99mTc-annexin V and 111In-antimyosin antibody uptake in experimental myocardial infarction in rats

2005 ◽  
Vol 33 (3) ◽  
pp. 239-245 ◽  
Author(s):  
Laure Sarda-Mantel ◽  
Jean-Baptiste Michel ◽  
François Rouzet ◽  
Geneviève Martet ◽  
Liliane Louedec ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Annexin V ◽  
Experimental Myocardial Infarction ◽  
Antimyosin Antibody ◽  
Antibody Uptake

111In antimyosin antibody uptake is related to the age of myocardial infarction

1991 ◽  
Vol 122 (6) ◽  
pp. 1583-1587 ◽  
Author(s):  
Shoumo Bhattacharya ◽  
Xiu-jie Liu ◽  
Roxy Senior ◽  
Diwakar Jain ◽  
Jeffrey A. Leppo ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Antimyosin Antibody ◽  
Antibody Uptake

Changes in localization of annexin V, a Ca2+ binding protein,in myocardium during repair process following experimental myocardial infarction

1999 ◽  
Vol 5 (3) ◽  
pp. 78
Author(s):  
Shigeru Toyoda ◽  
Takafumi Nakamachi ◽  
Hiroshi Nakamura ◽  
Hidehiko Suzuki ◽  
Hirotada Maezawa ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Binding Protein ◽  
Annexin V ◽  
Repair Process ◽  
Experimental Myocardial Infarction

scholarly journals Thrombus-targeting therapy with apyrase-annexin V fusion attenuates thrombosis without bleeding

2021 ◽  
Author(s):  
Ridong Chen ◽  
Dana Abendschein ◽  
Soon Seog Jeong ◽  
Thomas Wakefield ◽  
Jose Diaz ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Annexin V ◽  
Clinical Effectiveness ◽  
Experimental Myocardial Infarction ◽  
Antithrombotic Drugs ◽  
Thrombotic Occlusion ◽  
Targeting Therapy ◽  
Antithrombotic Efficacy ◽  
Clinical Conditions ◽  
Thrombotic Diseases

Abstract Antithrombotic therapy is essential to prevent thrombotic reocclusion in patients with acute myocardial infarction, stroke, or venous thromboembolism. However, current antithrombotic drugs cause bleeding that limits dose and clinical effectiveness. Previously, we reported that APT102 (AZD3366), a human apyrase optimized to scavenge extracellular ADP and ATP, exhibited potent antiplatelet efficacy without bleeding in experimental myocardial infarction and stroke. Here we describe APT402, an optimized fusion of APT102 and annexin V that uniquely inhibits both platelet and coagulation components of thrombus growth. APT402 preferentially bound to injured vessels and thrombus and prevented thrombotic occlusion in arterial and venous thrombosis models, without increasing bleeding. Thus, APT402 breaks the confounding link between antithrombotic efficacy and bleeding, pioneering a safe and effective approach to prevent and treat a broad range of thrombotic diseases, and may be particularly useful in clinical conditions associated with high bleeding risks.

Scintigraphic Detection of Experimental Myocardial Infarction with 99mTc-2,3-Dimercaptosuccinic Acid

1984 ◽  
Vol 23 (06) ◽  
pp. 317-319
Author(s):  
J. Novák ◽  
Y. Mazurová ◽  
J. Kubíček ◽  
J. Yižd’a ◽  
P. Kafka ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Intravenous Administration ◽  
Experimental Myocardial Infarction ◽  
Myocardial Infarctions ◽  
Clinical Use ◽  
Scintigraphic Imaging ◽  
Tissue Samples ◽  
Scintigraphic Finding

SummaryAcute myocardial infarctions were produced by ligature of the left frontal descending coronary artery in 9 dogs. The possibility of scintigraphic imaging with 99mTc-DMSA 4 hrs after intravenous administration was studied. The infarctions were 4, 24 and 48 hrs old. The in vivo scan was positive in only one dog with a 4-hr old infarction. The in vivo scans were confirmed by the analysis of the radioactivity in tissue samples. The accumulation of the radiopharmaceutical increased slightly in 48-hr old lesions; however, this increase was not sufficient for a positive scintigraphic finding. Thus, we do not recommend 99mTc-DMSA for clinical use in acute lesions.

A translational model of chronic heart failure in rats

2018 ◽  
pp. 136-148
Author(s):  
С.А. Крыжановский ◽  
И.Б. Цорин ◽  
Е.О. Ионова ◽  
В.Н. Столярук ◽  
М.Б. Вититнова ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Compensatory Hypertrophy ◽  
Experimental Myocardial Infarction ◽  
Left Ventricular Ejection ◽  
Translational Model ◽  
Innovative Drug ◽  
Ventricular Ejection Fraction

Цель исследования - разработка трансляционной модели хронической сердечной недостаточности (ХСН) у крыс, позволяющей, с одной стороны, изучить тонкие механизмы, лежащие в основе данной патологии, а с другой стороны, выявить новые биомишени для поиска и изучения механизма действия инновационных лекарственных средств. Методика. Использован комплекс эхокардиографических, морфологических, биохимических и молекулярно-биологических исследований, позволяющий оценивать и дифференцировать этапы формирования ХСН. Результаты. Динамические эхокардиографические исследования показали, что ХСН формируется через 90 дней после воспроизведения переднего трансмурального инфаркта миокарда. К этому времени у животных основной группы отмечается статистически значимое по сравнению со 2-ми сут. после воспроизведения экспериментального инфаркта миокарда снижение ФВ левого желудочка сердца (соответственно 55,9 ± 1,4 и 63,9 ± 1,6%, р = 0,0008). Снижение насосной функции сердца (на 13% по сравнению со 2-ми сут. после операции и на ~40% по сравнению с интактными животными) сопровождается увеличением КСР и КДР (соответственно с 2,49 ± 0,08 до 3,91 ± 0,17 мм, р = 0,0002, и с 3,56 ± 0,11 до 5,20 ± 0,19 мм, р = 0,0001), то есть к этому сроку развивается сердечная недостаточность. Результаты эхокардиографических исследований подтверждены данными морфометрии миокарда, продемонстрировавшими дилатацию правого и левого желудочков сердца. Параллельно проведенные гистологические исследования свидетельствуют о наличии патогномоничных для данной патологии изменений миокарда (постинфарктный кардиосклероз, компенсаторная гипертрофия кардиомиоцитов, очаги исчезновения поперечной исчерченности мышечных волокон и т.д.) и признаков венозного застоя в легких и печени. Биохимические исследования выявили значимое увеличение концентрации в плазме крови биохимического маркера ХСН - мозгового натрийуретического пептида. Данные молекулярно-биологических исследований позволяют говорить о наличии гиперактивности ренин-ангиотензин-альдостероновой и симпатоадреналовой систем, играющих ключевую роль в патогенезе ХСН. Заключение. Разработана трансляционная модель ХСН у крыс, воспроизводящая основные клинико-диагностические критерии этого заболевания. Показано наличие корреляции между морфометрическими, гистологическими, биохимическими и молекулярными маркерами прогрессирующей ХСН и эхокардиографическими диагностическими признаками, что позволяет использовать неинвазивный метод эхокардиографии, характеризующий состояние внутрисердечной гемодинамики, в качестве основного критерия оценки наличия/отсутствия данной патологии. Aim. Development of a translational model for chronic heart failure (CHF) in rats to identify new biotargets for finding and studying mechanisms of innovative drug effect in this disease. Methods. A set of echocardiographic, morphological, biochemical, and molecular methods was used to evaluate and differentiate stages of CHF development. Results. Dynamic echocardiographic studies showed that CHF developed in 90 days after anterior transmural myocardial infarction. By that time, left ventricular ejection fraction was significantly decreased in animals of the main group compared with rats studied on day 2 after experimental myocardial infarction (55.9 ± 1.4% vs . 63.9 ± 1.6%, respectively, p<0.0008). The decrease in heart’s pumping function (by 13% compared with day 2 after infarction and by approximately 40% compared to intact animals) was associated with increased ESD and EDD (from 2.49 ± 0.08 to 3.91 ± 0.17 mm, p = 0.0002, and from 3.56 ± 0.11 to 5.20 ± 0.19 mm, respectively, p = 0.0001); therefore, heart failure developed by that time. The results of echocardiographic studies were confirmed by myocardial morphometry, which demonstrated dilatation of both right and left ventricles. Paralleled histological studies indicated presence of the changes pathognomonic for this myocardial pathology (postinfarction cardiosclerosis, compensatory hypertrophy of cardiomyocytes, foci of disappeared transverse striation of muscle fibers, etc.) and signs of venous congestion in lungs and liver. Biochemical studies demonstrated a significant increase in plasma concentration of brain natriuretic peptide, a biochemical marker of CHF. Results of molecular studies suggested hyperactivity of the renin-angiotensin-aldosterone and sympathoadrenal systems, which play a key role in the pathogenesis of CHF. Conclusions. A translational model of CHF in rats was developed, which reproduced major clinical and diagnostic criteria for this disease. Morphometric, histological, biochemical, and molecular markers for progressive CHF were correlated with echocardiographic diagnostic signs, which allows using this echocardiographic, noninvasive method characterizing the intracardiac hemodynamics as a major criterion for the presence / absence of this pathology.

Technetium-99m Cysteine; A Novel Radiopharmaceutical for Detection of Experimental Myocardial Infarction in Rats

2010 ◽  
Vol 3 (4) ◽  
pp. 290-296 ◽  
Author(s):  
Mita Chatterjee Debnath ◽  
Urmi Roy ◽  
Kamal Krishna Halder ◽  
Bharat R. Sarkar ◽  
Samarendu Sinha ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Experimental Myocardial Infarction ◽  
Technetium 99M
Sign in / Sign up

Export Citation Format

Share Document