The Role of Ultrasound Examination in B-Scan Dynamic Examination of Common Carotid Arteries Intima-Media in People with Risk Factors of Atherosclerosis Development While Direct Antiotherogen Therapy

1997 ◽  
Vol 6 ◽  
pp. S42
Author(s):  
G Kountsevich
2002 ◽  
Vol 282 (1) ◽  
pp. R131-R138 ◽  
Author(s):  
Arlin B. Blood ◽  
Yu Zhao ◽  
Wen Long ◽  
Lubo Zhang ◽  
Lawrence D. Longo

Recently, we reported that, whereas in cerebral arteries of the adult a majority of norepinephrine (NE)-induced increase in intracellular Ca2+ concentration ([Ca2+]i) comes from release of the sarcoplasmic reticulum (SR) Ca2+ stores, in the fetus the SR Ca2+ stores are relatively small, and NE-induced increase in [Ca2+]i results mainly from activation of plasma membrane L-type Ca2+ channels (20). In an effort to establish further the role of L-type Ca2+ channels in the developing cerebral arteries, we tested the hypothesis that, in the fetus, increased reliance on plasmalemmal L-type Ca2+ channels is mediated, in part, by increased L-type Ca2+ channel density. We used3H-labeled (+)isopropyl-4-(2,1,3-benzoxadiazol-4-y1)-1,4-dihydro-(2,6-dimethyl-5-methoxycarbonyl)pyridine-3-carboxylate (PN200–110, isradipine) to measure L-type Ca2+ channel density (Bmax) in the cerebral arteries, common carotid artery (CCA), and descending aortae of fetal (∼140 gestation days), newborn (7–10 days), and adult sheep. In the cerebral and common carotid arteries, Bmax values (fmol/mg protein) of fetuses and newborns were significantly greater than those of adults. Western immunoblotting assay also revealed that the density of L-type Ca2+ channel protein in the cerebral arteries and CCA was about twofold greater in the fetus than the adult. Finally, compared with the adult, fetal cerebral arteries demonstrated a significantly greater maximum tension and [Ca2+]i in response to stimulation with the L-type Ca2+ channel agonist Bay K 8644. In addition, Bay K 8644-stimulated fetal vessels demonstrated a maximal tension and [Ca2+]isimilar to that observed in response to stimulation with 10−4 NE. These results support the idea that fetal cerebrovascular smooth muscle relies more on extracellular Ca2+ and L-type Ca2+ channels for contraction than does the adult and that this increased reliance is mediated, in part, by greater L-type Ca2+ channel density. This may have important implications in the regulation of cerebral blood flow in the developing organism.


2018 ◽  
Vol 3 (4) ◽  
pp. 229-233
Author(s):  
Balázs Oltean-Péter ◽  
István Kovács ◽  
Monica Chițu ◽  
Imre Benedek

Abstract Atherosclerosis is a systemic disease that most often affects the carotid arteries. Being usually asymptomatic in its early stages, it is diagnosed only in advanced stages, when treatment is more difficult and prognosis is poor. Carotid ultrasound (US) is the most commonly used method for diagnosing carotid artery disease and represents a proper method for screening in patients with cardiovascular (CV) risk factors. This paper shows the methodology and necessity of carotid imaging methods in patients at high risk of developing atherosclerotic lesions. We also review the findings that underline the need of carotid screening in patients with ischemic heart disease or with ischemic arteriopathy, showing that the carotid arteries are like ‘mirrors’ of the arterial system, which need to be assessed in every patient with CV risk factors, regardless of the presence or absence of symptoms.


2000 ◽  
Vol 22 (5) ◽  
pp. 543-554 ◽  
Author(s):  
Naoki Furuhashi ◽  
Seiji Miyazaki ◽  
Masanori Kamura ◽  
Shoichi Emura ◽  
Keigo Yasuda

1989 ◽  
Vol 9 (4) ◽  
pp. 500-505 ◽  
Author(s):  
Bjarne Grøgaard ◽  
Ludwig Schürer ◽  
Bengt Gerdin ◽  
Karl E. Arfors

The role of polymorphonuclear leukocytes (PMNLs) in postischemic delayed hypoperfusion in the rat brain was investigated. Cerebral ischemia was accomplished by reversible bilateral occlusion of the common carotid arteries for 15 min combined with bleeding to an MABP of 50 mm Hg. The animals of one group were depleted of their circulating PMNLs by intraperitoneal injections of an antineutrophil serum (ANS) prior to the experiment. All animals included in this group had fewer than 0.2 × 109 circulating PMNLs/L at the start of the experiments. In another group ANS was injected intravenously for 5 min starting 2 min after the ischemic insult. After 4 min of recirculation, the number of circulating PMNLs in this group was below 10% of the normal. Control animals were injected with the same amount of normal sheep serum or were not treated at all. Sixty minutes after termination of ischemia, the local blood flow in previously ischemic cerebral structures was 40–50% of the normal as measured with the [14C]iodoantipyrine technique. In animals treated with ANS prior to the ischemic insult, the postischemic blood flow in the frontal, sensorimotor, and parietal cortex as well as caudoputamen and thalamus was significantly higher than that in non-ANS-treated animals. Treatment with ANS immediately after the ischemic period caused no improvement of the local CBF. It is concluded that PMNLs are involved in the cerebral postischemic flow derangements seen in this model. Their effects seem to be exerted during ischemia or immediately upon reinstitution of blood flow.


2009 ◽  
Vol 15 (5) ◽  
pp. 551-554
Author(s):  
L. V. Melnikova

The paper addresses the dependence of common carotid arteries (CCA) remodeling parameters from systolic blood ressure value in patients with essential hypertension aged 30-62 years. Ultrasound examination of CCA and heart was arried out. Structural changes of CCA and central haemodynamic indices were estimated. Correlation between systolic blood pressure, CCA diameter and intima-media complex thickness was detected. Reduction of wall elasticity was revealed blood pressure increased.


2016 ◽  
Vol 4 (01) ◽  
pp. 19-30
Author(s):  
Neema Kanyal

Objective: To investigate the Role of Rauwolfia serpentina in stroke induced experimental dementia. Methods: Methanolic root extract of Rauwolfia serpentina(RS) at a dose of 10mg/kg,20mg/kg and 40mg/kg;p.o. was studied against global cerebral ischemia induced dementia by occluding both common carotid arteries. RS at a dose of 10mg/kg, 20mg/kg and 40mg/kg;p.o. were administered for 14 days before and 7 days after both common carotid arteries occlusion(BCCAO) and were continued during behavioral testing i.e. Morris water maze test and elevated plus maze test. At the end of all experiment mice brain were removed and TBARS level, SOD level and infract size were determined.Results : Occlusion of both common carotid arteries significantly increased escape latency time(ELT) during acquisition trial and decrease, time spent in target quadrant on morris water maze, an increase in escape latency time was also observed on elevated plus maze when measured after 7 days of occlusion.Furthermore, TBARS levels, SOD levels and infract size were also increased when measured after 12 days of occlusion. Administration of RS specially at a dose of 20mg/kg and 40mg/kg;p.o. significantly attenuated these alteration and show neuroprotective effect against oxidative stress, infract size and learning and memory impairment. Conclusions: These finding suggest that Rauwolfia serpentina may have a promising role as a prophylactic drug in stroke induced experimental dementia due to its neuroprotective effect. The phenolic compound like phenolic acid, flavanoids and tannins present in the plant.


2020 ◽  
Vol 22 (Supplement_M) ◽  
pp. M51-M59
Author(s):  
Ben Freedman ◽  
Hooman Kamel ◽  
Isabelle C Van Gelder ◽  
Renate B Schnabel

Abstract Atrial fibrillation (AF) and stroke are inextricably connected, with classical Virchow pathophysiology explaining thromboembolism through blood stasis in the fibrillating left atrium. This conceptualization has been reinforced by the remarkable efficacy of oral anticoagulant (OAC) for stroke prevention in AF. A number of observations showing that the presence of AF is neither necessary nor sufficient for stroke, cast doubt on the causal role of AF as a villain in vascular brain injury (VBI). The requirement for additional risk factors before AF increases stroke risk; temporal disconnect of AF from a stroke in patients with no AF for months before stroke during continuous ECG monitoring but manifesting AF only after stroke; and increasing recognition of the role of atrial cardiomyopathy and atrial substrate in AF-related stroke, and also stroke without AF, have led to rethinking the pathogenetic model of cardioembolic stroke. This is quite separate from recognition that in AF, shared cardiovascular risk factors can lead both to non-embolic stroke, or emboli from the aorta and carotid arteries. Meanwhile, VBI is now expanded to include dementia and cognitive decline: research is required to see if reduced by OAC. A changed conceptual model with less focus on the arrhythmia, and more on atrial substrate/cardiomyopathy causing VBI both in the presence or absence of AF, is required to allow us to better prevent AF-related VBI. It could direct focus towards prevention of the atrial cardiomyopathy though much work is required to better define this entity before the balance between AF as villain or bystander can be determined.


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