ИШЕМИЧЕСКОЕ ПОСТКОНДИЦИОНИРОВАНИЕ СЕРДЦА. АНАЛИЗ ЭКСПЕРИМЕНТАЛЬНЫХ И КЛИНИЧЕСКИХ ДАННЫХ

Published data on the impact of the experimental atherosclerosis on the infarct-limiting effect of ischemic postconditioning (IPost) are controversial. The reviewed data indicate that aging eliminates or reduces the infarct-limiting effect of postconditioning but does not affect the antiarrhythmic effect of IPost. Most of the experimental data reported that streptozotocin-induced diabetes removes the infarct-limiting effect of IPost. Regarding the second type of diabetes, information is contradictory: some authors argue that this diabetes completely eliminates the cardioprotective effect of IPost, others say that it only weakens but does not eliminate the infarct-limiting effect of IPost. Postconditioning in rats with high blood pressure prevents the appearance of reperfusion contractile dysfunction of the heart and provides the infarct-limiting effect. Cardiac hypertrophy, post-infarction remodeling and dilated cardiomyopathy have no effect on the infarct-reducing and inotropic effect of postconditioning. The majority of publications indicates that IPost enhances the inotropic and cardioprotective effect of cardioplegia. Data on the effect of postconditioning on the tolerance of the human heart to ischemia/reperfusion are limited and do not allow to make an unambiguous conclusion about whether IPost prevents reperfusion myocardial injury in cardiac patients.Литературные данные о влиянии экспериментального атеросклероза на инфаркт-лимитирующий эффект ишемического посткондиционирования (ИПост) носят противоречивый характер. Представленные данные свидетельствуют о том, что старение устраняет или ослабляет инфаркт-лимитирующий эффект посткондиционирования, но не влияет на антиаритмический эффект ИПост. Большинство экспериментальных данных сообщают о том, что стрептозотоцин-индуцированный диабет устраняет инфаркт- лимитирующий эффект ИПост. Относительно сахарного диабета 2-го типа сведения носят противоречивый характер: одни авторы утверждают, что подобный диабет полностью нивелирует кардиопротекторный эффект ИПост, другие говорят о том, что он только ослабляет, но не устраняет инфаркт-лимитирующий эффект ИПост. Посткондиционирование у крыс с повышенным артериальным давлением предупреждает появление реперфузионной сократительной дисфункции сердца и оказывает инфаркт-лимитирующий эффект. Гипертрофия сердца, постинфарктное ремоделирование и дилатационная кардиомиопатия не влияют на инфаркт-лимитирующий и инотропный эффект посткондиционирования. Согласно большинству публикаций, ИПост усиливает инотропный и кардиопротекторный эффект кардиоплегии. Данные о влиянии посткондиционирования на толерантность сердца человека к действию ишемии-реперфузии носят ограниченный характер и не позволяют сделать однозначный вывод о том, может ли ИПост предупреждать реперфузионные повреждения миокарда у кардиологических пациентов

Anisotropic Behavior of Knight Shift in Superconducting State of Na_xCoO_2yH_2O

The Co Knight shift was measured in an aligned powder sample of Na_xCoO_2yH_2O, which shows superconductivity at T_c \sim 4.6 K. The Knight-shift components parallel (K_c) and perpendicular to the c-axis (along the ab plane K_{ab}) were measured in both the normal and superconducting (SC) states. The temperature dependences of K_{ab} and K_c are scaled with the bulk susceptibility, which shows that the microscopic susceptibility deduced from the Knight shift is related to Co-3d spins. In the SC state, the Knight shift shows an anisotropic temperature dependence: K_{ab} decreases below 5 K, whereas K_c does not decrease within experimental accuracy. This result raises the possibility that spin-triplet superconductivity with the spin component of the pairs directed along the c-axis is realized in Na_xCoO_2yH_2O.Comment: 5 pages, 5 figures, to be published in Journal of Physical Society of Japan vol. 75, No.

Hearts from Mice Fed a Non-Obesogenic High-Fat Diet Exhibit Changes in Their Oxidative State, Calcium and Mitochondria in Parallel with Increased Susceptibility to Reperfusion Injury

High-fat diet with obesity-associated co-morbidities triggers cardiac remodeling and renders the heart more vulnerable to ischemia/reperfusion injury. However, the effect of high-fat diet without obesity and associated co-morbidities is presently unknown.To characterize a non-obese mouse model of high-fat diet, assess the vulnerability of hearts to reperfusion injury and to investigate cardiac cellular remodeling in relation to the mechanism(s) underlying reperfusion injury.Feeding C57BL/6J male mice high-fat diet for 20 weeks did not induce obesity, diabetes, cardiac hypertrophy, cardiac dysfunction, atherosclerosis or cardiac apoptosis. However, isolated perfused hearts from mice fed high-fat diet were more vulnerable to reperfusion injury than those from mice fed normal diet. In isolated cardiomyocytes, high-fat diet was associated with higher diastolic intracellular Ca2+ concentration and greater damage to isolated cardiomyocytes following simulated ischemia/reperfusion. High-fat diet was also associated with changes in mitochondrial morphology and expression of some related proteins but not mitochondrial respiration or reactive oxygen species turnover rates. Proteomics, western blot and high-performance liquid chromatography techniques revealed that high-fat diet led to less cardiac oxidative stress, higher catalase expression and significant changes in expression of putative components of the mitochondrial permeability transition pore (mPTP). Inhibition of the mPTP conferred relatively more cardio-protection in the high-fat fed mice compared to normal diet.This study shows for the first time that high-fat diet, independent of obesity-induced co-morbidities, triggers changes in cardiac oxidative state, calcium handling and mitochondria which are likely to be responsible for increased vulnerability to cardiac insults