Dynamic magnetic birefringence in a viscoelastic ferrocolloid.

A model is developed to describe the oscillations of optical anisotropy induced in a viscoelastic ferrocolloid (nanodispersion of magnetic particles) by an AC magnetic field. The viscoelasticity of the matrix (carrier medium) is assumed to obey the Jeffreys rheological scheme, whose advantage is that with the aid of just two viscous parameters and a single one for elasticity it enables one to vary the retarded mechanical response of the carrier from a weakly Maxwellian fluid to a medium with the rheology of a Kelvin gel. As the orientational motion of the particles driven by the AC field is always strongly affected by thermal motion, the occurring process is described with the aid of a kinetic (Fokker-Planck type) equation that combines diffusional and drift terms. On this basis, an exact evolution equation for the macroscopic optical anisotropy of a ferrocolloid is derived that is, however, just one link in an infinite chain of equations for statistical moments. The solution is obtained by applying effective field approximation: reducing the number of moment equations to their minimum and closing the chosen set. This solution is substituted to the scheme of a standard polarimetric set-up, and it is demonstrated how the peculiarities imparted by viscoelasticity should manifest themselves on the intensity of the light transmitted through the set up containing a ferrocolloid sample. This article is part of the theme issue 'Transport phenomena in complex systems (part 2)'.

Magnetic response of a viscoelastic ferrodispersion: From a nearly Newtonian ferrofluid to a Jeffreys ferrogel.

The theory of orientational motion of a Brownian magnetic nanoparticle embedded in a viscoelastic medium and subjected to a time-dependent uniform magnetic field is developed. The rheology of the viscoelastic environment of the particle is modeled by the Jeffreys scheme, which under variation of a minimal number of parameters is able to resemble a wide range of soft materials: from a weakly structured (nearly Newtonian) polymer solution to a gel. It is shown that in the Jeffreys model, the diffusional orientational motion of a particle is a combination of two modes, which could be associated with a fast motion within the polymer mesh cell and a slow displacement that involves deformation of the mesh, respectively. The dependencies of the reference times of both relaxation modes on the Jeffreys viscous and elastic parameters and temperature are found. It turns out that in substantially viscoelastic media, the rate of the slow mode (it dominates in relaxation) quadratically depends on the matrix temperature. This effect does not have analogs in linearly viscous systems. For an ensemble of magnetic nanoparticles in viscoelastic and gel Jeffreys matrices: (1) the dynamic magnetic susceptibility is derived and evaluated both within an exact approach and in a simple approximation; (2) the problem of magnetic relaxometry, i.e., evolution of magnetization after step-wise turning off the field, is solved; (3) the specific power loss caused by viscous dissipation generated by the particles under an ac field is analyzed as a function of the rheological parameters. Results (1) and (2) provide simple models for magnetic nanorheology; consideration (3) advances the physics of magnetic hyperthermia in viscoelastic and gel-like media.

Heart sensitivity to electrolyte composition of perfusion solution of rats after severe brain injury.

The in vitro model of isovolumic beating heart revealed enhanced sensitivity of the hearts from rats survived severe brain injury to concentration of Ca(2+), Na(+), and H(+) ions in the perfusion solution. Inhibition of myocardial contractile function after trauma was accompanied by destruction signs in cardiomyocyte sarcolemma and mitochondrial dysfunction.

Orientational kinetics of dipolar particles in a Maxwell fluid matrix: inertialess limit for the rotary microrheology.

We study magnetic response of an assembly of ferroparticles suspended in a viscoelastic matrix which is modeled by a Maxwell fluid with a unique stress relaxation time. The problem refers to the magnetic microrheology approach where deformational properties of a complex fluid are tested with the aid of embedded nanoparticle probes set to motion by an external ac magnetic field. A possibility is considered to simplify the description of the orientational kinetics of the system at the expense of neglecting inertia effects in particle rotary motion. It is shown that in this aspect a Maxwell matrix differs essentially from the Newtonian one. In the latter the inertialess approximation for the particles of the approximately 10nm size is valid practically unboundedly. For a viscoelastic matrix the inertialess approximation means an important restriction on the value of the stress relaxation time. Assuming weak nonequilibrium, the magneto-orientational relaxation times are found and low-frequency magnetic spectra of a viscoelastic suspension are determined in the presence of a constant (magnetizing) field.

[Myocardial contractility after brain injury].

Cardiac contractile function in the acute period after brain injury (BI) was studied on 158 non-inbred male albino rats, by using the isolated isovolumetrically contracted heart according to the procedure described by Fallen et al. The injured rats showed a significantly depressed left ventricular myocardial contractility during the hypoxic test, followed by reoxygenation, a lower positive chronic inotropic effect, and an increased diastolic defect with an enhanced rate of cardiac stimulation rates. Brain injury increased the dependence of cardiac performance on the concentration of Ca2+ in the perfused solution. The findings suggest the decreased resistance of the hearts of the rats that had sustained BI to pathogenetic factors.

Dynamic susceptibilities of an assembly of dipolar particles in an elastic environment.

Theoretical model to describe magnetodynamics of a ferrogel, i.e., an assembly of ferromagnetic nanoparticles embedded in a gel, is proposed. The reorientations of the particles are determined by the influence of the elastic matrix and the rotational Brownian motion. Due to the interplay between these two factors, the main parameter characterizing the static magnetic susceptibility of the system is the ratio of the elastic modulus of the matrix times particle volume to the thermal energy. It is shown that the main components of the dynamic magnetic-susceptibility tensor are determined by the combinations of the reference rates of several processes inherent to the system, namely, the elastic restoration of the particle orientation, Brownian rotary diffusion, and viscous relaxation of the particle angular momentum. In the framework of the model, absorption of the energy of an alternating external field by a ferrogel is studied. With allowance for the ever present interaction of elastic and Brownian forces, the effective relaxation times for the longitudinal and transverse components of the ferrogel magnetization are evaluated.

[Role of disorders of metabolism in rat myocardium and endotoxemia in the pathogenesis of post-resuscitation cardiodepression]. / Rol' narushenii metabolizma v miokarde krys i éndotoksemii v patogeneze postreanimatsionnoi kardiodepressii.

The model of 4-min clinical death due to acute blood loss was used to study cardiac contractility, myocardial metabolism and causes of endotoxemia in early postresuscitation period. The investigations were made on the whole body, isolated, isovolemically contracting heart and isolated papillary muscle. A marked reduction in functional myocardial reserves, maximal within the first 24 hours of postresuscitation, with dominant defects in relaxation was seen. Pathogenetic factors responsible for cardiodepression are the following: hypoxia, impairment of bioenergetics, hyperactivation of lipid peroxidation, acidosis, membrane destruction, endotoxemia.

[The membrane-protective effect of carnosine in the post-resuscitation period after acute lethal blood loss]. / Membranoprotektornoe deistvie karnozina v postreanimatsionnom periode posle ostroi smertel'noi krovopoteri.

Activation of serum enzymes in male rats was detected during the postresuscitation period after 4-6-min clinical death as a result of membrane destruction. Increase in the rate of lipid peroxidation and impairments of energy metabolism in the myocardium were responsible for destruction of cardiomyocyte biomembranes. Administration of carnosine (25 mg/kg body weight) simultaneously with compensation for blood loss obviated the membrane lipid bilayer destruction and contributed to the development of the optimal conditions for membrane-bound enzymes.

[The pathogenesis and correction of disorders of the heart rhythm in the early post-resuscitation period]. / K patogenezu i korrektsii narushenii ritma serdtsa v rannem postreanimatsionnom periode.

The frequency and nature of heart rhythm disturbances have been studied in experiments on random-bred male rats who survived 4- and 6-min clinical deaths of acute blood loss. Using correlation analysis it has been shown that the leading pathogenetic arrhythmogenic factors are: catecholamine excess, as well as excess of free fatty acids, lipid peroxidation products, lactate and Ca-ATPase inhibition. The efficacy of preventive (gutimin, inderal, oxipiridin-6, isoptin) and therapeutic (carnozin, creatinphosphate) use of the drugs affecting pathogenetic mechanisms of heart arrhythmias and thus stabilizing bioelectrical heart activity in the early postresuscitation period has been observed.

[Reperfusion injury of myocardial biomembranes after acute fatal hemorrhage and their correction with carnosine]. / Reperfuzionnye povrezhdeniia biomembran miokarda posle ostroi smertel'noi krovopoteri i ikh korrektsiia karnozinom.

Studies on inbred male rats revealed that ischemia associated with clinical death caused by haemorrhage with subsequent recirculation and reoxygenation during resuscitation led to an increase in enzyme activities in blood serum and perfusate passed through the coronary bed of isolated hearts, presumably due to impaired membrane integrity. Damage to cardiomyocyte membranes was caused by intensification of LPO concomitant with enhanced glycolysis and lactate accumulation in the cardiac muscle. Carnosine (25 mg/kg) injected simultaneously with recirculation and reoxygenation prevented membrane damage and created optimal conditions for the functioning of membrane enzymes.

Pathogenesis and pharmacorrection of early postresuscitation cardiac arrhythmia.

Effect of acute lethal blood loss on character and frequency of cardiac arrhythmias in postresuscitation period has been studied. Experiments were carried out on mongrel male rats resuscitated after 4- and 6-min clinical death caused by acute blood loss. Electric cardiac instability was found in early postresuscitation period. Pacemaker migration, paroxysmal ventricular tachycardia, blockades and extrasystole that lead to ventricular fibrillation were observed in 20 percent of cases. Supported by correlative analysis it has been established that the main arrhythmogenic factors are abundance of catecholamines, free fatty acids, dienic conjugates, lactate and inhibition of Ca dependent ATPase. Antiarrhythmogenic effects of antihypoxant gutimin, the beta-adrenoreceptor blocker inderal, antioxidant oxypiridin-6 were noticed after their separate administration before clinical death. The same effect of carnosine and phosphocreatine administered during resuscitation also was noticed.

[Effects of carnosine on systemic hemodynamics and myocardial metabolism in rats in the early postresuscitation period]. / Vliianie karnozina na sistemnuiu gemodinamiku i metabolizm miokarda krys v rannem postreanimnatsionnym periode.

It was demonstrated in experiments on male rats that acute lethal blood loss and subsequent resuscitation after 4- and 6-min clinical death induce lipid peroxidation processes, decreased antioxidant enzyme activity, cause activation of anaerobic glycolysis in the myocardium. This metabolic heart impairment causes hemodynamic instability in postresuscitation period. 25 mg/kg of carnosine injected during resuscitation decreased functional-metabolic heart impairments and hemodynamic disarrangement as well as early postresuscitation lethality. The authors attribute positive carnosine effect to its significant antioxidant activity.

[The use of carnosine for reducing the post-resuscitation damage to the heart following acute fatal blood loss]. / Ispol'zovanie karnozina dlia umen'sheniia postreanimatsionnykh povrezhdenii serdtsa posle ostroi smertel'noi krovopoteri.

The experiments on random-bred male rats have established that 4 and 6 min clinical death of acute blood loss initiated lipid peroxidation processes (LPO), causing biomembrane damage, enhanced adenyl nucleotide catabolism, activated glycolysis and glycogenolysis in the heart muscle and caused cardiac arrhythmias. Carnosine at a dose 25 mg/kg administered together with pumped blood enhanced resuscitation efficacy and reduced considerably lethality in the early rehabilitation period. A favourable effect of carnosine is associated with its ability to restrict LPO processes, inhibit glycolysis and glycogenolysis and create optimal conditions for the functioning of membrane-located lipid-dependent enzymes.

Functional metabolic heart impairment after acute lethal hemorrhage followed by resuscitation.

Effects of acute lethal blood loss on postresuscitation heart impairment has been studied. Experiments were performed in mongrel male rats anesthesized with sodium pentobarbital (25 mg/kg). Functional metabolic heart impairments have been evaluated in different terms after resuscitation by isolated perfused heart method (Fallen et al., J. Appl. Physiol, 22 (1967) 836-839). It has been established that maximal heart injury occurs in the first hours after resuscitation. It is supported by the following findings: depression of myocardium contractile function grew; enzyme excretion from cardiomyocytes in coronary flow increased: efficacy of glucose utilization by means of carried function decreased; pyruvate excretion in coronary flow elevated. Because of severe course of postresuscitation period functional metabolic heart disturbances are more pronounced and preserved for a long time.