic hypertension or the finding of minor parietal irregularities on the initial coronary arteriogram. Conclusion. Despite treatment with calcium channel blockers, persistent or recurrent episodes of angina are frequently observed whereas complications such as myocardial infarction or death are rare.

Coronary artery spasm in patients with normal or near normal coronary arteries. Long-term follow-up of 277 patients.

ACUTE LAMINITIS has long been attributed to factors or events that precede the onset of laminitis. Between 1759 and 1907 the overconsumption of grain, inflammation of the feet, suppression of perspiration (anhydrosis), excessive rest, excessive bleeding, road concussion, poor shoeing, unilateral weight bearing, sudden environmental temperature changes, prolonged standing (in the cold and aboard ships), diarrhea, and postpartum complications were all designated as causes. Today, commonly listed etiologic factors include ingestion of large amounts of grain, cold water, lush grass, or black walnut shavings, repeated concussion, endometritis or other severe infections, colic, exhaustion, stress, drug toxicities, and endocrine dysfunctions. At Texas A&M University (Table 1) the factors recorded as the cause presume a causal relationship between some preceding event and the acute laminitis. Logically, any event that precedes laminitis might be a cause, but etiologic validity depends on the definition of “cause” and the role that coincidence might have in the appearance of the disease.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1939-1676.1993.tb01012.x

The Role of Vascular Mechanisms in the Development of Acute Equine Laminitis

Prolonged exposure to hand-transmitted vibration can cause debilitating neural and vascular dysfunction in humans. It is unclear whether the pathophysiology involves simultaneous or sequential injury of arteries and nerves. The mechanism of vibration injury was investigated in a rat tail model, containing arteries and nerves structurally similar to those in the human hand. Tails were selectively vibrated for 1 or 9 days with the remainder of the animal at rest. One vibration bout of 4 h/day, 60 HZ, 5 g (49 m/s(2)) acceleration, injured endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor. Electron microscopy revealed that vibration for 9 days produced loss and thinning of endothelial cells, with activated platelets coating the exposed subendothelial tissue. Endothelial cells and arterial smooth muscle cells contained double membrane-limited, swollen processes indicative of vasoconstriction-induced damage. Laser doppler surface recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion. These findings indicate that early injury involves vasoconstriction and denuding of the arterial endothelium.

Vibration injury damages arterial endothelial cells.

Prolonged arterial constriction can cause damage to the artery itself. The purpose of this study was to define the intimal changes. Two muscular arteries of the rat were studied by electron microscopy 15 minutes to 7 days after L-norepinephrine had been dripped over the vessels. Endothelial damage was caused by the tight folding of the internal elastic lamina, which mechanically squeezed the cells. As the artery relaxed, the endothelium showed gaps, patches of thinned cytoplasm, and many adhesions between cells on opposite sides of intimal folds. The adhesions involved whole cells of cytoplasmic bridges stretched across the intimal "valleys." They were present up to one day; later they seemed to snap and disappear without causing further cellular damage. A survey of the literature shows that such adhesions can also develop in collapsed arteries postmortem. They explain the endothelial "bridges" previously described by others as a normal intimal structure.

Endothelial changes induced by arterial spasm.

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

G Majno

Author Tools

Chat about Author

Papers

Endothelial changes induced by arterial spasm.