Serial changes in coagulation and fibrinolysis studied among 42 patients admitted to hospital with a wide variety of injuries are reported. The first hours after trauma are dominated by an acceleration of fibrinolysis (clot lysis) and clotting time which are often followed by an abrupt rebound to prolonged fibrinolysis and normal clotting. Evidence is presented that acceleration of fibrinolysis is due to flooding of the circulation by plasminogen activator and that prolongation is probably due to an inhibitor. A prolonged prothrombin time, increased prothrombin consumption index, an acceleration of the heparin-retarded clotting time, and a fall in the platelet count are also frequent during the first hours after injury. There is evidence also of an early deficiency in factor V and the onset of a fall in factor VII and prothrombin. The following days are characterized by continued prolongation of fibrinolysis, a lengthening of clotting time, and an increased prothrombin consumption index suggestive of a defect in thrombo-plastin generation. Subsequent periods of prolonged fibrinolysis may develop. Prothrombin time often continues prolonged for one to three weeks and may vary phasically; plasma prothrombin and factor VII are reduced but there is now little change in factor V. The platelet count continues to fall for one to three days, then a thrombocytosis develops, often with abnormally high platelet levels, a week or so later. Plasma fibrinogen rises within 24 hours to reach a plateau maximum a few days later and levels remain high for prolonged periods in the severely injured. Various changes are related to or influenced by the severity of trauma. Mechanisms are discussed, including thrombosis in vivo, and reference is made to homeostatic significance and its possible breakdown.

https://jcp.bmj.com/content/jclinpath/17/1/1.full.pdf

Coagulation and fibrinolysis in injured patients

The effects of moderate and severe hemorrhage on the cardiac output and its distribution have been studied in the rat. In moderate hemorrhage, cerebral and adrenal blood flow are well maintained through localized vasodilatation while most other organs show increased vascular resistance and diminished blood flow. After severe hemorrhage, despite further changes in territorial resistances, the blood flow is not maintained in any area of the body.

Effect of Hemorrhage on the Cardiac Output and Distribution in the Rat

OVER the past several years considerable work has been done relative to shock and its possible relationship to intravascular coagulation of blood.1, 6–28, 34–38 It would seem desirable to summarize in one paper the significant results and offer a theory of shock which has been evolved from these stu

The Role of Intravascular Clotting in the Etiology of Shock

Transport of organic anions in the liver. An update on bile acid, fatty acid, monocarboxylate, anionic amino acid, cholephilic organic anion, and anionic drug transport

Purpose. A variety of methods exist which determine the rate and extent of intestinal absorption. The method described here employs an internal absorption reference probe and portal blood sampling in unanesthetized rat. 
Methods. Theophylline and tritiated water were selected as absorption reference probes since they are quantitatively absorbed in conscious rat. The fraction of an intestinal dose which reaches portal blood was determined from the resulting portal-systemic blood concentration gradients of the drug relative to the absorption probe. The absorption probes provide a means to calculate the drug mass reaching portal blood without the need of measuring the portal blood flow rate. The technique was evaluated with verapamil and a well-absorbed 5-lipoxygenase inhibitor, A-79035. 
Results. The fraction of an intrajejunal dose of A-79035 reaching the portal vein (FG) was 0.86 using theophylline as the absorption probe. Verapamil, which is susceptible to extensive hepatic first-pass elimination, was completely absorbed (FG = 0.98) within 1 hour, but was only 21.4% bioavailable. Absorption rate constants, estimated from initial appearance rates in portal blood, were used to monitor factors that affect drug absorption. For example, with a dose solution containing 30% PEG-400, the absorption rate constants of theophylline and A-79035 were significantly reduced. Anesthesia reduced the absorption rate constant for theophylline in rats by 40% compared to conscious animals. 
Conclusions. The technique detailed here allows reliable, direct measurement of intestinal absorption which may assist in characterizing oral dosing for novel therapeutic agents.

Method to estimate the rate and extent of intestinal absorption in conscious rats using an absorption probe and portal blood sampling.

Hemorrhagic shock was produced in anesthetized and unanesthetized dogs by bleeding to fixed arterial pressure levels for specified periods using Wiggers9 method. Blood was drawn through an ion exchange resin and at the end of the hypotension was reinfused simultaneously with the removed ions. Early in the hypotension there was usually some shortening of blood coagulation time. In the late hypotension and reinfusion period 75% of the dogs had a distinct prolongation of clotting time. Prothrombin activity and blood platelets showed a marked progressive decline during the shock period. Special tests indicated that the coagulation defect was mainly due to a decrease of labile factor in conjunction with a second deficiency, most likely prothrombin. There was no discernible deficiency of stable factor nor any release of heparinoids during the shock procedure. It is suggested that the hepatic anoxia and the resultant diminished production of labile factor and prothrombin contributes importantly to the clotting defect. Prior administration of heparin (10 mg/ kg) tended to lower mortality and increase survival time but did not afford critical protection against the development of irreversibility.

Coagulation mechanism and effect of heparin in hemorrhagic shock

During experimental hemorrhagic shock there was a large fall in oxygen saturation of portal, hepatic venous and inferior vena caval blood. Saturation levels were restored to about 90 per cent of the control values after reinfusion of the drawn blood.

Oxygen Saturation of Hepatic Blood During Hemorrhagic Shock in the Dog

A combined hemorrhagic—aortic occlusion shock was produced in dogs in order to study the effect of perfusion pressures in different aortic segments on the development of irreversible shock. Oxygen saturations of arterial, hepatic venous and inferior vena caval blood were determined before, during and after the shock procedure in order to assess the degree of anoxia prevailing in the different body segments. Perfusion of the thoracic aorta plus the coeliac and superior mesenteric arteries at 80 mm Hg mean pressure and the remaining abdominal aorta at 30 mm Hg for 2 1/2 hours resulted in lowered mortality and increased survival time compared with control groups in which conditions were similar except that the two upper abdominal arteries were perfused at the lower pressure. The protective effect of perfusion of the liver and upper splanchnic organs appears to be a specific one, i.e. not solely attributable to the decreased ischemic tissue mass involved. Mortality and survival in shock resulting from infradiaphragmatic aortic hypotension of 30 mm Hg for 2 1/2 hours was unaffected by variations in supradiaphragmatic aortic pressure within the range of 60–100 mm Hg.

Influence of differential aortic perfusion pressures in experimental shock.

Effect of splenectomy on oxygen saturation of hepatic blood in the anesthetized dog.

Summary1) A combination of hemorrhagic and partial aortic occlusion produces a controllable degree of hypotensive shock in the dog which closely resembles hemorrhagic shock. 2) The method provides an opportunity to study the effects of differential arterial perfusion of different body segments.

Secondary Shock in the Dog Produced by Total and Partial Aortic Occlusion.

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.

Robert A. Grace

Author Tools

Chat about Author