Coronavirus disease 2019-induced hypercoagulability and its clinical implications

2021 ◽  
pp. 021849232110691
Author(s):  
Ricardo Poveda-Jaramillo
Keyword(s):  
Blood Cells ◽  
Endothelial Damage ◽  
Clot Lysis ◽  
Clinical Implications ◽  
Oxygen Species ◽  
Angiotensin Converting Enzyme 2 ◽  
Pulmonary Capillaries ◽  
Endothelial Surface ◽  
The Right ◽  
D Dimer

Coronavirus disease 2019 is the disease produced by severe acute respiratory syndrome-coronavirus-2, which is introduced into the host’s cell thanks to the angiotensin-converting enzyme 2 receptor. Once there, it uses the cell’s machinery to multiply itself. In this process, it generates an immune response that stimulates the lymphocytes to produce cytokines and reactive oxygen species that begin to deteriorate the endothelial cell. Complement activation, through the complement attack complex and C5a, contributes to this endothelial damage. The different mediators further promote the expression of adhesion molecules on the endothelial surface, which encourages all blood cells to adhere to the endothelial surface to form small conglomerates, called clots, which obstruct the lumen of the small blood vessels. Furthermore, the mediators of clot lysis are inhibited. All this promotes a prothrombotic environment within the pulmonary capillaries that is reflected in the elevation of D-dimer. The only solution for this cascade of events seems to be the implementation of an effective anticoagulation protocol that early counteracts the changes induced by thrombi in the pulmonary circulation and reflected in the functioning of the right ventricle.

Ultrastructure of pulmonary microvasculature in acute endotoxemia

1978 ◽  
Vol 36 (2) ◽  
pp. 470-471
Author(s):  
R. G. Gerrity ◽  
M. Richardson
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Alveolar Epithelium ◽  
Endothelial Damage ◽  
Capillary Endothelium ◽  
Type Ii Cells ◽  
Type Ii ◽  
Interstitial Edema ◽  
Pulmonary Capillaries ◽  
Lung Ultrastructure ◽  
Fibrin Thrombi

Dogs were injected intravenously with E_. coli endotoxin (2 mg/kg), and lung samples were taken at 15 min., 1 hr. and 24 hrs. At 15 min., occlusion of pulmonary capillaries by degranulating platelets and polymorphonuclear leukocytes (PML) was evident (Fig. 1). Capillary endothelium was intact but endothelial damage in small arteries and arterioles, accompanied by intraalveolar hemorrhage, was frequent (Fig. 2). Sloughing of the surfactant layer from alveolar epithelium was evident (Fig. 1). At 1 hr., platelet-PML plugs were no longer seen in capillaries, the endothelium of which was often vacuolated (Fig. 3). Interstitial edema and destruction of alveolar epithelium were seen, and type II cells had discharged their granules into the alveoli (Fig. 4). At 24 hr. phagocytic PML's were frequent in peripheral alveoli, while centrally, alveoli and vessels were packed with fibrin thrombi and PML's (Fig. 5). In similar dogs rendered thrombocytopenic with anti-platelet serum, lung ultrastructure was similar to that of controls, although PML's were more frequently seen in capillaries in the former (Fig. 6).

The Occlusion Effect in Unilateral Functional Hearing Loss

1970 ◽  
Vol 13 (1) ◽  
pp. 37-40
Author(s):  
Gary Thompson ◽  
Marie Denman
Keyword(s):  
Hearing Loss ◽  
Bone Conduction ◽  
Low Frequency ◽  
Clinical Implications ◽  
The Right ◽  
Occlusion Effect

Bone-conduction tests were administered to subjects who feigned a hearing loss in the right ear. The tests were conducted under two conditions: With and without occlusion of the non-test ear. It was anticipated that the occlusion effect, a well-known audiological principle, would operate to draw low frequency bone-conducted signals to the occluded side in a predictable manner. Results supported this expectation and are discussed in terms of their clinical implications.

Hyperbaric treatment of air or gas embolism: current recommendations

2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  
Keyword(s):  
Animal Studies ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Endothelial Damage ◽  
Neurological Deficits ◽  
Breath Hold ◽  
Gas Embolism ◽  
Hyperbaric Treatment ◽  
Pulmonary Capillaries ◽  
Venous Gas Embolism

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

Altered fibrin clot structure/function in patients with antiphospholipid syndrome: association with thrombotic manifestation

2014 ◽  
Vol 112 (08) ◽  
pp. 287-296 ◽  
Author(s):  
Magdalena Celińska-Löwenhoff ◽  
Teresa Iwaniec ◽  
Agnieszka Padjas ◽  
Jacek Musiał ◽  
Anetta Undas
Keyword(s):  
Structure Function ◽  
Antiphospholipid Syndrome ◽  
Thrombotic Event ◽  
Fibrin Clot ◽  
Clot Lysis ◽  
Lag Phase ◽  
Lysis Time ◽  
Clot Structure ◽  
Clot Lysis Time ◽  
D Dimer

SummaryWe tested the hypothesis that plasma fibrin clot structure/function is unfavourably altered in patients with antiphospholipid syndrome (APS). Ex vivo plasma clot permeability, turbidity and susceptibility to lysis were determined in 126 consecutive patients with APS enrolled five months or more since thrombotic event vs 105 controls. Patients with both primary and secondary APS were characterised by 11% lower clot permeability (p<0.001), 4.8% shorter lag phase (p<0.001), 10% longer clot lysis time (p<0.001), and 4.7% higher maximum level of D-dimer released from clots (p=0.02) as compared to the controls. Scanning electron microscopy images confirmed denser fibrin networks composed of thinner fibres in APS. Clots from patients with “triple-antibody positivity” were formed after shorter lag phase (p=0.019) and were lysed at a slower rate (p=0.004) than in the remainder. Clots from APS patients who experienced stroke and/or myocardial infarction were 8% less permeable (p=0.01) and susceptible to lysis (10.4% longer clot lysis time [p=0.006] and 4.5% slower release of D-dimer from clots [p=0.01]) compared with those following venous thromboembolism alone. Multivariate analysis adjusted for potential confounders showed that in APS patients, lupus anticoagulant and “triple-positivity” were the independent predictors of clot permeability, while “triple-positivity” predicted lysis time. We conclude that APS is associated with prothrombotic plasma fibrin clot phenotype, with more pronounced abnormalities in arterial thrombosis. Molecular background for this novel prothrombotic mechanism in APS remains to be established.

COVID-19 AND STROKE: POSSIBLE CAUSES AND PATHOGENESIS (REVIEW)

Vestnik ◽  
2021 ◽  
pp. 103-106
Author(s):  
А.Е. Кожашева ◽  
С.О. Белесбек ◽  
Д.Ж. Абдимитова ◽  
Б.М. Сакен ◽  
А.П. Бориходжаева ◽  
...  
Keyword(s):  
Preventive Measures ◽  
Cerebrovascular Disorders ◽  
Endothelial Damage ◽  
Cytokine Release ◽  
Contributing Factors ◽  
Acute Cerebrovascular Accident ◽  
Von Willebrand ◽  
The Relationship ◽  
Willebrand Factor ◽  
D Dimer

Появляются доказательства того, что COVID-19 может вызывать выброс цитокинов, состояние гиперкоагуляции и повреждение эндотелия, которое может привести к острому нарушению мозгового кровообращения (ОНМК). В данной статье авторы обсуждают взаимосвязь между COVID-19 и ОНМК, и о возможных факторах, способствующих возникновению инсульта. Как свидетельствует увеличение D-димера, фибриногена, фактора VIII и фактора фон Виллебранда, инфекция SARS-CoV-2 вызывает коагулопатию, нарушает функцию эндотелия и способствует состоянию гиперкоагуляции. В совокупности это предрасполагает пациентов к цереброваскулярным нарушениям. Механизм, лежащий в основе COVID-19 и инсульта, требует дальнейшего изучения, равно как и разработка эффективных терапевтических или профилактических мер. Evidence is emerging that COVID-19 can cause cytokine release, hypercoagulable states, and endothelial damage that can lead to acute cerebrovascular accident (ACVI). In this article, the authors discuss the relationship between COVID-19 and stroke and the possible contributing factors to stroke. As evidenced by an increase in D-dimer, fibrinogen, factor VIII and von Willebrand factor, SARS-CoV-2 infection causes coagulopathy, disrupts endothelial function and hypercoagulability. Collectively, this predisposes patients to cerebrovascular disorders. The mechanism underlying COVID-19 and stroke requires further study, as does the development of effective therapeutic or preventive measures.

Prediction of persistent ventricular dilation by initial ventriculomegaly and clot volume in a porcine model

2021 ◽  
pp. 1-8
Author(s):  
Grace Y. Lai ◽  
William Chu Kwan ◽  
Karolina Piorkowska ◽  
Matthias W. Wagner ◽  
Pouya Jamshidi ◽  
...  
Keyword(s):  
Porcine Model ◽  
Autologous Blood ◽  
Ventricular Volume ◽  
Intraventricular Injection ◽  
Clot Lysis ◽  
Ventricular Dilation ◽  
Ventricular Volumes ◽  
Clot Burden ◽  
The Right ◽  
The Relationship

OBJECTIVE While intraventricular hemorrhage (IVH) is associated with posthemorrhagic ventricular dilation (PHVD), not all infants affected by high-grade IVH develop PHVD. The authors aimed to determine clot-associated predictors of PHVD in a porcine model by varying the amount and rate of direct intraventricular injection of whole autologous blood. METHODS Seven 1-week-old piglets underwent craniectomy and injection of autologous blood into the right lateral ventricle. They survived for a maximum of 28 days. MRI was performed prior to injection, immediately postoperatively, and every 7 days thereafter. T1-weighted, T2-weighted, and susceptibility-weighted imaging (SWI) sequences were used to segment ventricular and clot volumes. Spearman correlations were used to determine the relationship between blood and clot volumes and ventricular volumes over time. RESULTS The maximum ventricular volume was up to 12 times that of baseline. One animal developed acute hydrocephalus on day 4. All other animals survived until planned endpoints. The interaction between volume of blood injected and duration of injection was significantly associated with clot volume on the postoperative scan (p = 0.003) but not the amount of blood injected alone (p = 0.38). Initial postoperative and day 7 clot volumes, but not volume of blood injected, were correlated with maximum (p = 0.007 and 0.014) and terminal (p = 0.014 and 0.036) ventricular volumes. Initial postoperative ventricular volume was correlated with maximum and terminal ventricular volume (p = 0.007 and p = 0.014). CONCLUSIONS Initial postoperative, maximum, and terminal ventricular dilations were associated with the amount of clot formed, rather than the amount of blood injected. This supports the hypothesis that PHVD is determined by clot burden rather than the presence of blood products and allows further testing of early clot lysis to minimize PHVD risk.

Permeation of the luminal capillary glycocalyx is determined by hyaluronan

1999 ◽  
Vol 277 (2) ◽  
pp. H508-H514 ◽  
Author(s):  
Charmaine B. S. Henry ◽  
Brian R. Duling
Keyword(s):  
Blood Cell ◽  
Red Blood Cells ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Enzyme Treatment ◽  
Apical Surface ◽  
Bright Field ◽  
Endothelial Surface ◽  
The Difference

The endothelial cell glycocalyx influences blood flow and presents a selective barrier to movement of macromolecules from plasma to the endothelial surface. In the hamster cremaster microcirculation, FITC-labeled Dextran 70 and larger molecules are excluded from a region extending almost 0.5 μm from the endothelial surface into the lumen. Red blood cells under normal flow conditions are excluded from a region extending even farther into the lumen. Examination of cultured endothelial cells has shown that the glycocalyx contains hyaluronan, a glycosaminoglycan which is known to create matrices with molecular sieving properties. To test the hypothesis that hyaluronan might be involved in establishing the permeation properties of the apical surface glycocalyx in vivo, hamster microvessels in the cremaster muscle were visualized using video microscopy. After infusion of one of several FITC-dextrans (70, 145, 580, and 2,000 kDa) via a femoral cannula, microvessels were observed with bright-field and fluorescence microscopy to obtain estimates of the anatomic diameters and the widths of fluorescent dextran columns and of red blood cell columns (means ± SE). The widths of the red blood cell and dextran exclusion zones were calculated as one-half the difference between the bright-field anatomic diameter and the width of the red blood cell column or dextran column. After 1 h of treatment with active Streptomyces hyaluronidase, there was a significant increase in access of 70- and 145-kDa FITC-dextrans to the space bounded by the apical glycocalyx, but no increase in access of the red blood cells or in the anatomic diameter in capillaries, arterioles, and venules. Hyaluronidase had no effect on access of FITC-Dextrans 580 and 2,000. Infusion of a mixture of hyaluronan and chondroitin sulfate after enzyme treatment reconstituted the glycocalyx, although treatment with either molecule separately had no effect. These results suggest that cell surface hyaluronan plays a role in regulating or establishing permeation of the apical glycocalyx to macromolecules. This finding and our prior observations suggest that hyaluronan and other glycoconjugates are required for assembly of the matrix on the endothelial surface. We hypothesize that hyaluronidase creates a more open matrix, enabling smaller dextran molecules to penetrate deeper into the glycocalyx.

scholarly journals Antioxidant Compounds from Microalgae: A Review

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 549
Author(s):  
Noémie Coulombier ◽  
Thierry Jauffrais ◽  
Nicolas Lebouvier
Keyword(s):  
Antioxidant Activity ◽  
Natural Products ◽  
Mode Of Action ◽  
Natural Antioxidants ◽  
Culture Conditions ◽  
Antioxidant Compounds ◽  
Oxygen Species ◽  
Synthetic Antioxidants ◽  
Metabolic Plasticity ◽  
The Right

The demand for natural products isolated from microalgae has increased over the last decade and has drawn the attention from the food, cosmetic and nutraceutical industries. Among these natural products, the demand for natural antioxidants as an alternative to synthetic antioxidants has increased. In addition, microalgae combine several advantages for the development of biotechnological applications: high biodiversity, photosynthetic yield, growth, productivity and a metabolic plasticity that can be orientated using culture conditions. Regarding the wide diversity of antioxidant compounds and mode of action combined with the diversity of reactive oxygen species (ROS), this review covers a brief presentation of antioxidant molecules with their role and mode of action, to summarize and evaluate common and recent assays used to assess antioxidant activity of microalgae. The aim is to improve our ability to choose the right assay to assess microalgae antioxidant activity regarding the antioxidant molecules studied.

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