Colonic Diverticular and Vascular Diseases

2014 ◽  
pp. 499-526
Author(s):  
Bora Keum
Keyword(s):  
Vascular Diseases

The molecular mechanism of mechanotransduction in vascular homeostasis and disease

2020 ◽  
Vol 134 (17) ◽  
pp. 2399-2418
Author(s):  
Yoshito Yamashiro ◽  
Hiromi Yanagisawa
Keyword(s):  
Shear Stress ◽  
Blood Vessels ◽  
Vessel Wall ◽  
Vascular Diseases ◽  
Cell Interactions ◽  
Aortic Aneurysms ◽  
Cyclic Stretch ◽  
Mechanical Stimuli ◽  
Vascular Homeostasis ◽  
Matrix Cell

Abstract Blood vessels are constantly exposed to mechanical stimuli such as shear stress due to flow and pulsatile stretch. The extracellular matrix maintains the structural integrity of the vessel wall and coordinates with a dynamic mechanical environment to provide cues to initiate intracellular signaling pathway(s), thereby changing cellular behaviors and functions. However, the precise role of matrix–cell interactions involved in mechanotransduction during vascular homeostasis and disease development remains to be fully determined. In this review, we introduce hemodynamics forces in blood vessels and the initial sensors of mechanical stimuli, including cell–cell junctional molecules, G-protein-coupled receptors (GPCRs), multiple ion channels, and a variety of small GTPases. We then highlight the molecular mechanotransduction events in the vessel wall triggered by laminar shear stress (LSS) and disturbed shear stress (DSS) on vascular endothelial cells (ECs), and cyclic stretch in ECs and vascular smooth muscle cells (SMCs)—both of which activate several key transcription factors. Finally, we provide a recent overview of matrix–cell interactions and mechanotransduction centered on fibronectin in ECs and thrombospondin-1 in SMCs. The results of this review suggest that abnormal mechanical cues or altered responses to mechanical stimuli in EC and SMCs serve as the molecular basis of vascular diseases such as atherosclerosis, hypertension and aortic aneurysms. Collecting evidence and advancing knowledge on the mechanotransduction in the vessel wall can lead to a new direction of therapeutic interventions for vascular diseases.

Contrast-enhanced ultrasound of the abdominal aorta – current status and future perspectives

VASA ◽  
2019 ◽  
Vol 48 (2) ◽  
pp. 115-125 ◽  
Author(s):  
Xin Li ◽  
Daniel Staub ◽  
Vasileios Rafailidis ◽  
Mohammed Al-Natour ◽  
Sanjeeva Kalva ◽  
...  
Keyword(s):  
Real Time ◽  
Vascular Diseases ◽  
Aneurysm Rupture ◽  
Vasa Vasorum ◽  
Current Status ◽  
Contrast Enhanced Ultrasound ◽  
Aortic Diseases ◽  
Cross Sectional ◽  
Vascular Abnormalities ◽  
Contrast Enhanced

Abstract. Ultrasound has been established as an important diagnostic tool in assessing vascular abnormalities. Standard B-mode and Doppler techniques have inherent limitations with regards to detection of slow flow and small vasculature. Contrast-enhanced ultrasound (CEUS) is a complementary tool and is useful in assessing both the macro- and microvascular anatomy of the aorta. CEUS can also provide valuable physiological information in real-time scanning sessions due to the physical and safety profiles of the administered microbubbles. From a macrovascular perspective, CEUS has been used to characterize aortic aneurysm rupture, dissection and endoleaks post-EVAR repair. With regard to microvasculature CEUS enables imaging of adventitial vasa vasorum thereby assessing aortic inflammation processes, such as monitoring treatment response in chronic periaortitis. CEUS may have additional clinical utility since adventitial vasa vasorum has important implications in the pathogenesis of aortic diseases. In recent years, there have been an increasing number of studies comparing CEUS to cross-sectional imaging for aortic applications. For endoleak surveillance CEUS has been shown to be equal or in certain cases superior in comparison to CT angiography. The recent advancement of CEUS software along with the ongoing development of drug-eluting contrast microbubbles has allowed improved targeted detection and real-time ultrasound guided therapy for aortic vasa vasorum inflammation and neovascularization in animal models. Therefore, CEUS is uniquely suited to comprehensively assess and potentially treat aortic vascular diseases in the future.

Role of Emotional Processes in Cardio-vascular Diseases

2012 ◽  
Author(s):  
Suman Balhara ◽  
Nov Rattan Sharma ◽  
Amrita Yadav
Keyword(s):  
Vascular Diseases ◽  
Emotional Processes ◽  
Cardio Vascular

Decreasing systemic blood pressure impairs cerebral vascular reserves in patients with steno-occlusive cerebral vascular diseases: A repeated I-123 split dose spect study

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S404-S404
Author(s):  
Yasuyuki Kimura ◽  
Naohiko Oku ◽  
Katsufumi Kajimoto ◽  
Hiroki Kato ◽  
Makiko Tanaka ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Diseases ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Split Dose ◽  
Cerebral Vascular

A Mutation in Plasma Platelet-activating Factor Acetylhydrolase (Val279Phe) Is a Genetic Risk Factor for Cerebral Hemorrhage but not for Hypertension

1998 ◽  
Vol 80 (09) ◽  
pp. 372-375 ◽  
Author(s):  
Hidemi Yoshida ◽  
Tadaatsu Imaizumi ◽  
Koji Fujimoto ◽  
Hiroyuki Itaya ◽  
Makoto Hiramoto ◽  
...  
Keyword(s):  
Risk Factor ◽  
Genetic Risk ◽  
Platelet Activating Factor ◽  
Vascular Diseases ◽  
Genetic Risk Factor ◽  
Brain Hemorrhage ◽  
Platelet Activating Factor Acetylhydrolase ◽  
Paf Acetylhydrolase ◽  
Polymerase Chain ◽  
The Difference

SummaryPlatelet-activating factor (PAF) acetylhydrolase is an enzyme that inactivates PAF. Deficiency of this enzyme is caused by a missense mutation in the gene. We previously found a higher prevalence of this mutation in patients with ischemic stroke. This fact suggests that the mutation might enhance the risk for stroke through its association with hypertension. We have addressed this hypothesis by analyzing the prevalence of the mutation in hypertension. We studied 138 patients with essential hypertension, 99 patients with brain hemorrhage, and 270 healthy controls. Genomic DNA was analyzed for the mutant allele by the polymerase-chain reaction. The prevalence of the mutation was 29.3% (27.4% heterozygotes and 1.9% homozygotes) in controls and 36.2% in hypertensives and the difference was not significant. The prevalence in patients with brain hemorrhage was significantly higher than the control: 32.6% heterozygotes and 6.1% homozygotes (p <0.05). PAF acetylhydrolase deficiency may be a genetic risk factor for vascular diseases.

Relationship Between Fibrinopeptide A and Fibrinogen/Fibrin Fragment E in Thromboembolism, DIC and Various Non-Thromboembolic Diseases

1987 ◽  
Vol 58 (02) ◽  
pp. 758-763 ◽  
Author(s):  
G Mombelli ◽  
R Monotti ◽  
A Haeberli ◽  
P W Straub
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Liver Cirrhosis ◽  
Healthy Subjects ◽  
Vascular Diseases ◽  
Fibrinopeptide A ◽  
Normal Range ◽  
Collagen Vascular Diseases ◽  
Intravascular Coagulation ◽  
Fibrin Formation

SummaryIncreased fibrinopeptide A (FPA) levels have been reported in various non-thrombotic disorders, including cancer, acute myocardial infarction, liver cirrhosis and collagen vascular diseases. To investigate the significance of these findings, the present study combined the radioimmunoassay of FPA with that of fibrinogen/fibrin degradation fragment E (FgE) in the aforementioned disorders and compared the results with those observed in healthy subjects as well as in patients with thromboembolism and overt disseminated intravascular coagulation (DIC). Mean FPA and FgE in malignancy were 6.3 and 305 ng/ml, in myocardial infarction 5.6 and 98 ng/ml, in liver cirrhosis 2.7 and 132 ng/ml and in collagen vascular diseases 5.6 and 142 ng/ml. All these values were significantly higher than in healthy controls (mean FPA 1.6 ng/ml, mean FgE 49 ng/ml) but significantly lower than in thromboembolism (mean FPA 10.7 ng/ml, mean FgE 639 ng/ ml) and DIC (mean FPA 22.0 ng/ml, mean FgE 1041 ng/ml). The overall correlation between FPA and FgE was highly significant. Elowever, different disorders showed peculiar patterns in FPA, FgE and fibrinogen levels. In malignancy, a definite increase of FPA, FgE and plasma fibrinogen levels was observed. This finding probably indicates a compensated state of (intra- or extravascular) fibrin formation and lysis. Acute myocardial infarction was characterized by a high FPA to FgE ratio, which is interpreted to reflect acute thrombin generation and fibrin formation. FPA in cirrhosis was only marginally elevated with most single values within the normal range, indicating that intravascular coagulation was infrequent and unimportant in quantitative terms.

Stimulated Platelet Aggregation, Thromboxane B2 Formation and Platelet Sensitivity to Prostacyclin - A Critical Evaluation

1981 ◽  
Vol 45 (03) ◽  
pp. 204-207 ◽  
Author(s):  
Wolfgang Siess ◽  
Peter Roth ◽  
Peter C Weber
Keyword(s):  
Arachidonic Acid ◽  
Platelet Count ◽  
Platelet Aggregation ◽  
Reliable Method ◽  
Platelet Rich Plasma ◽  
Critical Evaluation ◽  
Vascular Diseases ◽  
Thromboxane B2 ◽  
Test Time ◽  
Stimulation Of

SummaryPlatelets have been implicated in the development of atherosclerotic and thrombotic vascular diseases. Evaluation of platelet aggregation in relation to endogenously formed compounds which affect platelet function may provide information of clinical and pharmacological relevance. We describe a method in which thromboxane B2 (TXB2) formation was analyzed following stimulation of platelet-rich plasma (PRP) with ADP, 1-epinephrine, collagen, and arachidonic acid. In addition, we determined platelet sensitivity to prostacyclin following ADP- and collagen-induced platelet aggregation. The parameters under study were found to depend on the platelet count in PRP, on the type and dose of the aggregating agent used, and on the test time after blood sampling. By standardization of these variables, a reliable method was established which can be used in clinical and pharmacological trials.

Raised Plasma Homocysteine: An Emerging Risk Factor for Ischaemic Heart Disease

1970 ◽  
Vol 19 (2) ◽  
pp. 87-93
Author(s):  
MS Kabir ◽  
AAS Majumder ◽  
AW Chowdhury ◽  
SA Haque ◽  
AQM Reza ◽  
...  
Keyword(s):  
Risk Factor ◽  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Plasminogen Activator ◽  
Research Work ◽  
Vascular Diseases ◽  
Plasminogen Activator Inhibitor ◽  
Plasma Homocysteine ◽  
Type I ◽  
Activator Inhibitor Type

Only one half to two thirds of atherosclerotic vascular diseases can be explained by classical risk factors like smoking, diabetes mellitus, hypertension, dyslipidaemia, family history of premature atherosclerotic vascular diseases, physical inactivity, obesity etc. Some other variables appear to contribute to the development of atherosclerotic vascular diseases which include estrogen deficiency, lipoprotein (a), plasma fibrinogen, plasminogen-activator inhibitor type I, endogenous tissue plasminogen activator (tPA), C-reactive protein and homocysteine. Over the last several years, investigators undertook extensive research work, in home and abroad, to determine the contribution of plasma homocysteine in the pathogenesis of atherosclerotic vascular diseases. So far the research work indicates, raised plasma homocysteine appears to be a potential risk factor for ischaemic heart disease.   doi: 10.3329/taj.v19i2.3158 TAJ 2006; 19(2): 87-93

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