Dysglycemia, in this survey defined as impaired glucose tolerance (IGT) or type 2 diabetes, is common in patients with coronary artery disease (CAD) and associated with an unfavorable prognosis. This European survey investigated dysglycemia screening and risk factor management of patients with CAD in relation to standards of European guidelines for cardiovascular subjects. RESEARCH DESIGN AND METHODS The European Society of Cardiology's European Observational Research Programme (ESC EORP) European Action on Secondary and Primary Prevention by Intervention to Reduce Events (EUROASPIRE) V (2016-2017) included 8,261 CAD patients, aged 18-80 years, from 27 countries. If the glycemic state was unknown, patients underwent an oral glucose tolerance test (OGTT) and measurement of glycated hemoglobin A 1c. Lifestyle, risk factors, and pharmacological management were investigated. RESULTS A total of 2,452 patients (29.7%) had known diabetes. OGTT was performed in 4,440 patients with unknown glycemic state, of whom 41.1% were dysglycemic. Without the OGTT, 30% of patients with type 2 diabetes and 70% of those with IGT would not have been detected. The presence of dysglycemia almost doubled from that selfreported to the true proportion after screening. Only approximately one-third of all coronary patients had completely normal glucose metabolism. Of patients with known diabetes, 31% had been advised to attend a diabetes clinic, and only 24% attended. Only 58% of dysglycemic patients were prescribed all cardioprotective drugs, and use of sodium-glucose cotransporter 2 inhibitors (3%) or glucagon-like peptide 1 receptor agonists (1%) was small. CONCLUSIONS Urgent action is required for both screening and management of patients with CAD and dysglycemia, in the expectation of a substantial reduction in risk of further cardiovascular events and in complications of diabetes, as well as longer life expectancy.

Key Words: calcium Ⅲ vascular smooth muscle Ⅲ endothelium P recapillary arterioles are the final generation of terminal arterioles. They have diameters Ͻ30 m and determine local blood flow to tissues via capillary beds, as opposed to the gross distribution of blood and control of pressure, performed by the larger conducting vessels and resistance arteries. Little direct investigation of Ca signaling, structure, and contractility has been possible in live, intact precapillary arterioles, because their small size virtually precludes dissection. Although vital microscopy and related techniques have produced useful information, 1-3 they are not well suited to investigations of cellular function, signaling, or morphology. 4 A decreased role for the internal Ca store in small vessels has been suggested, 5,6 but generally the paucity of information in precapillary arterioles has led to the processes found in larger vessels, eg, integration of neuronal and endothelial signals, 3,7-9 being extrapolated to precapillary arterioles. However, consideration of the differences in their function, innervation, and amount of tone would suggest that the mechanisms and signaling controlling precapillary arterioles may differ from those present in other vessels. 10,11 In addition to neurohormonal stimulation of myocytes, the endothelium via Ca signals and NO-and/or EDHF-mediated effects, can also affect vascular tone. [12][13][14][15] Little is known concerning endothelial Ca signals in precapillary arterioles or their contribution to relaxation; indeed, it is unclear how relevant flow-, pressure-, or shear-mediated relaxing mechanism are to these smaller vessels. 1,11 We now report unique mechanistic signaling data from in situ precapillary arterioles in 2 host tissues, obtained with confocal imaging of intracellular Ca, and directly compare the results with a well-characterized larger vessel, the mesenteric artery (Ϸ230 m in diameter). 16 -19 We show, for the first time, that Ca signals induced by agonists in precapillary arteriolar myocytes rely exclusively on Ca release from the sarcoplasmic reticulum (SR) mediated by inositol 1,4,5-trisphosphate (IP 3 ) receptors (IP 3 Rs). As the signals do not pass and coordinate between cells, exquisite local control in segments of precapillary arterioles is achieved. The endothelium has no effect on agonist-induced tone but abolishes Ca spikes and contraction produced by L-type Ca channel entry. Thus, uniquely within the arterial system, in precapillary arterioles a single myocyte influences a significant part of the vessel and blood flow to the surrounding region.

In endothelial cells there remain uncertainties in the details of how Ca2+ signals are generated and maintained, especially in intact preparations. In particular the role of the sarco-endoplasmic reticulum Ca2+-ATPase (SERCA), in contributing to the components of agonist-induced signals is unclear.The aim of this work was to increase understanding of the detailed mechanism of Ca2+ signalling in endothelial cells using real time confocal imaging of Fluo-4 loaded intact rat tail arteries in response to muscarinic stimulation. In particular we have focused on the role of SERCA, and its interplay with capacitative Ca2+ entry (CCE) and ER Ca2+ release and uptake. We have determined its contribution to the Ca2+ signal and how it varies with different physiological stimuli, including single and repeated carbachol applications and brief and prolonged exposures.In agreement with previous work, carbachol stimulated a rise in intracellular Ca2+ in the endothelial cells, consisting of a rapid initial phase, then a plateau upon which oscillations of Ca2+ were superimposed, followed by a decline to basal Ca2+ levels upon carbachol removal. Our data support the following conclusions: (i) the size (amplitude and duration) of the Ca2+ spike and early oscillations are limited by SERCA activity, thus both are increased if SERCA is inhibited. (ii) SERCA activity is such that brief applications of carbachol do not trigger CCE, presumably because the fall in luminal Ca2+ is not sufficient to trigger it. However, longer applications sufficient to deplete the ER or even partial SERCA inhibition stimulate CCE. (iii) Ca2+ entry occurs via STIM-mediated CCE and SERCA contributes to the cessation of CCE. In conclusion our data show how SERCA function is crucial to shaping endothelial cell Ca signals and its dynamic interplay with both CCE and ER Ca releases.

Сибирский государственный медицинский университет, г. Томск (1) Красноярский государственный медицинский университет им. В.Ф. Войно-Ясенецкого, г. Красноярск (2)Распределение жировой ткани и ее количество (преобладание висцерального жирового депо), размер адипоцитов (гипертрофия клеток) могут являться опреде-ляющим фактором риска развития метаболических нарушений. В работе исследо-вано влияние аэробных и анаэробных физических нагрузок на морфометрические параметры мезентериальной и подкожной жировой ткани у крыс с ожирением, ин-дуцированным высокожировой диетой.Установлено, что у животных, находившихся на высокожировой диете, уве-личение массы подкожной жировой ткани сопровождается преобладанием адипо-цитов малых размеров, что возможно играет адаптивную роль и защищает эктопи-ческие ткани от липотоксичности.Анаэробные физически нагрузки снижают удельную массу мезентериальной жировой ткани у животных, находившихся на стандартной диете.При высокожировой диете анаэробные физические нагрузки в большей степе-ни снижают удельную массу и размер адипоцитов в мезентериальной жировой тка-ни, в то время как аэробные в подкожной.Ключевые слова: жировая ткань, адипоциты, высокожировая диета, физические нагрузки.Ожирение в настоящее время явля-ется одним из распространенных хрони-ческих заболеваний и приобретает харак-тер глобальной эпидемии. Избыточный вес и ожирение приводят не только к косметическому дефекту, но и к развитию тяжелых и социально значимых заболе-ваний, таких как сахарный диабет, ише-мическая болезнь сердца, гипертониче-ская болезнь и другие [1, 2].Выделяют два основных жировых депо: висцеральное и подкожное, при этом висцеральное депо у грызунов пред-ставлено мезентериальной, забрюшинной и эпидидимальной жировой тканью [5].Увеличение массы жировой ткани идет двумя путями: за счет увеличения объема клеток-адипоцитов (гипертрофии) и увеличения числа адипоцитов (гипер-плазии). Известно, что у людей при избы-точном питании увеличение подкожной жировой ткани в ягодично-бедренной области происходит за счет увеличения числа клеток, а области передней брюш-ной стенки за счет увеличения размера адипоцитов [20]. У крыс, находившихся на высокожировой диете, развитие мезен-териальной и эпидимальной жировой ткани преимущественно происходит за счет гипертрофии клеток, в то время как