Statistical approach on the inter-yarn friction behavior of the dual-phase STF/ρ-Aramid impregnated fabrics via factorial design and 3D-RSM.

Shear thickening fluids (STFs) refer to non-Newtonian fluids of the dilatant variety, wherein their viscosity experiences a significant surge with an escalation in the shear rate. In this investigative work, the friction behavior between yarns (pull-out) and absorption of static and kinetic energy during the phenomenon of friction between yarns in STFs are performed by monophase (MP-STF) adding nano SiO2 and dual-phase (MP-STF) adding carbon nanotubes. The ρ-Aramid fabrics were reinforced via the "foulard process", and carried out on MP-STF, and DP-STF/ρ-Aramid-impregnated fabrics to evaluate and compare with the enhancement in interfacial friction properties between yarns. The results showed that DP-STF has more significant than MP-STF and MP-STF in ultimate load, kinetic shear stress, static shear stress, and friction energy level effects. The DP-STF exhibits various friction enhancement mechanisms at the yarn interface, leading to higher absorption of static and kinetic energy related to interfacial friction, as indicated by the results obtained. Furthermore, the DP-STF/ρ-Aramid impregnated fabrics exhibited ultimate load (22.23 ± 0.522 N), kinetic shear stress (35.73 ± 0.850 MPa*100), static shear stress (36.28 ± 0.900 MPa*100), and friction energy level (610.33 ± 0.250). Increased ultimate load (581.7% and 180.7%), kinetic shear stress (621.4% and 174.6%), static shear stress (550.5% and 159.1%), and friction energy level (680.2 and 186.7%) compared to WT-STF and MP-STF, respectively. The current discoveries hold immense potential for various applications in the fields of engineering and smart material technologies. These applications span a multiplicity of industries, including sports products, medical advancements, space technology, as well as protective and shielding products.

Effects of UV sensitivity and accelerated photo-aging on stab resistance of ρ-aramid fabrics impregnated with shear thickening fluids (STFs).

The use of Kevlar in the field of ballistic and stabbing protection has been studied by researchers in polymeric composites for this purpose. This study presents complementary knowledge on energy absorption and dissipation in ρ-aramid fabric impregnated with shear thickening fluids (STFs), especially aiming to obtain better protection against impacts that are deeply associated with STFs, as well as color change, accelerated aging (QUV), and penetration depth (drop tower test). In addition, Scanning Electron Microscopy (SEM), and Fourier transform infrared spectroscopy (FTIR) was performed. The research shows that there was a good distribution of STF particles on the ρ-Aramid fabric surface, promoting increased friction between the interfilament and the yarns, further increasing performance and, consequently, improving the energy absorption and dissipation mechanism and, also, the penetration effectiveness in relation to non-impregnated ρ-Aramid fabric. Regarding the protection efficiency against UV exposure (250-400 nm region), there was a significantly decreased compared to those non-impregnated Kevlar® woven with STFs. The FTIR analysis showed that the conditions of aging, after exposure to UV, did not produce new functional groups, that is, there was no chemical modification. Finally, Kevlar fabric impregnated with STFs improved penetration depth performance with the blades independent of the blade type with up to 81% increase in resistance. This result was improved due to interactions between the nanoparticles present in STFs, yarns, and even high-performance woven impregnated with shear-thickening fluids.

Spontaneous emission in inertial and dissipative nematic liquid crystals: the role of critical phenomena.

We develop a rigorous, field-theoretical approach to the study of spontaneous emission in inertial and dissipative nematic liquid crystals (LCs), disclosing an alternative application of the massive Stückelberg gauge theory to describe critical phenomena in these systems. This approach allows one not only to unveil the role of phase transitions in the spontaneous emission in LCs but also to make quantitative predictions for quantum emission in realistic nematics of current scientific and technological interest in the field of metamaterials. Specifically, we predict that one can switch on and off quantum emission in LCs by varying the temperature in the vicinities of the crystalline-to-nematic phase transition, for both the inertial and dissipative cases. We also predict from first principles the value of the critical exponent that characterizes such a transition, which we show not only to be independent of the inertial or dissipative dynamics, but also to be in good agreement with experiments. We determine the orientation of the dipole moment of the emitter relative to the nematic director that inhibits spontaneous emission, paving the way to achieve directionality of the emitted radiation, a result that could be applied in tuneable photonic devices such as metasurfaces and tuneable light sources.

The blockade of angiotensin AT1 and aldosterone receptors protects rats from synthetic androgen-induced cardiac autonomic dysfunction.

AIM: This study aimed to evaluate the combined effects of exercise and antagonists of the angiotensin II and aldosterone receptors on cardiac autonomic regulation and ventricular repolarization in rats chronically treated with nandrolone decanoate (ND), a synthetic androgen. METHODS: Thirty male Wistar rats were divided into six groups: sedentary, trained, ND-treated, trained and ND-treated, trained and treated with both ND and spironolactone, and trained and treated with both ND and losartan. ND (10 mg kg(-1) weekly) and the antagonists (20 mg kg(-1) daily) of the angiotensin II AT1 (losartan) and aldosterone (spironolactone) receptors were administered for 8 weeks. Exercise training was performed using a treadmill five times each week for 8 weeks. Following this 8-week training and treatment period, electrocardiogram recordings were obtained to determine the time and frequency domains of heart rate variability (HRV) and corrected QT interval (QTc). RESULTS: Nandrolone decanoate treatment increased the QTc interval and reduced the parasympathetic indexes of HRV (RMSSD, pNN5 and high-frequency power) in sedentary and trained rats. The ratio between low- and high-frequency power (LF/HF) was higher in ND-treated groups. Both losartan and spironolactone treatments prevented the effects of ND on the QTc interval and the HRV parameters (RMSSD, pNN5, high-frequency power, and the LF/HF ratio). CONCLUSION: Our results show that chronic treatment with a high dose of ND induces cardiac parasympathetic dysfunction and disturbances in ventricular repolarization in both sedentary and exercised rats. Furthermore, inhibiting the renin-angiotensin-aldosterone system using losartan, or spironolactone, prevented these deleterious effects.

Cardiac autonomic dysfunction in anabolic steroid users.

This study aimed to evaluate if androgenic-anabolic steroids (AAS) abuse may induce cardiac autonomic dysfunction in recreational trained subjects. Twenty-two men were volunteered for the study. The AAS group (n = 11) utilized AAS at mean dosage of 410 ± 78.6 mg/week. All of them were submitted to submaximal exercise testing using an Astrand-Rhyming protocol. Electrocardiogram (ECG) and respired gas analysis were monitored at rest, during, and post-effort. Mean values of VO2 , VCO2 , and VE were higher in AAS group only at rest. The heart rate variability variables were calculated from ECG using MATLAB-based algorithms. At rest, AAS group showed lower values of the standard deviation of R-R intervals, the proportion of adjacent R-R intervals differing by more than 50 ms (pNN50), the root mean square of successive differences (RMSSD), and the total, the low-frequency (LF) and the high-frequency (HF) spectral power, as compared to Control group. After submaximal exercise testing, pNN50, RMSSD, and HF were lower, and the LF/HF ratio was higher in AAS group when compared to control group. Thus, the use of supraphysiological doses of AAS seems to induce dysfunction in tonic cardiac autonomic regulation in recreational trained subjects.

Cardiac effects of anabolic steroids: hypertrophy, ischemia and electrical remodelling as potential triggers of sudden death.

Anabolic-androgenic steroids (AAS) are synthetic testosterone derivatives developed to maximise anabolic activity and minimise androgenic activity. AAS abuse is widespread among both athletes and non-athletes at fitness centres and is becoming a public health issue. In addition to their atherogenic, thrombogenic and spastic effects, AAS have direct cardiotoxic effects by causing hypertrophy, electrical and structural remodelling, and contractile dysfunction and by increasing the susceptibility to ischemic injuries. All of these factors contribute to an increased risk of ventricular arrhythmias and sudden cardiac death.

Photocatalytic activity and UV-protection of TiO2 nanocoatings on poly(lactic acid) fibres deposited by pulsed magnetron sputtering.

The application of nanocoatings in the textile finishing is increasingly being explored because they open a whole new vista of value-addition possibilities in the textile sector. In the present work, low temperature pulsed DC magnetron sputtering method was used to create functional TiO2 nanocoatings on poly(lactic acid) textile fibres surfaces. In this study, the principal objectives in the application of TiO2 nanocoatings to textile materials are to impart UV protection functions and self-cleaning properties to the textile substrates. The TiO2 films were characterized by X-ray diffraction, scanning electron microscopy, atomic force microscopy, transmission electron microscopy, UV-visible spectroscopy and contact angle analysis. The Photocatalytic activity of the films was tested by measuring the photodegradation rates of rhodamine-B dye aqueous solution under UV light irradiation. The ultraviolet protection function was tested according to the Australian/New Zealand standards. It was observed that the TiO2 nanocoatings on poly(lactic acid) fibres showed an excellent ultraviolet protection (> 40) function and the photocatalytic efficiency was maintained even after a strong washing treatment.

The negative inotropic action of canrenone is mediated by L-type calcium current blockade and reduced intracellular calcium transients.

BACKGROUND AND PURPOSE: Adding spironolactone to standard therapy in heart failure reduces morbidity and mortality, but the underlying mechanisms are not fully understood. We analysed the effect of canrenone, the major active metabolite of spironolactone, on myocardial contractility and intracellular calcium homeostasis. EXPERIMENTAL APPROACH: Left ventricular papillary muscles and cardiomyocytes were isolated from male Wistar rats. Contractility of papillary muscles was assessed with force transducers, Ca(2+) transients by fluorescence and Ca(2+) fluxes by electrophysiological techniques. KEY RESULTS: Canrenone (300-600 micromol L(-1)) reduced developed tension, maximum rate of tension increase and maximum rate of tension decay of papillary muscles. In cardiomyocytes, canrenone (50 micromol L(-1)) reduced cell shortening and L-type Ca(2+) channel current, whereas steady-state activation and inactivation, and reactivation curves were unchanged. Canrenone also decreased the Ca(2+) content of the sarcoplasmic reticulum, intracellular Ca(2+) transient amplitude and intracellular diastolic Ca(2+) concentration. However, the time course of [Ca(2+)](i) decline during transients evoked by caffeine was not affected by canrenone. CONCLUSION AND IMPLICATIONS: Canrenone reduced L-type Ca(2+) channel current, amplitude of intracellular Ca(2+) transients and Ca(2+) content of sarcoplasmic reticulum in cardiomyocytes. These changes are likely to underlie the negative inotropic effect of canrenone.

Cardiac effects of oxytocin: is there a role for this peptide in cardiovascular homeostasis?

Oxytocin is well known for its role in reproduction. However, evidence has emerged suggesting a role in cardiovascular and hydroelectrolytic homeostasis. Although its renal effects have been characterized, the cardiac ones have not been much studied. Therefore, we aimed to investigate the cardiac effects of oxytocin both in vivo and in vitro. In unanesthetized rats (n=6) intravenous oxytocin (1 mug) decreased dP/dt(max) by 15% (P<0.05) and heart rate by 20% (P<0.001), at the first minute after injection. dP/dt(max) was still lower in OT-treated rats than in controls (n=8) after 15 min (P<0.05), while heart rate returned to control values after 5 min. In isolated hearts, oxytocin was able to promote negative inotropic and chronotropic effects. Perfusion with 10(-5), 10(-6) and 10(-7)M oxytocin resulted in approximately 60% (P<0.01), 25% (P<0.01) and 10% (P<0.05) reduction of left ventricle developed pressure, without effect in lower concentrations (10(-10) to 10(-8) M). Also, dP/dt(max) was reduced by 45 and 20% (10(-5) e 10(-6) M; P<0.01), while diastolic pressure raised and heart rate fell only with 10(-5)M oxytocin (P<0.05). Intravenous oxytocin (1 mug; n=6) increased arterial pressure by 22% at the first minute (+23+/-3 mm Hg; P<0.001), returning to control value thereafter. Thus, oxytocin is able to promote directly negative inotropic and chronotropic effects, but its in vivo effect also involves a reflex mechanism, originated from its pressor effect.

cGMP-mediated inhibition of cardiac L-type Ca(2+) current by a monoclonal antibody against the M(2) ACh receptor.

The effects of a monoclonal antibody (B8E5) directed against the second extracellular loop of the muscarinic M(2) receptor were studied on the L-type Ca(2+) currents (I(Ca,L)) of guinea pig ventricular myocytes using the whole cell patch-clamp technique. Similar to carbachol, B8E5 reduced the isoproterenol (ISO)-stimulated I(Ca,L) but did not significantly affect basal I(Ca,L). Atropine blocked the inhibitory effect of B8E5. The electrophysiological parameters of ISO-stimulated I(Ca,L) were not modified in presence of B8E5. Inhibition of I(Ca,L) by B8E5 was still observed when intracellular cAMP was either enhanced by forskolin or maintained constant by using a hydrolysis-resistant cAMP analog (8-bromoadenosine 3',5'-cyclic monophosphate) or by applying the phosphodiesterase inhibitor IBMX. The effect of B8E5 was mimicked by 8-bromoguanosine 3',5'-cyclic monophosphate, a potent stimulator of cGMP-dependent protein kinase, and prevented by a selective inhibitor of nitric oxide-sensitive guanylyl cyclase [1H-(1,2,4)oxadiazolo[4,3-a]quinoxaline-1-one]. These results indicate that the antibody B8E5 inhibits the beta-adrenergic-stimulated I(Ca,L) through activation of the M(2) muscarinic receptor and further suggest that the antibody acts not via the classical pathway of decreasing intracellular cAMP, but rather by increasing cGMP.

Induction of in vitro heart block is not restricted to affinity purified anti-52 kDa Ro/SSA antibody from mothers of children with neonatal lupus.

The ability of affinity purified anti-52 kDa Ro/SSA antibody from patients without obstetric history of neonatal lupus to cause heart block using an experimental model was investigated. IgG-enriched fractions from sera of 20 systemic lupus erythematosus (SLE) and one Sjögren's syndrome (SS) all positives for anti-Ro/SSA antibodies as detected by CIE, were perfused on isolated whole rabbit hearts. Only six (29%) samples induced A-V block, five of them presenting low anti-Ro/SSA titre. All of them recognized the 52 kDa isoform on ELISA whereas only one had a concomitant binding to the 60 kDa protein. Moreover, affinity purified antibodies from two sera previously known to induce A-V block were obtained by affinity chromatography using a column containing the full-length 52 kDa Ro/SSA fusion protein. Paired eluate and effluent devoid of anti-52 kDa activity from the same patient were individually perfused in whole hearts. The ability to cause cardiac blockade was restricted to the affinity anti-52 kDa eluates. In addition, anti-52 kDa eluates from three IgG fractions that primarily failed to induce blockade remained ineffective. The present study has added to our knowledge that affinity anti-52 kDa Ro/SSA antibodies from mothers with healthy infants are capable of causing in vitro cardiac conduction disturbances. A prospective follow up of these patients will better delineate the clinical usefulness of this experimental model.

Ca2+-entry blockade by CAF603, a carotane sesquiterpene isolated from Trichoderma virens.

Isometric tension recordings and patch-clamp methods were combined to explore the functional effects and mechanisms of action of 8-daucene-3,4-diol (CAF603), a carotane sesquiterpene isolated from the fungus Trichoderma virens. CAF603 (1-100 microM) inhibited the spontaneous motility of guinea-pig portal vein, duodenum and ileum, and the Ca2+-induced tension of depolarized ileum strips. These effects were not antagonized by either iberiotoxin or glyburide. CAF603 increased the spontaneous motility of guinea-pig detrusor muscle, but inhibited the contraction induced by high-KCl, depolarizing salines. CAF603 blocked L-type Ca2+ channel currents of rabbit cardiac myocytes. It is proposed that Ca2+-entry blockade accounts for the inhibitory effects of CAF603 on smooth muscle contractility, whereas the stimulation of spontaneous motility of detrusor muscle is ascribed to blockade of Ca2+-activated K+ (BKCa) channel currents. The latter interpretation is consistent with the allosteric modulation of charybdotoxin binding to BKCa in smooth muscle membranes [Lee et al., 1995. J. Nat. Prod. 58, 1822-1828].

Sera from chronic chagasic patients with complex cardiac arrhythmias depress electrogenesis and conduction in isolated rabbit hearts.

BACKGROUND: Immune dysfunction has long been proposed as a mechanism for the etiopathogenesis of the chronic phase of Chagas' disease. Antibodies of chagasic patients have been shown to interfere with electric and mechanical activity of embryonic myocardial cells in culture. Here, we demonstrate that antibodies derived from a group of chronic chagasic patients are able to induce disturbances in the electrogenesis and conduction in isolated adult rabbit hearts. METHODS AND RESULTS: Sera from chronic chagasic patients with complex cardiac arrhythmias (ChA+) decreased heart rate (from 131+/-26 to 98+/-37 bpm [mean+/-SD]; n=6; P<.05) in isolated rabbit hearts when perfused at a dilution of 1:100 (vol:vol) by the Langendorff method. Sera from another experimental group of four chronic chagasic patients without complex arrhythmias (ChA-) and two control groups composed of five Wolff-Parkinson-White (WPW) syndrome patients and five orthopedic surgery patients did not affect heart rate when tested under similar conditions. In addition, sera from five of six ChA+ patients and from one WPW patient induced AV conduction blockade. Effects of the sera from ChA+ patients are due to their IgG fractions. Both serum and IgG effects are blocked by atropine (10 micromol/L). CONCLUSIONS: Antibodies of ChA+ patients decrease heart rate and induce AV conduction block in isolated adult rabbit hearts through activation of muscarinic receptors.

Electrophysiological properties of L-type Ca2+ currents in isolated adult mouse ventricular myocytes.

The whole-cell configuration of the patch-clamp technique was used to analyze the electrophysiological characteristics of the L-type calcium current (ICa) in single ventricular myocytes from hearts of adult mice. In Tyrode solution, ICa activated ar -30mV peaked at 0 mV, and reverted near +60 mV, the peak current density was -8.1 +/- 2.5 pA/pF (N = 14). In a Na(+)- and K(+)-free solution containing 12 microM tetrodotoxin, and 10 mM Ca2+ or Ba2+ as charge carrier, the current-voltage relationship and the voltage dependence of inactivation were shifted about 10 mV to more depolarized voltages. The maximum Ba2+ current was two-times greater than the maximum Ca2+ current. The voltage dependencies of steady-state activation and inactivation were determined within the range of -70 to l mV and fitted with Boltzmann relations. The Ca2+ current showed half-maximal activation at -9.94 +/- 3.86 mV (slope factor (k) = 5.9 +/- 0.68 mV) and half-maximal inactivation at -27.65 +/- 5.74 mV (k = 6.37 +/- 2.79 mV), while the Ba2+ current showed half-maximal activation at -0.35 +/- 2.43 mV (k = 6.0 +/- 0.84 mV) and half-maximal inactivation at -20.33 +/- 2.40 mV (k = 5.36 +/- 1.10 mV). The time course of recovery of Ba2+ current from inactivation could be described using a single exponential function with a time constant of 83.37 msec. The overlap of activation and inactivation curves suggests the existence of an L-type Ca2+ window current with a maximal amplitude near -20mV.

Eletrophysiological properties of L-type Ca2+ currents in isolated adult mouse ventricular myocytes

The Whole-cell configuration of the patch-clamp technique was used to analyze the electrophysiological characteristics of the L-type calcium current (Ica) in single ventricular myocytes from hearts of adult mice. In Tyrode solution, ICa activated at -30 mV peaked at 0mV, and reverted near +60 mV. At 0mV, the peak current density was -8.1 + 2.5 pA/pF (N = 14). In a Na+ - and K+ -free solution containing 12 muM tetrodotoxin, and 10 mM Ca2+ or Ba2+ as charge carrier, the current-voltage relationship and the voltage dependence of inactivation were shifted about 10 mV to more depolarized voltages. The maximum Ba2+ current was two-times greater than the maximum Ca2+ current. The voltage dependencies of steady-state activation and inactivation were determined within the range of -70 to +50 mV and fitted with Boltzmann relations. The Ca2+ current showed half-maximal activation at -9.94 + 3.86 mV (slope factor (k) = 5.9 + 0.68 mV) and half-maximal inactivation at -27.65 + 5.74 mV (k = 6.37 + 2.79 mV), while the Ba2+ current showed half-maximal activation at -0.35 + 2.43 mV (k = 6.0 + 0.84 mV) and half-maximal inactivation at -20.33 + 2.40 mV (k = 5.36 + 1.10 mV). The time course of recovery of Ba2+ current from inactivation could be described using a single exponential function with a time constant of 83.37 msec. The overlap of activation and inactivation curves suggests the existence of an L-type Ca2+ window current with a maximal amplitude near -20mV.

Effects of extracellular sodium, quinidine, and ryanodine on slow response excitability in rabbit atrial trabeculae.

1. We investigated Na(+)-Ca2+ exchange and the involvement of the sarcoplasmic reticulum in frequency-dependent slow response excitability enhancement in rabbit atrial trabeculae. 2. Slow responses were induced in a modified Tyrode solution containing high K+ and Ba2+ and conventional electrophysiological techniques were used for stimulating and recording membrane potentials. 3. Under these conditions, the frequency-dependence of slow response excitability can be demonstrated with excitability enhancement as stimulation frequency is increased (0.25 to 1.0 Hz). 4. The frequency-dependent excitability enhancement depends on external Na+, increasing in high-[Na+]o (173.8 mM) and decreasing in low-[Na+]o (103.8 mM) media. 5. Quinidine (10 microM) and ryanodine (10 microM) decrease frequency-dependent slow response excitability enhancement. 6. These results indicate that the Na(+)-Ca2+ exchange might have an important role in frequency-dependent excitability enhancement of slow responses. Moreover, we suggest that the control of internal Ca2+ by the sarcoplasmic reticulum might have an additional role in regulating the excitability enhancement process in depolarized atrial trabeculae.

Effects of extracellular sodium, quinidine, and ryanodine on slow response excitability in rabbit atrial trabeculae

1. We investigated Na(+)-Ca2+ exchange and the involvement of the sarcoplasmic reticulum in frequency-dependent slow response excitability enhancement in rabbit atrial trabeculae. 2. Slow responses were induced in a modified Tyrode solution containing high K+ and Ba2+ and conventional electrophysiological techniques were used for stimulating and recording membrane potentials. 3. Under these conditions, the frequency-dependence of slow response excitability can be demonstrated with excitability enhancement as stimulation frequency is increased (0.25 to 1.0 Hz). 4. The frequency-dependent excitability enhancement depends on external Na+, increasing in high-[Na+]o (173.8 mM) and decreasing in low-[Na+]o (103.8 mM) media. 5. Quinidine (10 microM) and ryanodine (10 microM) decrease frequency-dependent slow response excitability enhancement. 6. These results indicate that the Na(+)-Ca2+ exchange might have an important role in frequency-dependent excitability enhancement of slow responses. Moreover, we suggest that the control of internal Ca2+ by the sarcoplasmic reticulum might have an additional role in regulating the excitability enhancement process in depolarized atrial trabeculae

Cellular mechanism of the conduction abnormalities induced by serum from anti-Ro/SSA-positive patients in rabbit hearts.

In this study, IgG fractions from sera of SLE patients with anti-Ro/SSA or anti-Ro/SSA and anti-La/SSB activity were tested in Langendorff preparations of adult rabbit hearts, aiming to reproduce the cardiac manifestations observed in neonatal lupus in an experimental model. The hearts were perfused with normal Tyrode's solution for 30 min, followed by perfusion with Tyrode's containing 0.3 mg/ml of anti-Ro/SSA- (or anti-Ro/La-) positive IgG (nine sera), anti-ribonucleoprotein (RNP)-positive IgG (five sera), or IgG fractions from normal donors (five sera). In one third of the experiments done with anti-Ro/La-positive IgG, heart block was observed. With the remaining fractions, a decrease in heart rate of 17.1% was observed, but normal sinus rhythm was maintained. The IgG fractions with anti-RNP activity (five experiments) and from normal sera (six experiments) reduced heart rates by 12.9 and 3.3%, respectively, but heart block was not observed. To further characterize the cellular mechanisms involved in the conduction disturbances observed in the whole rabbit hearts, we conducted experiments with ventricular myocytes isolated from young rabbit hearts, studied by whole cell patch-clamp technique. In these experiments, the slow inward currents were analyzed during the superfusion of the cell with normal Tyrode's solution and 5 min after superfusion with Tyrode's solution containing 0.3 mg/ml of anti-Ro/SSA- (or anti-Ro/La-) positive IgG (five sera), anti-RNP-positive IgG (three sera), or IgG from normal donors (four sera). Resting and action potential amplitudes were not affected by any of the sera used. The anti-Ro/SSA IgG fraction induced a mean reduction in the peak slow inward current of 31.6%. IgG fractions with anti-RNP activity reduced slow inward current by 4.4%, whereas IgG fractions from normal donors increased this current by 3.3%. IgG-free fractions from sera of patients with anti-Ro/SSA activity did not alter the peak slow inward current. These results show, for the first time, that the presence of anti-Ro/SSA or anti-Ro/SSA and anti-La/SSB antibody activity in IgG fractions from lupus patients' sera can induce cardiac conduction disorders similar to those observed in neonatal lupus.

Frequency-dependent excitability enhancement in isolated ventricular myocardial cells.

The understanding of the mechanisms underlying the frequency-dependent slow response excitability enhancement has been hindered by the problems inherent in multicellular preparations. These include ion accumulation/depletion in intercellular spaces and difficulties in the spatial control of transmembrane voltage. In the present communication we show that isolated ventricular cells exposed to a depolarizing (high potassium-barium containing) solution present electrophysiological properties similar to those of multicellular preparations: stable resting potential of -45.2 +/- 0.7 mV (mean +/- SEM, N = 57) in 75% of the cells and spontaneous activity in the remaining 25% (maximum diastolic potential of -41.9 +/- 1.2 mV, N = 19); high input resistance and slow response, under current clamp conditions. Under whole cell voltage clamp conditions with -45 mV holding potential, transient outward and delayed potassium currents as well as typical L type calcium channel are present. These cells also present the frequency-dependent excitability enhancement of the slow response, with the threshold stimulus at 1 Hz corresponding to about 50% of that obtained at 0.1 Hz. Thus, isolated ventricular cells constitute a suitable model for the study of frequency-dependent excitability enhancement of the slow response.

Frequency-dependent excitability enhancement in isolated ventricular myocardial cells

The understanding of the mechanisms underling the frquency-dependent slow response ecitability enhancement has been hndered by the problem inhyerent in multicellular preparations. These include ion acdcumulation/depletion in intercellular space and difficulties in the spatial control of transmembrane voltage. In the present communication we show that isolated ventricular cells exposed to a depolarizing (high potassium-barium containing) solution present electrophysiological properties similar to those of mulcellular preparations: stable resting potential of -45.2 ñ 0.7 mV (mean ñ SEM, N = 57) in 75% of the cells and spontaneous activity in the remaining 25% (maximum diatolic potential of -41.9 ñ 1.2 mV, N=19)ñ high input resistance and slow response, under current clamp conditions. Under whole cell voltage clamp conditions with -45 mV holding potential, transient outward and delayed potassium currents as well as typical L type calcium channel are present. These cells also present thye frequency-dependent excitability enhancement of the slow response, with the threshold stimulus at 1 Hz corresponding to about 50% of that obtained at 0.1 Hz. Thus, isolated ventricular cells constitute a suitable model for the study of frequency-dependent exitability enhancement of the slow response