Ganglioside participation in the regulation of free-radical reactions in brain membranes]

The effect of monosialoganglioside GM1 on induced free radical reactions in the synaptosomal and myelin membranes induced by Fe(2+)-H2O2 system was studied. The formation of free radicals was determined by measuring luminol-dependent chemoluminescence. It was found that preincubation of the membranes with GM1 (10(-11)-10(-6) M) and 12 or 12-palmitate, 13-acetate phorbol ester (10(-7)-10(-6) M) or alpha-tocopherol (10(-6) M) results in the decrease of chemiluminescent response. The inhibiting effect of alpha-tocopherol (but not of other compound tested) takes place without any preincubation as well. When the effect of GM1 was studied over a wide range of GM1 concentrations, a biphasic kinetics was observed, the highest per cent of inhibition of chemoluminescence being found at 10(-8) M. The data obtained provide evidence that the inhibition of free radical reactions in the brain membranes by nanomolar concentration of GM1 is not due to its interaction with lipid radicals. The results suggested that the inhibiting effect of GM1 is mediated through signal transduction system.     

Effect of the critical fragmentation of erythrocyte membranes]

After sonification of erythrocyte membranes, some changes were registered in these including a loss of their ability to structural rearrangements caused by cAMP (ESR-spectroscopy and luminescence data), an increase in cAMP binding and aggregation of intramembrane particles (freeze-fracture data). These findings suggest a non-identity of the structural organization in membranes and in their fragments. The cooperative nature of membrane structural modification at ultrasonic fragmentation is shown.     

Phosphoinositide content in the erythrocyte membranes of rats with spontaneous hypertension]

The values of triphosphoinositides (TPI) and monophosphoinositides (MPI) contents per 1 mg of membrane protein in the erythrocyte hosts of spontaneously hypertensive rats (SHR) constitute 178 and 74%, respectively, of that in the erythrocyte hosts of normotensive rats (NR). The total amount of phosphoinositides in the erythrocyte hosts of NR is more than 120% of the total amount of these lipids, in the erythrocyte hosts of SHR.     

Role of catalase in myocardial protection against ischemia in heat shocked rats

It was recently reported that in rats exposure to heat shock leads to appearance of a myocardial heat shock protein (HSP 70) and to an increase in myocardial catalase activity. This correlated with an improvement in post-ischemic function either in Langendorff-perfused hearts after low-flow ischemia or in working hearts after short-term, no-flow ischemia. We investigated the effect of the same hyperthermic treatment on functional recovery from no-flow ischemia of various durations in isolated working rat hearts performing at high or low external workloads. Rats were heated to core temperature of 42° C for 15 min. No significant protein oxidation (% oxidized methionine) was observed 2.5 hr after treatment. A protein with migration characteristics similar to HSP 70 was observed in hearts of heat shocked rats 24 hr after this treatment while their myocardial catalase activity was not increased. Hearts of similarly treated rats were excised 24 hr after hyperthermia and perfused in a working mode with Krebs-Henseleit buffer (1.25 mM Ca²⁺, 11 mM glucose). At 15 cm H₂O preload and 100 cm H₂O afterload after 30 min no-flow ischemia, control hearts recovered to 36.9%, 2%, 47.6%, and 21.5% of the preischemic values of heart rate-peak systolic pressure product (RPP), aortic output, coronary flow, and cardiac output, respectively. After only 25 min of ischemia the respective recovered values were 61.6%, 11.5%, 58.7%, and 33.5%. Throughout the recovery period these hemodynamic values were consistently higher in hearts of heat shocked animals than in those of control hearts but the differences were not statistically significant. After 25 min ischemia only 2 out of 7 control hearts recovered some aortic output, whereas in the heat shocked animals all 5 hearts recovered. After only 20 min of no-flow ischemia and at a lower workload (12.5 cm H₂O preload and 75 cm H₂O afterload), control hearts recovered to 85.1% of RPP, 54.1% of aortic output, and 68.3% of cardiac output. None of these variables was significantly improved by heat shock pretreatment. In summary, we were unable to demonstrate a similar degree of protective effect of heat shock pretreatment as compared to other reports where both HSP 70 and increased catalase activity were present. The reason(s) could be related to lack of induction of myocardial catalase activity in our study.     

The mechanism of the action of dalargin in experimental myocardial ischemia]

In acute experiments on cats it has been shown that dalargin possess antiarrhythmic affect in myocardial ischemia. Antiarrythmic effect of dalagrig may be connected both with reflex and with direct action of dalargin on neurons structure, which     

The sequelae of transient myocardial ischemia in chronic experiments]

Reversible short-term and local myocardial ischemia in non-anaesthetized dogs involved a functional (if changing the activity of CPK) and morphologic aftereffect. At the same time it is possible to find some mechanisms of compensation (in chronic experiment).     

Time of day and occurrence of myocardial ischemia]

A 24-hour Holter ECG was registered in 130 patients with the ischemic heart disease with or without the history of myocardial infarction treated in out-patient clinic. Two hundred thirty seven episodes of myocardial ischemia were detected. These episodes developed between 6.00 and 8.00 a.m., 12.00 and 4.00 p.m., and 6.00 and 8.00 p.m.     

竹红菌甲素对红细胞膜和几种磷脂脂质体膜的流动...

In this paper, the photodamage of Hypocrellin A to the fluidity of human erythrocyte membranes and some kinds of membranes of phospholipid liposomes was investigated by measuring the changes in fluorescence polarization of the membranes. The results showed that the photosensitization effect of HA caused the decrease of membrane fluidity of the phospholipid (DPPC, DPPC/DPPE, phospholipid of erythrocyte membranes) liposomes. The DPPC and DPPC/DPPE liposomes were more sensitive to the damage than the phospholipid liposomes of erythrocyte membranes. To human erythrocyte membranes, the photodamage effect of HA caused its fluidity first increased and then, with the increment of illumination time, decreased. To spectrin-depleted and trypsin-treated erythrocyte membranes, this kind of change in fluidity was inhibited. All of the results indicated that phospholipids and proteins play different roles in the photodamage of HA to the fluidity of membranes. Membrane proteins, especially spectrin, were the key factor involved in the changes of the fluidity.     

Glycerol-induced baroprotection in erythrocyte membranes

A system for applying hydrostatic pressures up to 10,000 atm upon cell suspensions for time intervals from a few seconds to several minutes is described. The K+ content of toad red blood cells was used as an indication of the degree of membrane injury induced by the hyperbaric condition. It is practically not affected for pressures up to 2000 atm in experiments lasting 3 or 10 min. falling markedly for pressures of 5000 or 8000 atm. The duration of the applied pressure and its intensity are additive regarding the magnitude of the baroinjury. Glycerol, a cryoprotective agent. at 4.0 M, confers partial but significant baroprotection, which is characterized by a smaller decline of the cell K+ content of the glycerol-treated cells in comparison to the untreated cells, submitted to the same conditions of pressure and time. Baroinjury is compatible with a reversible mechanism. However, irreversible membrane damage occurs for a pressure of 8000 atm applied for 10 min. Baroinjury is discussed in terms of alterations of the lipid leaflet or of membrane proteins, and the mechanism of baroprotection in terms of stabilization of membrane components, under the effect of high pressure, by the association of glycerol with the proteins or the phosphate head groups of phospholipids.     

Mechanisms of the structural changes in erythrocyte membranes under the action of a shift in pH]

The effect of pH shifts (5--10) on erythrocyte "ghosts" has been studied using the IR spectroscopy. The process of regulation has been shown to take place within pH 7.15--8 range involving both protein (transition testified by absorption band changes 1520, 1540, 1635, 1645, 1585, 1696, 3305 CM-1) and lipid membrane components testified by absorption band splits 1745, 1470, 1380, 720 AND 1242 cm-1. The transition from a lesser to a higher regulating state of membrane structure happens unevenly, since the above changes take place within the narrow pH 7.15--8 interval, near the homeostase limit, being never observed at pH 5--7.15 or 8--10. It is supposed that the increase in regulation of both protein, phospholipid and lipid membrane fields is of phasic nature which presumably constitutes the basis for pH action mechanism as a regulation factor.     

PPAR-gamma activation fails to provide myocardial protection in ischemia and reperfusion in pigs

Peroxisome proliferator-activated receptor (PPAR)-gamma modulates substrate metabolism and inflammatory responses. In experimental rats subjected to myocardial ischemia-reperfusion (I/R), thiazolidinedione PPAR-gamma activators reduce infarct size and preserve left ventricular function. Troglitazone is the only PPAR-gamma activator that has been shown to be protective in I/R in large animals. However, because troglitazone contains both alpha-tocopherol and thiazolidinedione moieties, whether PPAR-gamma activation per se is protective in myocardial I/R in large animals remains uncertain. To address this question, 56 pigs were treated orally for 8 wk with troglitazone (75 mg x kg(-1) x day(-1)), rosiglitazone (3 mg x kg(-1) x day(-1)), or alpha-tocopherol (73 mg x kg(-1) x day(-1), equimolar to troglitazone dose) or received no treatment. Pigs were then anesthetized and subjected to 90 min of low-flow regional myocardial ischemia and 90 min of reperfusion. Myocardial expression of PPAR-gamma, determined by ribonuclease protection assay, increased with troglitazone and rosiglitazone compared with no treatment. Rosiglitazone had no significant effect on myocardial contractile function (Frank-Starling relations), substrate uptake, or expression of proinflammatory cytokines during I/R compared with untreated pigs. In contrast, preservation of myocardial contractile function and lactate uptake were greater and cytokine expression was attenuated in pigs treated with troglitazone or alpha-tocopherol compared with untreated pigs. Multivariate analysis indicated that presence of an alpha-tocopherol, but not a thiazolidinedione, moiety in the test compound was significantly related to greater contractile function and lactate uptake and lower cytokine expression during I/R. We conclude that PPAR-gamma activation is not protective in a porcine model of myocardial I/R. Protective effects of troglitazone are attributable to its alpha-tocopherol moiety. These findings, in conjunction with prior rat studies, suggest interspecies differences in the response to PPAR-gamma activation in the heart.     

Course of acute myocardial ischemia in dogs depending on the pharmacological background]

In acute myocardial ischemia of dogs glycogen is mobilized most completely and its break down products are utilized most efficaciously after administration of izatin rather than after gamma-hydroxybutyric acid (GABA) and guthymin. Izatin potentiates a beneficial effect of GABA on myocardial energy efficiency.     

Fluorescence studies of the aged erythrocyte membranes

The most important purpose of this research is to characterize by means of fluorescence polarization the structural and functional changes which occur in the membrane of the human erythrocytes during aging process. Our results provide evidence of a significant increase of membrane fluidity in the deep lipid core and in the lipid/protein boundary, in the aged erythrocytes. These features are associated with a rigidity of the membrane surface, as revealed by the anisotropy increase of a specific probe suitable for monitoring the membrane protein behaviour. These modifications could be considered as one of the mechanisms which contribute to alter erythrocyte rheological properties sufficiently to be recognised and removed within circulation.