Alpha1 desensitization of the heart during adaptation to stress]

Results of the experiments evidence that a combination of three factors, limiting the Ca2+ concentration increase in myocardial cell, can play a role in the cardioprotective effect of adaptation of rats to short-term immobilization stress (every second day for a month) are presented. Those factors are as follows: desensitization of alpha 1-adrenoreceptors, M-cholinoreceptors up-regulation and reduced number of voltage-dependent Ca2+ channels in the myocardial membranes.     

Participation of heart prostaglandins in cardioprotective cross-effects of adaptation to stress and hypoxia

An adaptation to stress and hypoxia was found to increase the baseline PGE content in the myocardium. The data obtained suggest that the activation of the myocardial system of protective PGs is an important link in the cardioprotective effects of adaptation.     

Phosphorylation of rhodopsin as a possible mechanism of adaptation.

Light-induced phosphorylation of rhodopsin has been extensively studied by a number of investigators from a biochemical point of view. However, little is known about the physiological function of this reaction. The slow rates measured for phosphorylation and dephosphorylation suggest that it may be involved in visual adaptation rather than in excitation. This paper presents biochemical data obtained from phosphorylation experiments in isolated photoreceptor membranes as well as in the physiological system of whole retinas and living animals. An attempt is made to compare the phosphorylation reaction with visual adaptation hypotheses taken from the electrophysiological literature. Finally, effects of cyclic nucleotide metabolism on the sensitivity of photoreceptors are presented and discussed.     

Control of seed coat thickness and permeability in soybean : a possible adaptation to stress

Although the seed coat, through its thickness and permeability, often regulates seed germination, very little is known about the control of its development. Using soybean (Glycine max [L.] Merrill) explants, podbearing cuttings in which defined solutions can be substituted for the roots, we have demonstrated that cytokinin and mineral nutrients moving through the xylem can control soybean seed coat development. Lack of cytokinin and minerals in the culture solution, causes a thicker, less permeable seed coat to develop. The seeds with thickened coats will imbibe water rapidly if scarified; furthermore, these scratched seeds also germinate and produce normal plants. Inasmuch as stress (e.g. drought) decreases mineral assimilation and cytokinin production by the roots, the resulting delay in germination could be an adaptive response to stress.     

The stress of mortally dangerous conditions: the individual psychophysiological mechanisms of adaptation in life-threatening situations

Investigation into the mechanisms of the individual psychophysiological adaptation to life-threatening situations was performed. The data analysis of evoked potentials induced with verbal stimuli in 30-50-msec exposures was executed. Cross-correlation and wavelet analysis, as well as neurone algorithms were used to define total brain response to each stimulus and its duration. Correlation of the estimated parameters with subconscious aspects of psychic activity is discussed. Results of the studies performed with this neurosemantie method in various groups of subjects perceiving threat to life in the course of their performance, are presented. Described changes in the subconscious response mechanisms can help to clarify the direction for creation of new approaches with psychological correction and support.     

Comparative evaluation of the protective effect of adaptation to short-term stress exposures in damage to the heart and portal vein from long-term stress

The effect of the preliminary adaptation to short-term stress actions carried out under different conditions was studied in the myocardium and vascular smooth muscle damaged by long-term immobilization stress. The preliminary adaptation performed under "sparing" conditions was shown to protect more effectively the right atrial myocardium and portal vein against damages induced by long-term immobilization than that carried out under stringent conditions. The sparing adaptation allowed avoiding the appearance of the structural "price" of the adaptation, i.e. the depression of myocardial contractile function induced by adaptation itself.     

Deliberate heart arrest in man and its possible mechanism

A case of deliberate 7-second heart arrest is described. It is assumed that the effect is the result of voluntary self-irritation of peritoneal receptors by means of rhythmical diaphragm muscle contractions realized in conditions of preliminary breathing arrest.     

On the possible mechanism of cell cycle synchronization

The influence of exchanges of lipids and antioxidants (AO) between the cells on the cell proliferation is studied in the frame of the membrane model of the cell cycle. It is shown theoretically that the easy-oxidative lipids exchange favours the synchronization of cell division, while the AO exchange leads to desynchronization. The analytical consideration and some numerical estimations are carried out. The qualitative consequences accessible to experimental verification are discussed.     

On the possible role of focal cooling of the heart in the mechanism of repetitive ventricular extra beats

The role of myocardial foci in the mechanism of ventricular arrhythmias was studied by local cooling of the intact dog heart. At normal heart rate conduction delay in the focus is not sufficient to account for re-entry of impulses. However, a premature stimulus applied near the refractory period caused sudden prolongation of conduction giving rise to nonstimulated extra beats, arising probably as a result of re-entry. The phenomenon is presumably due to the fact that at this time a large portion of the fibres has not yet recovered excitability. With increasing size of the focus, there is increased asynchrony of recovery of excitability and premature stimuli falling later in the cycle are able to produce reentry. A negative correlation exists between cycle length and conduction delay and a positive correlation between cycle length and the coupling interval, i.e. the time interval between a premature stimulus and the first nonstimulated extra beat.     

Brain angiotensin receptors and adaptation to stress

In this short review, we hypothesize that the central renin-angiotensin system might participate to the initiation of compensatory responses to a stressor agent. Regulation of the expression of the brain angiotensin receptors might constitute a primary molecular mechanism by which this protecting action would take place. We illustrate this possibility by investigating the expression of the angiotensin type 1 receptor in the hypothalamus in response to systemic and neurogenic stressors.     

Physiological adaptation of the heart to pathological overloading

Chronic overloading of the rat heart induces a cascade of adaptational events that compensate for the increase in work. At the myocardial level there are two types of adaptational mechanisms: qualitative, represented by the isomyosin changes leading to an improved efficiency; and quantitative, the hypertrophy. We present new approaches exploring possible adaptational changes at other levels within the myocardial cell. Studies of heart overload were performed either in young rats with experimental aortic stenosis or in humans with chronic compensatory hypertrophy. By means of double immunofluorescence labeling of isolated myocytes with anti-V1 and anti-V3 myosin immunoglobulins, we showed that the shift from high- to low-ATPase isomyosins occurs rapidly after aortic stenosis (2-3 days). Cardiac myocytes were shown to be poor in tubulin but a microtubule pattern was clearly visualized by an immunofluorescence approach. Their role in the onset of adaptational processes after aortic stenosis in not yet clear. On the other hand, we showed that in humans, contrary to small rodents, the adaptational process at the isomyosin level is very small or nonexistent.     

植物对水淹胁迫的响应与适应

水淹是植物遭受的主要的非生物胁迫之一.水淹胁迫使植物处于周期或长期的厌氧或缺氧状态,限制植物的需氧呼吸和维持生命活动所需的能量产生,导致土壤还原势的降低和有毒物质的积累,从而对植物的生存构成严重威胁.在长期的进化过程中,一些植物能够忍耐短期或长期的水淹生境而存活下来.目前分析植物感知水淹胁迫的主要途径为感知体内氧浓度的降低和感知体内乙烯浓度的增加.淹水胁迫下植株的适应策略主要包括:1)茎的伸长生长、不定根和通气组织的形成等形态学方面的适应;2)代谢途径的改变,淹水植物主要通过厌氧代谢获得维持生命的能量;3)通过体内乙烯、赤霉素和脱落酸等激素含量水平的改变来调节生理活动或形态、解剖等方面的变化;4)抗氧化酶系统对厌氧胁迫植株体内有毒的活性氧自由基的清除.运用分子生物学和生物信息学等手段找出由水淹胁迫诱导的相关基因并对其进行克隆,繁殖与培育具有耐水淹能力强的植物种类、品种和生态型,将是从事植物抗水淹胁迫研究的科研人员的目标和方向.     

Loss of adaptation to oxidative stress as a mechanism for aortic damage in aging rats

Cells are armed with a vast repertoire of antioxidant defence mechanisms to prevent the accumulation of oxidative damage. The cellular adaptive response is an important antioxidant mechanism against physiological and pathophysiological oxidative alterations in a cell's microenvironment. The aim of this paper was to study, in the rat aorta, whether this adaptive response and the inflammation associated with oxidative stress were expressed throughout the aging process. We examined the rat aorta, as it is a very sensitive tissue to oxidative stress. Male Wistar rats of 1.5, 3, 12, 18 and 24 months of age were used. Superoxide anion (O2(-)) generation; levels of two antioxidant enzymes, superoxide dismutase (SOD) and catalase; and the levels of prostaglandin E2 (PGE2), an inflammatory marker, were measured. The results for rats at different ages were compared with those for 3 months of age. A balance between production of O2(-) and SOD activity was found in the aorta of rats from 1.5 to 12 months old. Oxidative stress was present in the aorta of old animals (18-24 months), due to a failure in the mechanisms of adaptation to oxidative stress. The observed increase in PGE2 levels in these rats reflected an inflammatory response. All together suggest that vascular oxidative stress and the inflammatory process observed in the old groups of rats could be closely related to vascular aging. Our results also remark the importance of the adaptative response to oxidative stress.     

Glutathione system adaptation to acute stress in the heart of rats during different regimes of hypoxia training

The intensity of lipid peroxidation (LPO), reduced and oxidized glutathione (GSH and GSSG) contents, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase (G-6-PDH), and NADP-isocitrate dehydrogenase (NADP-IDH) activities were studied in the heart of male rats exposed to two modes of intermittent hypoxic training (IHT): I-breathing in normobaric chamber with 7% O2 gas mixture for 5 min with 15 min normoxic intervals 4 times daily during 3 weeks; II-breathing by 12% O2 gas mixture in the same manner). After adaptation to hypoxia, the rats were subjected to 6h-immobilization stress. It has been shown that stress action after IHT (regime I) caused the increase in LPO and the shift of GSH/GSSG to disulfides. A disbalance in antioxidative defense system was determined by the decrease in glutatione peroxidase, G-6-PDH activities, and GSH content. The support of glutathione reductase activity under stress in this group with simultaneous decrease of enzyme activity in the pentose phosphate pathway was realized through the participation of NADP-IDH. Hypoxic training in regime II induced LPO decrease in the heart tissue after stress. The increase in the heart GSH content, optimal balance of glutathione-related enzymes in this group evidences for the dependence of adaptation effects on the vigor of hypoxic exposition. Our results suggest the active participation of glutathione system in the formation of adaptation reactions under the extreme factor influences through the action on intracellular red/ox potential as well as effectiveness of antioxidant defense.     

Increased enzymatic activity of antioxidant protection of the heart in the adaptation of rats to short-term stress exposure

It has been shown that adaptation to short-term emotional-painful stresses leads to an increase in antioxidant enzyme activities but does not change vitamin E content in the myocardium. The most labile enzyme was catalase (35% increase). During stress in nonadapted animals the enzyme activity decreased, as compared to the control, while in the group of adapted animals with subsequent stress the activity was even higher than in the control. During initiation of lipid peroxidation in the heart homogenates in vitro there was a 3-fold increase and a 1%-fold decrease in the oxidation intensity in rats exposed to stress and in adapted animals, respectively. The role of adaptation activation of cardiac antioxidant system in the prevention of stress-induced heart damage is discussed.