scholarly journals Correlations between morphological changes in platelet aggregates and underlying endothelial damage in cerebral microcirculation of mice.

Stroke ◽  
1993 ◽  
Vol 24 (12) ◽  
pp. 1968-1976 ◽  
Author(s):  
S Said ◽  
W I Rosenblum ◽  
J T Povlishock ◽  
G H Nelson
Keyword(s):  
Morphological Changes ◽  
Endothelial Damage ◽  
Cerebral Microcirculation ◽  
Platelet Aggregates

GpIbα-VWF blockade restores vessel patency by dissolving platelet aggregates formed under very high shear rate in mice

Blood ◽  
2014 ◽  
Vol 123 (21) ◽  
pp. 3354-3363 ◽  
Author(s):  
Audrey Le Behot ◽  
Maxime Gauberti ◽  
Sara Martinez De Lizarrondo ◽  
Axel Montagne ◽  
Eloïse Lemarchand ◽  
...  
Keyword(s):  
Shear Rate ◽  
Endothelial Damage ◽  
Cross Linking ◽  
High Shear ◽  
External Layer ◽  
Vessel Lumen ◽  
Key Points ◽  
Vessel Patency ◽  
Platelet Aggregates ◽  
Very High

Key Points Following endothelial damage, platelet cross-linking during closure of the vessel lumen is mediated by GpIbα-VWF interactions. Disruption of GpIbα-VWF interactions restores vessel patency by specifically disaggregating the external layer of occlusive thrombi.

Effect of Dextran 70 on the Platelet Distribution of Ex Vivo Thrombi

1979 ◽  
Author(s):  
M. åberg ◽  
A. Rausing ◽  
U. Hedner ◽  
S.-E. Bergent
Keyword(s):  
Light Microscopy ◽  
Factor Viii ◽  
Healthy Volunteers ◽  
Platelet Function ◽  
Small Dose ◽  
Ex Vivo ◽  
Morphological Changes ◽  
Dextran 70 ◽  
Platelet Aggregates

Infusion of dextran 70 impairs the function of factor VIII and increases the lysability of ex vivo thrombi. To find out whether this increased lysability is accompanied by any morphological changes of the thrombi dextran was infused into four healthy volunteers and one patient with von Wiilebrand’s disease. Dextran was also given to four dogs with 51Cr labelled platelets and 1-1abelled fibrinogen. The thrombi were studied in light microscopy and the distribution of isotopes measured. Dextran caused marked changes in the morphology of the thrombi. The platelet aggregates constituting the head were not formed and the platelets were more evenly distributed in the thrombi. The changes were most pronounced 2-4 hours after the infusion. In the patient with von Wiilebrand’s. disease the structure of the thrombus was abnormal already before the infusion of dextran. Even a small dose of dextran given to this patient prevented the formation of a platelet head. When factor VIII concentrate was given the platelet aggregates constituting the head of thrombus again formed. The findings indicate that factor VIII is of importance for the formation and coherence of the platelet aggregates in ex vivo thrombi. Dextran given intravenously reduces platelet aggregabiIity by impairing the function of factor VIII. The alteration of platelet function, accompanied bv profound changes in the morphology of ex vivo thrombi, may explain the increase in lysability which has been previously shown by us.

INTRACELLULAR CA++ MOBILIZATION IN GRAY PLATELET SYNDROME. ELECTRONMICROSCOPIC STUDIES ON AEQUORIN LOADED PLATELETS

1987 ◽  
Author(s):  
K Mori ◽  
S Suzuki ◽  
K Sugai ◽  
Y Akutsu ◽  
M Ishikawa ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Peripheral Blood Smear ◽  
Buffer Solution ◽  
A 23187 ◽  
Tubular System ◽  
Intracellular Ca ◽  
Trace Line ◽  
Platelet Aggregates ◽  
Gray Platelet Syndrome ◽  
Second Peak

Light microscopic examinations on platelets in Gray Platelet Syndrome(GPS) showed peculiar gray colored platelets due to deficiency in ^-granules on the peripheral blood smear by May-Grunwald-Giemsa stain. Besides α-granule deficiency, however, several morphological abnormalities, especially abnormal features of dense tubular system(DTS) etc., were recognized in the transmission electronmicroscopic examinations. In the platelet function tests, release abnormalities rather than storage-pool deficiency were noted. We were strongly interested in the relationships between these morphological and functional abnormalities, because DTS in the platelets have been thought to be main storage sites of intracellular Ca ion.We examined the intracellular Ca++ mobilization using aequo-rin loaded platelets by means of Lumi-aggregometer(Salzman's method) under the stimulation of A-23187 and thrombin, and also morphological changes of platelets during the process of platelet aggregation by light |ipd transmission electronmicroscope.Intracellular Ca concentration increased dose-dependently after addition of A-23187 in both normal and GPS platelets. Namely, besides the first peak of emission which located at the same site as normal control, the slowly appearing second peak were recognized on the trace line by the addition of A-23187 and also abnormal by thrombin in GPS platelets. Transmission electronmi-crographs showed insufficient contraction of platelet-aggregates and malformation or wide appearance of pseudopods by the addition of A-23187 and thrombin. Most of the contractile gels, which were usually seen in the center of the platelets, were slightly enlarged and eccentric in the position. Delayed intracellular Ca mobilization were also noted even in the buffer solution containing EGTA.From above mentioned results, intracellular Ca++ mobilization were abnormal and these low and delayed mobilization were thou -ght to be related with prominent abnormal morphology, especially abnormalities of DTS in the GPS platelets.

scholarly journals Increase in Platelet Volume and Aggregability in Adenosine Diphosphate Induced Pulmonary Micro Thromboembolism and Effect of Acetylsalicylic Acid Treatment

1977 ◽  
Author(s):  
T. Motomiya ◽  
H. Yamazaki
Keyword(s):  
Platelet Count ◽  
Acetylsalicylic Acid ◽  
Morphological Changes ◽  
Adenosine Diphosphate ◽  
Central Vein ◽  
Platelet Volume ◽  
Small Vessels ◽  
T Wave ◽  
Platelet Aggregates ◽  
Premature Beats

Several reports suggest that functional and morphological changes of platelet may occur in atherosclerotic and thromboembolic diseases and acetylsalicylic acid (ASA) has been considered as one of the possibly beneficial treatments of such conditions. Thirty male rabbits including 7 pretreated with ASA 200 mg/Kg p.o. for 4 days were catheterized. ECG, respiration, arterial and central venous pressures were recorded throughout the experiment. ADP 2 mg/Kg was injected into the central vein and citrated blood was obtained before, 30 seconds, 3, 10 and 45 minutes after the injection for platelet studies. Platelet count and volume were measured using with a Coulter Counter Zbl coupled with a Channelyzer C-1000. Platelet aggregability was determined by a Sienco aggregometer. Within several seconds after completion of ADP injection the animal developed bradycardia, premature beats, ischemic ST-T wave changes, hypotension, apnea and convulsion. Histology of the lung revealed small vessels being obstructed with platelet aggregates. In rabbits received ASA developed less bradycardia and hypotension and no ischemic ST-T wave changes, apnea or convulsion. Platelet count decreased at 30-second and increased at 10-minute after injection. Significant increases in platelet volume and aggregability were noted with no overt change in platelet morphology at 3 and 10 minutes after ADP injection. Correlation between platelet volume and aggregability was significant (r=0.60, P<0.05). This experiment demonstrated that platelet size or volume is not only dependent on its age but changes transiently under certain circumstances such as thrombosis. Treatment with ASA prevented cardiorespiratory disorders and changes in platelet volume and aggregability induced by administration of ADP.

scholarly journals Mechanisms Underlying Endothelin-1 Level Elevations Caused by Excessive Fluoride Exposure

2016 ◽  
Vol 40 (5) ◽  
pp. 861-873 ◽  
Author(s):  
Liyan Sun ◽  
Yanhui Gao ◽  
Wei Zhang ◽  
Xiaona Liu ◽  
Bingyun Li ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Umbilical Vein ◽  
Culture Fluid ◽  
Endothelial Damage ◽  
Control Group ◽  
Expression Levels ◽  
Endothelin 1 ◽  
Fluoride Exposure ◽  
Ras Activation ◽  
Umbilical Vein Endothelial Cells

Objective: To explore the mechanisms underlying endothelin-1 (ET-1) elevations induced by excessive fluoride exposure. Methods: We measured serum and bone fluoride ion content and plasma ET-1 levels and compared these parameters among different groups in an animal model. We also observed morphological changes in the aorta and endothelium of rabbits. In cell experiments, human umbilical vein endothelial cells (HUVECs) were treated with varying concentrations of NaF for 24h, with or without 10 µM U0126 pretreatment for 1 h. ET-1 levels in culture fluid and intracellular reactive oxygen species (ROS) levels, as well as ET1 gene, endothelin-converting enzyme-1 (ECE-1), extracellular signal-regulating kinase 1/2 (ERK1/2), pERK1/2 expression levels and RAS activation were measured and compared among the groups. Results: Plasma ET-1 levels of rabbits increased significantly in fluorinated groups compared with those in the control group. The rabbit thoracic aortas became slightly hardened in fluorinated groups compared with those in the control group, and some vacuoles were present in the endothelial cell cytoplasm of the rabbits in fluorinated groups. In our cell experiments, ET1 gene and ECE-1 expression levels in HUVECs and ET-1 expression levels in the cell culture supernatants increased significantly in some experimental groups compared with those in the control group. These trends paralleled the changes in intracellular ROS levels, RAS activation, and the pERK1/2-to-ERK1/2 ratio. After U0126 was added, ECE-1 expression and ET-1 levels decreased significantly. Conclusion: Excessive fluoride exposure leads to characteristic endothelial damage (vacuoles), thoracic aorta hardening, and plasma ET-1 level elevations in rabbits. In addition, the ROS-RAS-MEK1/2-pERK1/2/ERK1/2 pathway plays a crucial—and at least partial—role in ET-1 over-expression, which is promoted by excessive fluoride exposure.

Minimum vascular occlusive force

1979 ◽  
Vol 51 (5) ◽  
pp. 662-668 ◽  
Author(s):  
Manuel Dujovny ◽  
Norman Wakenhut ◽  
Nir Kossovsky ◽  
Carl W. Gomes ◽  
Ranjit K. Laha ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Vessel Diameter ◽  
Endothelial Damage ◽  
Content Type ◽  
Small Vessels ◽  
Variable Force ◽  
Force Clamp ◽  
Theoretical Results ◽  
Increased Pressure

✓ A mathematical analysis of the minimum occlusion force necessary to occlude small vessels based on the parametric influence of blood pressure, vessel diameter, clamp width, and vessel shape after clamping was performed. The results were confirmed by in vivo experimentation with 60 rat aortas (of 1.8 to 2.4 mm caliber) using a variable-force clamp gauge developed in our laboratory. Experimental and theoretical results differed by only 3 gm. Scanning electron microscopy revealed that the initial changes in the endothelium occurred in smaller radii of curvature. Increased pressure resulted in gross morphological changes across the vessel. The minimum occlusion force (as determined by the variable-force clamp gauge) produced only minimal endothelial damage.

Effects of spaceflight on morphology of the rat adenohypophysis

1994 ◽  
Vol 77 (3) ◽  
pp. 1411-1420 ◽  
Author(s):  
K. Thapar ◽  
K. Kovacs ◽  
E. Horvath ◽  
L. Stefaneanu ◽  
E. Chambers ◽  
...  
Keyword(s):  
Anterior Pituitary ◽  
Structural Integrity ◽  
Space Shuttle ◽  
Morphological Changes ◽  
Secretory Activity ◽  
Endothelial Damage ◽  
Morphological Response ◽  
Endocrine Activity ◽  
Adenohypophyseal Cell ◽  
Vascular Elements

To determine the effects of spaceflight on the anterior pituitary gland, the adenohypophyses of rats after a 7-day spaceflight aboard the space shuttle Endeavor (STS-54) were investigated by histology, immunohistochemistry, morphometry, electron microscopy, and in situ hybridization and were compared with synchronous control rats. Morphometry revealed the corticotrophs of space-flown rats to be significantly enlarged, demonstrating 46–48% increases in mean cell, nuclear, and cytoplasmic areas. These corticotrophs also exhibited striking ultrastructural signs of heightened secretory activity. Furthermore, their expression of proopiomelanocortin mRNA, the transcript encoding the precursor protein from which adrenocorticotropic hormone is posttranslationally cleaved, was also significantly enhanced, a finding consistent with their hypersecretory state. Gonadotrophs also exhibited significant increments in mean nuclear, cell, and cytoplasmic areas of 22, 45, and 51%, respectively; however, they were not accompanied by ultrastructural evidence of increased secretory function. There were no morphological changes in somatotrophs, lactotrophs, or thyrotrophs, nor were there any significant changes in the overall frequency of any one adenohypophyseal cell type in comparison with control. The structural integrity of all adenohypophyseal secretory and vascular elements was preserved after spaceflight, as there was neither evidence of necrosis nor other forms of cellular injury in spaceflown specimens. Capillaries were patent, and neither endothelial damage nor thrombosis was noted. These data suggest that spaceflight is accompanied by a selective morphological response in the anterior pituitary, one characterized by hypertrophy of both corticotrophs and gonadotrophs and by enhanced endocrine activity of the former.

L-NMMA in brain microcirculation of mice is inhibited by blockade of cyclooxygenase and by superoxide dismutase

1992 ◽  
Vol 262 (5) ◽  
pp. H1343-H1349 ◽  
Author(s):  
W. I. Rosenblum ◽  
H. Nishimura ◽  
G. H. Nelson
Keyword(s):  
Superoxide Dismutase ◽  
Acetylsalicylic Acid ◽  
Platelet Adhesion ◽  
Competitive Inhibition ◽  
Endothelial Damage ◽  
Cerebral Microcirculation ◽  
Relaxing Factor ◽  
Pial Arterioles ◽  
Endothelium Derived Relaxing Factor ◽  
Brain Microcirculation

As previously reported, NG-monomethyl-L-arginine (L-NMMA) constricted pial arterioles, inhibited dilation of pial arterioles by acetylcholine (ACh) or L-arginine (L-Arg), and enhanced platelet adhesion/aggregation at sites of endothelial damage. However, all of these effects were inhibited by local application of 20 micrograms/ml indomethacin (Indo). When 100 micrograms/ml acetylsalicylic acid were used instead of Indo, the acid also blocked the effects of L-NMMA. Superoxide dismutase (SOD; 50 U/ml) blocked the constriction produced by L-NMMA and also blocked the constriction produced by N omega-nitro-L-arginine (NNA). SOD also prevented L-NMMA from blocking dilation by ACh. SOD itself had no effect on diameter or on the response to ACh, norepinephrine, or BaCl2. The effects of L-NMMA and of Indo were also selective. Thus L-NMMA did not inhibit dilation by prostacyclin or bradykinin, and Indo did not inhibit dilation by prostacyclin. Indo did not interfere with the ability of arginase to enhance platelet adhesion/aggregation or with the ability of ACh or L-Arg to inhibit adhesion/aggregation. We conclude that in mouse cerebral microcirculation the ability of L-NMMA and NNA to constrict arterioles, the ability of L-NMMA to inhibit dilation by ACh or L-Arg and the ability of L-NMMA to enhance platelet adhesion/aggregation are all related to interference with phenomena dependent on "classical" endothelium-derived relaxing factor (EDRFACh). However, in this preparation the action of L-NMMA or NNA may not be due to competitive inhibition of the enzyme producing EDRFACh from L-Arg. Rather, L-NMMA and NNA appear to activate cyclooxygenase with resultant production of superoxide, which inactivates EDRFACh.

Clinical Correlations

1975 ◽  
Vol 33 (03) ◽  
pp. 417-425 ◽  
Author(s):  
Sean Moore
Keyword(s):  
Dietary Lipid ◽  
Endothelial Damage ◽  
Relative Importance ◽  
Human Atherosclerosis ◽  
Platelet Aggregates ◽  
Clinical Correlations ◽  
Clinical Tools ◽  
Lipid Supplement ◽  
Relationship Of ◽  
The Relationship

SummaryThere are two aspects which are clinically relevant in the relationships among thrombosis and arteriosclerosis. First, the relationship of thrombosis to atherogenesis. Thrombosis is closely related to endothelial injury and there is recent evidence that repeated or continuous endothelial damage leads to the development of all the lesions seen in human atherosclerosis. This occurs in the absence of dietary lipid supplement. The relative importance of the parts played by injury and thrombosis in this process need further delineation. Secondly, established arteriosclerotic disease is associated with thrombosis. This thrombosis is usually mural, seldom occlusive. Embolism by platelet aggregates which has been well described in the retinal and cerebral circulations may affect other vascular territories such as the heart and the kidney. Such a mechanism may explain some cases of otherwise unexplained sudden cardiac death and some cases of hypertension. We need better clinical tools to detect the occurrence of thrombo-embolism and to monitor it’s progress. Measures to modify thrombosis and embolism may be as useful or more useful than those we currently employ in the clinical management of atherosclerotic disease.

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