International journal of cardiology · 2005
Platelet and leukocyte adhesion and activation in unstable angina and post-PTCA.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Serrano Carlos V, Rocha Giraldez Roberto, Fernandes Juliano de Lara, Nicolau José Carlos, Zweier Jay L, Ramires José Antonio F
Аннотация
BACKGROUND: Unstable atherosclerotic plaques activate blood cells which may adhere to the coronary endothelium causing vessel occlusion. However, it is unknown if different clinical syndromes associated with plaque rupture induce similar blood cell activation and adhesion to the endothelium.
METHODS: We studied changes in adhesion molecule expression of platelets (GPIIb/IIIa), neutrophils--CD18, CD11b and L-selectin--and monocytes (CD14) after interaction with active lesions of patients with stable angina subjected to PTCA and patients with unstable angina (UA). Generation of superoxide (SO) radicals from PMNs and PMN sequestration in the coronary circulation were also assessed. Blood samples were collected from the aorta (Ao) and coronary sinus (CS) before and 15 min after PTCA (n=13) and within the first 48 h of UA (n=12).
RESULTS: PTCA induced a marked up-regulation of CD18, CD11b, CD14 and GPIIb/IIIa with L-selectin shedding and reduced SO formation, whereas only minor L-selectin down-regulation and decreased SO production indicated activation in UA. However, a significant decrease in neutrophil count in the CS compared to the Ao was only observed in UA.
CONCLUSIONS: The magnitude of cellular activation depends on the underlying clinical setting and just partially contributes to cell adhesion to the endothelium which might be modulated by different extent of vascular occlusion and shear forces.
METHODS: We studied changes in adhesion molecule expression of platelets (GPIIb/IIIa), neutrophils--CD18, CD11b and L-selectin--and monocytes (CD14) after interaction with active lesions of patients with stable angina subjected to PTCA and patients with unstable angina (UA). Generation of superoxide (SO) radicals from PMNs and PMN sequestration in the coronary circulation were also assessed. Blood samples were collected from the aorta (Ao) and coronary sinus (CS) before and 15 min after PTCA (n=13) and within the first 48 h of UA (n=12).
RESULTS: PTCA induced a marked up-regulation of CD18, CD11b, CD14 and GPIIb/IIIa with L-selectin shedding and reduced SO formation, whereas only minor L-selectin down-regulation and decreased SO production indicated activation in UA. However, a significant decrease in neutrophil count in the CS compared to the Ao was only observed in UA.
CONCLUSIONS: The magnitude of cellular activation depends on the underlying clinical setting and just partially contributes to cell adhesion to the endothelium which might be modulated by different extent of vascular occlusion and shear forces.