©М.О. Гончарь СТАН ФУНКЦІОНАЛЬНОЇ АДАПТАЦІЇ СЕРЦЕВО-СУДИННОЇ СИСТЕМИ У ДІТЕЙ ПІСЛЯ ХІРУРГІЧНОЇ КОРЕКЦІЇ ВРОДЖЕНИХ ВАД СЕРЦЯ Харківський національний медичний університет СТАН ФУНКЦІОНАЛЬНОЇ АДАПТАЦІЇ СЕРЦЕВО-СУДИННОЇ СИСТЕМИ У ДІТЕЙ ПІСЛЯ ХІРУРГІЧНОЇ КОРЕКЦІЇ ВРОДЖЕНИХ ВАД СЕРЦЯ. В результаті обстеження 148 школярів у 73,7% пацієнтів, які були прооперовані з приводу вроджених вад серця, у віддалені терміни спостереження виявлено зниження рівня фізичноїпрацездатності за даними велоергометрі!. У 22,1% дітей встановлено добру толерантність до фізичного навантаження, у 4,2%-задовільну, у 70,7%-знижену, низьку-у 3,0% хворих. Незадовільну толерантність до фізичного навантаження мають діти з комбінованими вадами серця, що мали ускладнення до оперативної корекції. СОСТОЯНИЕ ФУНКЦИОНАЛЬНОЙ АДАПТАЦИИ СЕРДЕЧНО-СОСУДИСТОЙ СИСТЕМЫ У ДЕТЕЙ ПОСЛЕ ХИРУРГИЧЕСКОЙ КОРРЕКЦИИ ВРОЖДЕННЫХ ПОРОКОВ СЕРДЦА. В результате обследования 148 пациентов у 73,7% детей, прооперированных по поводу врожденных пороков сердца, в отдаленные сроки наблюдения по данным велоэргометрии выявлено снижение уровня физической работоспособности. У 22,1% детей выявлена хорошая толерантность к физической нагрузке, у 4,2%-удовлетворительная, у 70,7 %-сниженная, низкая-у 3,0% больных. Неудовлетворительную толерантность кфизической нагрузке имеют дети с комбинированными пороками сердца, имевшие осложнения при оперативной коррекции. CONDITION OF CARDIOVASCULAR FUNCTIONAL ADAPTATION IN CHILDREN AFTER SURGICAL TREATMENT OF CONGENITAL HEART DISEASE. 148 patients after surgical treatment of congenital heart disease have been observed. 73,7% children had impaired tolerance to physical exertion during bicycle ergometry, among them 70,7% patients with decreased and 3,0% with low level. 22,1% children have shown good and 4,2%-satisfactory exercise tolerance. Poor tolerance to physical exertion was typical in children with combined congenital heart disease who had complications during surgery. Ключові слова: вроджені вади серця, міокардиальна дисфункція, велоергометрія. Ключевые слова: врожденные пороки сердца, миокардиальная дисфункция, велоэргометрия.

Genistein causes L-arginine/NO-dependent vasodilation in forearm vasculature of human subjects with similar potency to 17beta-estradiol and potentiates endothelium-dependent vasodilation to acetylcholine.

Background-Phosphodiesterase type 5 (PDE5) inhibitors (eg, sildenafil) are a novel, orally active approach to the treatment of pulmonary arterial hypertension. The role of natriuretic peptides in the response to sildenafil was examined in mice lacking NPR-A, a guanylyl cyclase-linked natriuretic peptide receptor, in which pulmonary hypertension was induced by hypoxia. Methods and Results-Mice homozygous for NPR-A (NPR-Aϩ/ϩ ) and null mutants (NPR-A Ϫ/Ϫ ) were studied. Sildenafil inhibited the pressor response to acute hypoxia in the isolated perfused lungs of both genotypes. This effect was greater in the presence of atrial natriuretic peptide in the perfusate in NPR-A ϩ/ϩ mice but not NPR-A Ϫ/Ϫ animals. In vivo, NPR-A mutants had higher basal right ventricular (RV) systolic pressures (RVSPs) than did NPR-A ϩ/ϩ mice, and this was not affected by 3 weeks of treatment with sildenafil (25 mg · kg Ϫ1 · d Ϫ1 ). Both genotypes exhibited a rise in RVSP and RV weight with chronic hypoxia (10% O 2 for 21 days); RVSP and RV weight were reduced by continuous sildenafil administration in NPR-A ϩ/ϩ mice, but only RVSP showed evidence of a response to the drug in NPR-A Ϫ/Ϫ mice. The effect of sildenafil on hypoxia-induced pulmonary vascular muscularization and cyclic GMP levels was also blunted in NPR-A Ϫ/Ϫ mice. Conclusions-The natriuretic peptide pathway influences the response to PDE5 inhibition in hypoxia-induced pulmonary hypertension, particularly its effects on RV hypertrophy and vascular remodeling. Key Words: hypertension, pulmonary Ⅲ natriuretic peptides Ⅲ remodeling P ulmonary arterial hypertension is a life-threatening condition for which therapeutic options are limited. Phosphodiesterase type 5 (PDE5) inhibitors (eg, sildenafil) are under investigation as a novel, orally active therapy for this condition. PDE5 is abundant in the lung and hydrolyses cyclic GMP, a mediator of vasorelaxation and antitrophic effects in vascular tissue. 1-3 Chronic PDE5 inhibition has been shown to elevate pulmonary cyclic GMP levels and abrogate hypoxia-induced pulmonary hypertension and vascular remodeling in animal models, and to reduce pulmonary artery pressure in primary pulmonary hypertension. 4 -8 The major factors stimulating cyclic GMP synthesis in pulmonary vascular tissue are nitric oxide (NO) and the natriuretic peptides (atrial natriuretic peptide [ANP], brain natriuretic peptide [BNP], and c-type natriuretic peptide [CNP]). 9 Natriuretic peptide levels are elevated in all forms of pulmonary hypertension and may influence the response to PDE5 inhibitors in this condition. The cardiovascular response to the natriuretic peptides is transduced by NPR-A, a guanylyl cyclase-linked receptor. 10,11 We have examined the effect of sildenafil in mice lacking functional NPR-A exposed to hypoxia, a commonly used model of experimental pulmonary hypertension. Methods AnimalsNPR-A receptor-deficient mice (NPR-A Ϫ/Ϫ ) were bred in-house from stock and produced as described previously. 10,11 Studies were conducted on homozygous NPR-A ϩ/...

Those patients who survive to adulthood with a systemic right ventricle experience low mortality and good functional status up to 40 years of age. However, there is a substantial burden of atrial tachyarrhythmia, and this occurs significantly earlier in those with transposition of the great arteries-atrial switch. Management of atrial tachyarrhythmia, along with systemic right ventricular dysfunction and systemic atrioventricular valve regurgitation, is likely to be the major challenge for this group of patients over the next decade.