Therapeutic effect of diagnostic ultrasound on enzymatic thrombolysis

2004 ◽  
Vol 91 (06) ◽  
pp. 1078-1083 ◽  
Author(s):  
Cristiana Lupi ◽  
Guido Lazzerini ◽  
Piero Chiarelli ◽  
Antonio L’Abbate ◽  
Daniele Rovai ◽  
...  
Keyword(s):  
Venous Blood ◽  
Normal Subjects ◽  
Vascular Wall ◽  
Diagnostic Ultrasound ◽  
In Vitro Models ◽  
Mechanical Index ◽  
Ultrasound Exposure ◽  
Tissue Plasminogen ◽  
Artery Disease

SummaryIf delivered at elevated intensity, ultrasound potentiates enzymatic clot dissolution; however, an elevated acoustic intensity damages vascular wall and favors reocclusion. This study’s aim was to investigate whether exposure to high-frequency, lowintensity ultrasound generated by a diagnostic scanner enhances enzymatic thrombolysis, and if this effect differs in clots from blood of normal subjects and of patients with coronary artery disease (CAD). Venous blood samples were drawn from 10 healthy volunteers and from 10 CAD patients on chronic medical treatment, which also included aspirin. Each sample generated 2 radiolabelled clots, which were positioned in 2 in vitro models filled with human plasma recirculating at 37°. One clot was exposed to acetyl salicylic acid (60 μg/ml), tissue plasminogen activator (3 μg/ml) and heparin (1 IU/ml), while the other was exposed to the same medications plus ultrasound (2.5 MHz, mechanical index = 1.0) for 3 hours. Enzymatic thrombolysis was measured as solubilization of radiolabel. Normal subjects and patients did not significantly differ as to coagulation parameters, weight, volume and density of the clots, and fibrinolytic activity (p = 0.794). Ultrasound exposure did not influence thrombolysis in clots of normal subjects (p = 0.367), while it enhanced the dissolution of clots of CAD patients (p = 0.013). The enhancement was equal to 51% at 5 minutes, 32% at 15 minutes, 27% at 30 minutes, 20% at 1 hour and 19% at 3 hours (p < 0.05). Diagnostic ultrasound enhances enzymatic dissolution of clots generated from the blood of CAD patients, likely due to chronic treatment and in particular to aspirin.

scholarly journals Do patients with thromboembolic disease have circulating platelet aggregates?

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 205-209 ◽  
Author(s):  
FH Kohanna ◽  
MH Smith ◽  
EW Salzman
Keyword(s):  
Platelet Rich Plasma ◽  
Venous Blood ◽  
Adenosine Diphosphate ◽  
Normal Subjects ◽  
Thromboembolic Disease ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Lower Ratio

Reports of circulating platelet aggregates (ie, microemboli) in thromboembolism and other vascular disorders are based on a method (Wu and Hoak , 1974) in which venous blood is collected via scalp vein needle and tubing into either formaldehyde, which fixes aggregates, or EDTA, which disperses them. The ratio of platelet counts in platelet- rich plasma (PRP) from the two blood samples after centrifugation is interpreted as a measure of platelet aggregates in the circulation in vivo. We compared this standard Wu and Hoak technique with a modified one, in which blood was drawn directly into a syringe, and with a third method that avoided centrifugation by counting single platelets in whole blood. Both modified techniques could detect aggregates generated in vitro with adenosine diphosphate (ADP). In 12 normal subjects, the three methods were equivalent, but in 37 patients with thromboembolic disorders, the standard Wu and Hoak method gave a lower ratio than the other methods. Similar results were found in a subset of eight patients with myocardial infarction. Heparin treatment of patients did not influence the results. The data suggest that formation of platelet aggregates occurred during venipuncture. Platelets may be hyperactive in patients with thromboembolic disease and may form aggregates in vitro during collection, but the concept of chronic microembolism in such patients should be reassessed.

Measurement of lactate formation from glucose using [6-3H]- and [6-14C]glucose in humans.

1990 ◽  
Vol 259 (3) ◽  
pp. E397 ◽  
Author(s):  
A Virkamäki ◽  
I Puhakainen ◽  
N Nurjhan ◽  
J E Gerich ◽  
H Yki-Järvinen
Keyword(s):  
Lactate Dehydrogenase ◽  
Plasma Glucose ◽  
Venous Blood ◽  
Normal Subjects ◽  
Glutamic Pyruvic Transaminase ◽  
Plasma Lactate ◽  
Lactate Formation ◽  
Extrahepatic Tissues ◽  
Specific Activities

To assess the validity of determining the origin of plasma lactate from the ratio of lactate and glucose specific activities (SA) during infusion of labeled glucose, normal subjects received infusions of [6-3H]- and [6-14C]glucose for 4 h after a 12 h fast, and, on another day, cold glucose labeled with both tracers during 4-6 h of hyperinsulinemia (approximately 650 microU/ml). Basally, less lactate was derived from plasma glucose when measured with [6-3H]glucose (27 +/- 2%) than with [6-14C]glucose (40 +/- 2%, P less than 0.001). Insulin did not increase the percent of lactate derived from plasma glucose when measured with [6-3H]glucose (29 +/- 2%) but did increase when measured with [6-14C]glucose (60 +/- 4%). The arterialized blood (A) [3H]lactate SA was 30-40% higher (P less than 0.01) than deep venous blood (V) [3H]lactate SA, whereas A and V [14C]lactate SA were similar. During conversion of alanine to lactate with glutamic-pyruvic transaminase (GPT) and lactate dehydrogenase (LDH) in vitro, 32 +/- 2% of 3H in [3-3H]alanine was found in water and 68 +/- 2% in lactate. During infusion of [6-3H]- and [6-14C]glucose, the ratio of [14C]alanine to lactate SA (0.88 +/- 0.05) was less than the ratio of [3H]alanine to lactate SA (0.31 +/- 0.03, P less than 0.001). In conclusion 1) loss of 3H relative to 14C from position 6 in glucose occurs during lactate formation in extrahepatic tissues possibly due to the GPT reaction (alanine conversion to pyruvate), and 2) even under supraphysiologic hyperinsulinemic conditions not all of plasma lactate originates from plasma glucose.

Blood markers of fibrinolysis system and vascular wall state in neonates born to mothers with preeclampsia

2021 ◽  
Author(s):  
И.Г. Попова ◽  
С.Б. Назаров ◽  
О.Г. Ситникова ◽  
Г.Н. Кузьменко ◽  
М.М. Клычева ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Venous Blood ◽  
Vascular Wall ◽  
Endothelial Damage ◽  
Control Group ◽  
Blood Levels ◽  
Hemorrhagic Complications ◽  
Tissue Plasminogen ◽  
Pai 1

Введение. Новорожденные, родившиеся у матерей с патологией во время беременности, составляют группу высокого риска тромботических и геморрагических осложнений, которые повышаются при наличии у новорожденных перинатальной патологии. Цель исследования: оценить показатели, характеризующие состояние системы фибринолиза и сосудистой стенки в крови новорожденных, родившихся у матерей с преэклампсией (ПЭ), для прогнозирования риска тромботических и геморрагических осложнений у таких детей. Материалы и методы. Обследовано 60 новорожденных, родившихся у матерей с ПЭ. Контрольную группу составили 30 новорожденных от матерей без ПЭ. Исследовали венозную кровь, взятую у новорожденных на 3–5-е сутки жизни. В крови определяли уровень тканевого активатора плазминогена (t-РА), ингибитора тканевого активатора плазминогена (PAI-1) и тромбомодулина. Результаты. Выявлено, что у новорожденных от матерей с ПЭ на 3–5-е сутки жизни отмечаются признаки повреждения эндотелия и повышение фибринолитической активности крови, на что указывает повышение содержания t-РА, PAI-1 и тромбомодулина в крови. Заключение. Полученные данные свидетельствуют о риске развития геморрагических осложнений у таких детей. Background. Neonates born to mothers with pathology during pregnancy are at high risk of thrombotic and hemorrhagic complications that are increased if neonates have perinatal pathology. Objectives: to assess blood parameters characterizing fibrinolysis and vascular wall of neonates born to mothers with preeclampsia (РЕ), to predict the risk of hemorrhagic complications in these children. Patients/Methods. 60 neonates born to mothers with РЕ were examined. The control group consisted of 30 neonates born to mothers without РЕ. We studied levels of tissue plasminogen activator (t-PA), inhibitor of tissue plasminogen activator (PAI-1) and thrombomodulin (TM) in venous blood taken from neonates on the 3–5th days of life. Results. In neonates born to mothers with PE we revealed on the 3–5th days of life increased blood levels of t-PA, PAI-1 and TM that characterized endothelial damage and increased blood fibrinolytic activity. Conclusions. The data obtained indicate the risk of hemorrhagic complications development in these children.

Plasma 4-pregnene-17α,20α-diol-3-one (17α,20α-dihydroxyprogesterone) and 17α-hydroxyprogesterone in man

1983 ◽  
Vol 102 (2) ◽  
pp. 271-276 ◽  
Author(s):  
Judith A. Whitworth ◽  
Aldona Butkus ◽  
J. P. Coghlan ◽  
D. A. Denton ◽  
Dianne Saines ◽  
...  
Keyword(s):  
Venous Blood ◽  
Plasma Concentrations ◽  
Normal Subjects ◽  
Dietary Sodium ◽  
Lower Amplitude ◽  
Induced Hypertension ◽  
Male Subjects ◽  
Mineralocorticoid Activity

Abstract. Investigation of the mechanisms involved in ACTH induced hypertension in sheep led to delineation of the major role of 4-pregnene-17α,20α-diol-3-one (17α,20α-OHP) in ovine adrenal venous blood. It has been shown in this model of steroid induced hypertension that 17α,20α-OHP is 'hypertensinogenic' i.e. capable of raising blood pressue when infused concurrently with the major mineralocorticoid and glucocorticoid steroid hormones, but in itself it has no significant blood pressure elevating effect and no significant glucocorticoid or mineralocorticoid activity. The present study examines the regulation of 17α,20α-OHP and 17α-hydroxyprogesterone (17-OHP) in man. The plasma concentration of 17α,20α-OHP in normal ambulant subjects (n = 29) bled at 08.00 to 10.00 h was 14.5 ± 0.8 nmol/l compared with 17-OHP 7.8 ± 0.6 nmol/l. Administration of ACTH (20 μg/kg/day) to normotensive male subjects (n = 6) produced after 5 days of rise in 17α,20α-OHP from 16.6 ± 2.2 to 48.9 ± 7.9 nmol/l and in 17-OHP from 10.9 ± 1.12 to 29.3 ± 4.2 nmol/l. In normal subjects, 17α,20α-OHP had a diurnal rhythm similar to that of cortisol but of lower amplitude. Plasma concentrations of both steroids rose with stepped 30 min ACTH infusions and were suppressed by dexamethasone administration. Angiotensin II infusion, dietary sodium restriction and 9α-fluorocortisol administration had no effect on plasma 17α,20α-OHP. There was no change in 17α,20α-OHP throughout the menstrual cycle but 17-OHP increased during the luteal phase of the cycle. 17-OHP was lower in women on oral contraceptives than in control women, but values for 17α,20α-OHP were unchanged. The mean plasma clearance rate for 17α,20α-OHP in 3 normal subjects was 30.2 l/day/kg, similar to that for aldosterone (31.2 l/day/kg). Unlike the sheep there was no in vitro conversion of 17-OHP to 17α,20α-OHP in human blood. These studies show that 17α,20α-OHP is present in human plasma in higher concentration than 17-OHP. The secretion of 17α,20α-OHP appears to be primarily under the control of ACTH.

The effect of 40 kHz ultrasound on tissue plasminogen activator-induced clot lysis in three in vitro models

2004 ◽  
Vol 30 (11) ◽  
pp. 1545-1552 ◽  
Author(s):  
Marlien Pieters ◽  
Rob T. Hekkenberg ◽  
Marrie Barrett-Bergshoeff ◽  
Dingeman C. Rijken
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
In Vitro Models ◽  
Clot Lysis ◽  
Tissue Plasminogen

Arterial Plasma Potassium Measured Continuously during Exercise in Man

1984 ◽  
Vol 67 (4) ◽  
pp. 427-431 ◽  
Author(s):  
R. A. F. Linton ◽  
M. Lim ◽  
C. B. Wolff ◽  
P. Wilmshurst ◽  
D. M. Band
Keyword(s):  
Transmembrane Potential ◽  
Venous Blood ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Normal Subjects ◽  
Receptor Sensitivity ◽  
Blood Samples ◽  
Hepatic Venous Blood ◽  
Arterial Plasma

1. Five continuous records of arterial plasma potassium were obtained from three normal subjects during brief periods (5–7 min) of exercise (100 W). 2. In two of these subjects hepatic venous blood samples were withdrawn at 0.5–1.0 min intervals and analysed in vitro for plasma potassium. 3. Arterial plasma potassium rose rapidly at the start of exercise from 3.8 ± 0.3 mmol/l (mean ± sd) to plateau levels of 5.4 ± 0.1 mmol/l. 4. One of the above subjects and a further subject were studied after β-blockade with propranolol. This resulted in an exaggerated rise in arterial plasma potassium during exercise. 5. Hepatic venous potassium measurements indicated that the liver probably had little effect on potassium changes during exercise. 6. The changes in arterial plasma potassium during exercise are rapid and substantial. If transmitted to the extracellular fluid these changes would alter cell transmembrane potential and might as a result alter receptor sensitivity.

Increase in Serum Ionized Calcium during Exercise

1977 ◽  
Vol 53 (6) ◽  
pp. 579-586 ◽  
Author(s):  
S. Pors Nielsen ◽  
T. Falch Christiansen ◽  
O. Hartling ◽  
J. Trap-Jensen
Keyword(s):  
Blood Lactate ◽  
Venous Blood ◽  
Recovery Period ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Normal Subjects ◽  
Ionized Calcium ◽  
Serum Ionized Calcium

1. Normal subjects showed an average increase in serum ionized calcium (Ca2+) concentration of 0·11 mmol/l in peripheral venous blood 10 min after onset of bicycle exercise at 70% of maximum aerobic capacity. The corresponding mean rise in serum total calcium concentration was 0·21 mmol/l. 2. The change in serum Ca2+ as result of acidification was studied in 20 normal subjects by carbon dioxide equilibration in vitro followed by measurement of serum Ca2+. The log serum Ca2+ was inversely proportional to serum pH. 3. The Δlog serum Ca2+/ΔpH in vitro was similar to the Δlog serum Caa+/ΔpH in vivo during exercise, this ratio, however, being somewhat greater during the first minute of exercise. 4. Serum Ca2+ returned to normal values about 20 min after stopping exercise as the pH returned to normal, but the fall immediately after stopping exercise was more pronounced than that due to the change in pH, as predicted from the studies in vitro. 5. Blood lactate concentration rose from 0·86 to 8·41 mmol/l after 10 min exercise, but the rise in blood lactate during exercise was slower than the rise in serum Ca2+. Also the fall during the recovery period was delayed compared with the fall in serum Ca2+. 6. It is suggested that the rise in serum Ca2+ during severe muscular exercise might be important for the physiological adaptations during work, and for bone metabolism.

A Theoretical Model of the Role of Brain Stem Nuclei in Alcohol-Mediated Arrhythmogenesis in Older Adults

2003 ◽  
Vol 4 (3) ◽  
pp. 218-231 ◽  
Author(s):  
Joan A. Masters ◽  
Joanne S. Stevenson
Keyword(s):  
Older Adults ◽  
Theoretical Model ◽  
Brain Stem ◽  
Population Aging ◽  
In Vitro Models ◽  
Future Research ◽  
Autonomic Pathways ◽  
Artery Disease

Uncertainty about the mechanism of alcohol-mediated arrhythmogenesis and the effect of alcohol use on arrhythmic risk among older adults is an increasing concern in light of population aging and recent reports that moderate alcohol consumption may protect older adults against coronary artery disease. In this review, a theoretical model of the role of brain stem nuclei in alcohol-mediated arrhythmogenesis in older adults is developed. The model is based on the hypothesis that the effects of alcohol on central autonomic pathways of cardiac control may alter the threshold for alcohol-mediated arrhythmogenesis among older adults. Findings from multiple lines of research including cellular, electrophysiological, epidemiological, experimental, and clinical studies in human, animal, and in vitro models were synthesized in developing the model. Suggestions for future research on the topic of alcohol-mediated arrhythmogenesis in older adults are offered.

Stimulation of Ca2+ influx by endothelin-1 is subject to negative feedback by elevated intracellular Ca2+

1991 ◽  
Vol 260 (6) ◽  
pp. C1273-C1281 ◽  
Author(s):  
L. L. Muldoon ◽  
H. Enslen ◽  
K. D. Rodland ◽  
B. E. Magun
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Wall ◽  
In Vitro Models ◽  
Tumor Promoter ◽  
Local Concentration ◽  
Endothelin 1 ◽  
Stimulation Of

Endothelin-1 (ET-1) has been shown to require Ca2+ influx for activation of vascular smooth muscle in vivo, but in vitro models show that ET-1 mobilizes intracellular Ca2+ and is independent of extracellular Ca2+. We present data that suggest ET-1 modulates cellular responses through a dual mechanism involving both phosphatidylinositol turnover and Ca2+ channel activation. Addition of low concentrations of ET-1 (less than 10(-9) M) to serum-deprived quiescent Rat-1 cells stimulated Ca2+ influx while having little effect on diacylglycerol (DG) release or intracellular Ca2+ levels. In contrast, higher concentrations of ET-1 (greater than 10(-9) M) stimulated intracellular Ca2+ transients and release of inositol trisphosphate (IP3) and DG but did not activate Ca2+ uptake. Stimulation of Ca2+ influx at low [ET-1] could not be accounted for by depletion of intracellular IP3-sensitive pools. Neither the stimulation of Ca2+ influx at low [ET-1] nor the inhibitory actions of high [ET-1] could be mimicked by the activation of protein kinase C. We tested the hypothesis that elevated intracellular Ca2+ was inhibitory for Ca2+ influx. When intracellular Ca2+ transients were maintained below approximately 165 nM by chelation with BAPTA or BAPTA derivatives with altered affinity for Ca2+, Ca2+ influx was stimulated over the entire range of ET-1 concentrations. In addition, experimentally elevating intracellular Ca2+ levels with the tumor promoter thapsigargin abolished ET-1-stimulated Ca2+ influx. These data suggest that the biological consequences of ET-1 release may be determined by local concentration differences. Thus in vascular smooth muscle cells ET-1 may act either to mobilize intracellular Ca2+ or to promote Ca2+ influx, depending on the distance from the endothelial cell source in the vascular wall. The activation of different processes by low and high ET-1 concentrations may determine the physiological response to ET-1 stimulation in vivo.

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