Acid-base balance of spinal cord fluid in the post-resuscitation period]

Experiments were conducted on dogs which had sustained a 10-minute circulatory arrest caused by electrotrauma; the acid-base balance of the cerebrospinal fluid (CSF) and the blood was studied during the postreanimation period. Although the systemic uncompensated acidosis persisted in the course of the first hour of the postreanimation period, compensation of the CSF acidosis occurred much earlier and the pH was maintained at the initial level for 6 hours. Despite a high lactate concentration for a period of 3 hours of the postreanimation period the bicarbonate concentration remained near the initial one at this period.     

Correction of disorders of the system of blood aggregation regulation by ionol in the post-resuscitation period

In the experiments on white rats resuscitated after a 7-minute mechanical asphyxia, phase disorders in the indices of the system of regulation of aggregate state of the blood in postresuscitation period have been revealed. They appear in the shape of a syndrome of disseminated intravascular blood coagulation with the development of hypercoagulation phase by the 3rd hour. Prophylactic introduction of ionol in a dose of 100 mg/kg in 48, 24 and 1 hour before the experiment prevents the development and progressing of the above syndrome.     

Lymphatic bed of the heart in the post-resuscitation period

In the experiment performed on 96 rabbits, by means of silver nitrate impregnation and Gerota mass injection methods, changes in the epicardial lymphatic bed have been investigated after 5-minutes' clinical death caused by hemorrhage. During first hours after resuscitation certain signs of the lymphatic drenage activation are revealed. In most of the animals the specific density of the lymphatic bed increases, capillaries and postcapillaries dilate, hyperargirophilia of cytoplasm and nuclei of endotheliocytes appears. In the animals sacrificed against the background of a severe state (with certain, signs of a pronounced hypoxia), there are dystrophically and degeneratively altered endotheliocytes. This is accompanied with hyper- hypoargyrophilia of endothelium, fragmentation of its cell borders, with deterioration of injection ability of the lymph outflow pathways. In the rabbits survived, by the 7th-14th days a gradual normalization of the parameters studied takes place.     

Blood rheology in myocardial infarction and hypertension

Blood rheology was studied in patients with acute myocardial infarction (AMI) and essential hypertension (EH), and the results were correlated with in vivo hemodynamic functions. Blood viscosity (eta B) was elevated as a result of sequential changes of a number of parameters, including increases in hematocrit, plasma fibrinogen and alpha 2-globulin, an enhancement of red cell aggregation and a reduction of red cell filterability in plasma. Total peripheral resistance (TPR) was elevated upon admission, due to increases in both the vascular hindrance (ZS) and eta B. During recovery, the eta B became normalized; alterations in eta B were accompanied by parallel changes in TPR and an inverse change in plasma volume (PV). In EH patients, the increase in eta B showed a correlation with arterial pressure. For both established and borderline hypertensives, the rheological changes were most prominent in the high renin subgroups. In mild EH, the elevation of eta B was compensated by a decrease in ZS (vasodilation), keeping the TPR essentially normal. In EH with higher arterial pressure, the elevation of eta B was accompanied by a normal ZS without compensatory vasodilation, and hence TPR rose to exacerbate the hypertension. These results suggest that the elevation of eta B may be an early event in the development of EH and that its role must be considered with concurrent cardiovascular functions. In EH there is a significant correlation between left ventricular mass and eta B. Experimental manipulations of the hematocrit level in spontaneously hypertensive rats led to a corresponding variation of arterial pressure. The available data implicate a significant role of eta B in the pathophysiology of AMI and EH. Further interdisciplinary, longitudinal studies are needed tin order to unravel the complicated pathophysiological changes in myocardial infarction and hypertension.     

Anti-inflammatory effects of exercise training in the early period after myocardial infarction

The aim of this investigation was to determine the effect of exercise training on the levels of plasma cytokines and acute phase reactants in the early post acute myocardial infarction (AMI) period. Sixty patients were enrolled into this three-week cardiac rehabilitation study. The mean time from AMI was 7.08 +/- 1.60 days, and the patient mean age was 60 +/- 10 years. Subjects were randomly assigned to one of the two groups: the control group treated with standard measures, and the group with additional regular moderate-intensity exercise training. Physical activity was based on the ergospirometry test results. Apart from clinical follow-up and routine laboratory analysis we determined the levels of plasma cytokines: tumor necrosis factor (TNF-alpha), soluble TNF-alpha receptor 1 (TNF-alphaSR1), interleukin (IL)-8, IL-10, and acute phase reactants: high sensitivity C-reactive protein (hsCRP) and fibrinogen. The obtained results confirmed the hypothesis that the early post AMI period is an inflammatory state the intensity of which gradually decreases with standard treatment during the first month after AMI, while including patients into early exercise training improves their inflammatory profile by decreasing the level of acute phase reactant and TNF-alphaSR1.     

miRNA在心肌梗死中的作用及其机制研究进展

急性心肌梗死（AMI）是最常见的心血管事件,具有高发病率和高死亡率,严重威胁人类生命健康。微小RNA（miRNA）通过调节心肌细胞炎症、纤维化、细胞自噬及新生血管形成的表型机制发挥功能。本综述探讨了心肌梗死后miRNA上调及下调的分子机制,以及miRNA对心肌梗死早期诊断中的价值。     

Effects of clinical death and pre-administered inderal on adrenoreactivity of the heart in post-resuscitation period

Acute lethal blood loss followed by resuscitation was found to decrease noradrenaline and increase epinephrine levels in heart muscle in experiments on mongrel male rats which significantly increase heart beta-adreno-receptors sensitivity to exogenous noradrenaline. Preliminary inderal injection prevents excessive heart beta-adreno-receptors stimulation by catecholamines, considerably reduces post-resuscitation rhythmic disturbances and prevents ventricular fibrillation which significantly decreases early post-resuscitation lethality.     

The endothelin system and its role in acute myocardial infarction

Immediately after an acute myocardial infarction (AMI) or in models of ischemia-reperfusion injury, cardiac endothelin (ET) system is markedly activated, and plasma levels of ET are increased. In the heart, expression of the main components of the ET system (ET-1 peptide, both receptor subtypes ETA and ETB, though not endothelin converting enzyme) are increased both at the gene level and protein level, in the viable myocardium, and--even more substantially--in the necrotic area. Despite these conspicuous abnormalities, the role of ET in this setting remains unclear. In the absence of human data, most short-term studies in animals (in terms of hours to up to 8 days post-AMI) and in the reperfused ischemic heart, have found beneficial effects of ET receptor blockade on survival rate, incidence of arrhythmias, cardiac function, and morphology. In contrast, many studies in which a long-term ET inhibition was started immediately post-infarction and the late effects were examined in animals with ensuing chronic heart failure (14-100 days postinfarction), adverse effects were also observed, such as scar thinning, further ventricular dilation, or even a worse survival rate. It appears that the ET system plays a dual role during the early post-AMI period. At present, it is not clear whether the short-term beneficial effects or long-term adverse effects of ET receptor blockade would prevail. Acute use of short-acting ET receptor antagonists in patients with AMI complicated by an acute heart failure is an attractive possibility that also remains to be investigated.     

A role for decorin in the remodeling of myocardial infarction.

Because the small leucine-rich proteoglycan decorin has been implicated in regulation of collagen fibrillogenesis leading to proper extracellular matrix assembly, we hypothesized it could play a key role in cardiac fibrosis following myocardial infarction. In this study we ligated the left anterior descending coronary artery in wildtype and decorin-null mice to produce large infarcts in the anterior wall of the left ventricle. At early stages post-coronary occlusion the myocardial infarction size did not appreciably differ between the two genotypes. However, we found a wider distribution of collagen fibril sizes with less organization and loose packing in mature scar from decorin-null mice. Thus, we tested the hypothesis that these abnormal collagen fibrils would adversely affect post-infarction mechanics and ventricular remodeling. Indeed, scar size, right ventricular remote hypertrophy, and left ventricular dilatation were greater in decorin-null animals compared with wildtype littermates 14 days after acute myocardial infarction. Echocardiography revealed depressed left ventricular systolic function between 4 and 8 weeks post-ischemia in the decorin-null animals. These changes indicate that decorin is required for the proper fibrotic evolution of myocardial infarctions, and that its absence leads to abnormal scar tissue formation. This might contribute to aneurysmal ventricular dilatation, remote hypertrophy, and depressed ventricular function.     

Morphological characteristics of the small intestine and translocation of intestinal microflora in the post-resuscitation period]

Morphologic investigations were studied in rats during 1-3 hours after clinical death of the acute hemorrhage. The combination of morphologic and microbiologic methods obtained allow to describe the destruction of intestine wall and translocation of bacteria in the tissue and organs. In 3 days after clinical death the structure of small intestine regenerates, but the vital bacteria were isolated in the tissues and organs.     

The role of inflammation in the reparative process in experimental myocardial infarction

Experiments carried out on 91 dogs have shown that changes in the inflammatory process course result in complicated postinfarction repair of myocardium, disagreement in the development, i.e. in desynchronization of necrotic repair processes in the myocardial infarction zone. It is supposed that regulation of the myocardial infarction healing by inflammation can be one of the efficient methods of its therapy.     

Energy potential of the cerebral cortex in the pre-agonal and post-resuscitation period after acute blood loss

In experiments on dogs it was revealed that during the preagonal period, after a four-hour hypovolemic hypotension, the content of ATP was reduced in the gray matter of the brain by 38 percent, and of ADP and AMP increased by 121 percent and 875 percent, respectively. Reflecting these shifts the energy charge potential decreased from 0.931 to 0.733 (P less than 0.05). At the early and remote postrescucitation period the content of metabolites and of energy charge potential failed to differ from the initial level.