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The theoretical simulation of single Pb atom motion in faulted and unfaulted halves of a Si(1 1 1)-(7 × 7) surface were performed using the kinetic Monte Carlo method. Modifying diffusion barriers within the unit cell, the results were fitted to STM observations over a wide temperature range between 50 and 300 K. The average activation energy of a single atom jump was estimated to be approximately 0.1–0.2 eV, giving a diffusion coefficient of ≈3 × 10 −5 cm 2 s −1 at 300 K inside the Si(1 1 1)-(7 × 7) unit cell.

The adsorption of Cu atoms on the Si(1 1 1)-7×7 surface was studied by scanning tunnelling microscopy. The flash up to ∼550 °C stimulates a reaction leading to the massive re-arrangement of the surface resulting in the formation of 7×7 domains separated by disordered regions. Mostly, copper atoms are concentrated in these regions. Isolated Cu atoms were found incorporated in 7×7 reconstruction on the domains surface.

The adsorption of Cu atoms on a Si(1 1 1)-7×7 surface was studied using scanning tunnelling microscopy. Two different kinds of clusters were found at room temperature and we associate them with copper atoms embedded in subsurface layers. Short annealing at ∼550 °C stimulates a reaction, leading to the substitution of corner Si adatoms in the 7×7 unit cell. This configuration is stable with respect to continuing thermal processing.

The temperature-dependent coexistence of Si 0.28 Pb 0.72 /Si( 111) and Si(111)-( 1 ×1)-Pb phases was investigated using scanning tunneling microscopy. An area of (I x 1)-Pb islands was monitored as a function of temperature ranging from room temperature up to 400°C. The movie strategy was applied in order to acquire successive images of a selected region. It was found that this area fluctuates quasi-periodically in time, with amplitude depending on temperature. The strongest fluctuations (up to 10% of the mean area value) were observed at 210°C. These fluctuations were restricted to the defect-free parts of the island perimeter, the rest of the ( 1 ×1)-Pb phase being stable. A further increase in temperature lead to a monotonous temperature-dependent decrease in ( 1 ×1)-Pb areas. This decrease was observed to be strongly tip-influenced at temperatures slightly above 210°C, while at higher temperatures the desorption of Pb atoms prevailed.

Recently, a review of APS experimental results on the electron scattering investigation was published. In the frame of this work ultrathin layers were deposited by in situ evaporation on polycrystalline substrates. Ti, Cr, Mn and Ni were chosen as substrates and deposits and APS signal intensities were measured as functions of the overlayer thickness and energy interval of electrons taken into account as signal carriers. Among other quantitative results it was observed that the number of tertiary electrons created at the disappearance of one elastically reflected electron at a threshold potential depended on the overlayer thickness. This effect remained unexplained. In the present work an attempt to interpret this behaviour is made in terms of different escape depths of electrons contributing to the APS or DAPS signal.

In this contribution we show that the screening effect around the Si dopant atoms in GaAs can be observed not only at low temperature, as reported earlier, but also at room temperature.

Appearance potential spectroscopy (APS) was introduced in the early seventies as a relatively simple surface sensitive analytical technique. Later, various processes involved in APS signal formation have been investigated, making use of sophisticated experimental set-ups. In this way, APS became a possible tool for studying electron transport processes in the surface region of solids. In the experimental part of the submitted work that represents a considerable extension of the previously obtained results, ultrathin layers were deposited by in situ evaporation on polycrystalline substrates. Ti, Cr, Mn and Ni were chosen as substrates and deposits in a series of overlayer experiments. The L 3 , L 2 and L 1 (if possible) subshell signal intensities have been measured as a function of the overlayer thickness. Auger spectra have also been taken to monitor the cleanliness of the substrates and the overlayers. The discrete model of the APS signal formation according to Eckertova, instead of the common exponential model, offered the possibility of fitting the experimental results. Its parameters represent the probabilities of the basic types of electron interactions related to one atomic layer. Approximate values of these quantities have been calculated.

Contributions of electrons with different energies to Auger electron appearance potential spectroscopy (AEAPS) have been investigated. Appearance potential spectra amplitude dependences have been measured for Ti, Cr, Mn and Ni by means of a previously exploited method using a spherical three-grid retarding field system. The effective dimensionless coefficient σ eff , representing the number of slow electrons emitted at the disappearance of one elastically reflected electron at a threshold potential, ranges from 2.7 to 3.5 for L 2,3 subshells and from 9 to 11 for L 1 subshells. These results have been accounted for in terms of fast, highly probable Coster–Kronig transitions which turned out to be the only possibility for relaxation of the L 1 subshells of the materials under investigation. This explanation has been supported by a direct comparison with both former and recent experimental results. © 1997 Elsevier Science B.V.

The time evolution of fractal objects is ivestigated. A mechanism of iterative development is suggested based on the partial scaling of the initiator-generator fractals. The approach enables us to estimate the Hausdorff dimension of the resulting objects. An example is given from the modeling of catalytic gas-solid reactions.

Ultrathin chromium layers of increasing thickness were deposited on titanium substrates under UHV conditions. AFM was used to check the surface morphology and to optimize the evaporation parameters. In-situ AES and APS measurements were performed on these samples. The APS overlayer and substrate signal intensities, as a function of the overlayer thickness, have been measured. Instead of the common exponential model of the overlayer signal rise and the substrate signal attenuation, respectively, the discrete model according to Eckertova was used to fit the experimental results. Its parameters represent the probabilities of the basic types of the electron interactions at one atomic layer. Approximate values of these quantities have been calculated.

Two types of brown coal, oxyhumolite and peat were studied with respect to their ability to remove heavy metals from waste waters. The results showed that the calcium loaded form of these materials can be effectively used for metal extraction by ion exchange with calcium. The proposed method can be recommended for concentrations of metals less than 10 mM.

Chronic hypertension may have a negative impact on the myocardial response to ischemia. On the other hand, intrinsic ischemic tolerance may persist even in the pathologically altered hearts of hypertensive animals, and may be modified by short- or long-term adaptation to different stressful conditions. The effects of long-term limitation of living space (ie, crowding stress [CS]) and brief ischemia-induced stress on cardiac response to ischemia/reperfusion (I/R) injury are not yet fully characterized in hypertensive subjects. The present study was designed to test the influence of chronic and acute stress on the myocardial response to I/R in spontaneously hypertensive rats (SHR) compared with their effects in normotensive counterparts. In both groups, chronic, eight-week CS was induced by caging five rats per cage in cages designed for two rats (200 cm(2)/rat), while controls (C) were housed four to a cage in cages designed for six animals (480 cm(2)/rat). Acute stress was evoked by one cycle of I/R (5 min each, ischemic preconditioning) before sustained I/R in isolated Langendorff-perfused hearts of normotensive and SHR rats. At baseline conditions, the effects of CS were manifested only as a further increase in blood pressure in SHR, and by marked limitation of coronary perfusion in normotensive animals, while no changes in heart mechanical function were observed in any of the groups. Postischemic recovery of contractile function, severity of ventricular arrhythmias and lethal injury (infarction size) were worsened in the hypertrophied hearts of C-SHR compared with normotensive C. However, myo-cardial stunning and reperfusion-induced ventricular arrhythmias were attenuated by CS in SHR, which was different from deterioration of I/R injury in the hearts of normotensive animals. In contrast, ischemic preconditioning conferred an effective protection against I/R in both groups, although the extent of anti-infarct and anti-arrhythmic effects was lower in SHR. Both forms of stress may improve the altered response to ischemia in hypertensive subjects. In contrast to short-term preconditioning stress, chronic psychosocial stress was associated with a higher risk of lethal arrhythmias and contractile failure in normotensive animals exposed to an acute ischemic challenge.

The coexistence of Si~111!-~131!-Pb and Si0.28Pb0.72 /Si(111) phases was investigated using scanning tunneling microscopy. Reversible phase transition Si~111!-~131!-Pb,Si~111!-c(53A3)-Pb at TC’230 °C was observed. Simultaneously, small regions with surface charge ordered states were found on Si0.28Pb0.72 /Si(111) indicating a charge density wave phase transition. Both phases were found to be stable in the temperature interval from T’2240 °C up toTC . @S0163-1829~99!10243-1# Phase transitions and ordering in two dimensions ~2D! represent an important field of surface physics, both from a theoretical and applied point of view. Recently, the understanding of these processes in metal/semiconductor interfaces has improved due to the growing availability of scanning tunnelling microscopy ~STM!. 1‐3 STM has played a decisive role in revealing that in principle there are two kinds of temperature-driven 2D phase transitions possible. The first type involves the rearrangement of adsorbate atoms at a certain transition temperature TC , e.g., the transition of a close packed b-(A33A3)R30°,(131) in Pb/Ge~111! at TC ’180 °C, 2 or similarly incommensurate closed-packed (A3 3A3)R30°,(131) in Pb/Si~111!. 3,4 The second type incor

The direct evolution of submonolayer two-dimensional Au phases on the $\mathrm{Si}(111)\ensuremath{-}(7\ifmmode\times\else\texttimes\fi{}7)$ surface was studied in real time using the spectroscopic photoemission and low energy electron microscope located at the synchrotron radiation source ELETTRA. A finite area covered by 1 monolayer (ML) of gold with a steplike transition zone was prepared by evaporation in situ. Subsequent annealing resulted in the spread of the Au layer and the formation of laterally extended $\mathrm{Si}(111)\ensuremath{-}(5\ifmmode\times\else\texttimes\fi{}1)\ensuremath{-}\mathrm{Au}$ and $\mathrm{Si}(111)\ensuremath{-}(\sqrt{3}\ifmmode\times\else\texttimes\fi{}\sqrt{3})R30\ifmmode^\circ\else\textdegree\fi{}\ensuremath{-}\mathrm{Au}$ surface reconstructions. At a temperature around 970 K, the boundary of the gold-covered region propagates on the clean $\mathrm{Si}(111)\ensuremath{-}(7\ifmmode\times\else\texttimes\fi{}7)$ and exhibits a nonlinear dependence on time. The ordered $\mathrm{Si}(111)\ensuremath{-}(5\ifmmode\times\else\texttimes\fi{}1)\ensuremath{-}\mathrm{Au}$ plateau develops a separated front moving with constant velocity. Two values of the Au diffusion coefficients were estimated at a temperature of about 985 K: (1) ${D}_{7\ifmmode\times\else\texttimes\fi{}7}=5.2\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}8}{\mathrm{cm}}^{2}{\mathrm{s}}^{\ensuremath{-}1}$ as the average diffusion coefficient for Au on a clean $\mathrm{Si}(111)\ensuremath{-}(7\ifmmode\times\else\texttimes\fi{}7)$ surface in the concentration range from 0.4 ML up to 0.66 ML and (2) ${D}_{5\ifmmode\times\else\texttimes\fi{}1}=1.2\ifmmode\times\else\texttimes\fi{}{10}^{\ensuremath{-}7}{\mathrm{cm}}^{2}{\mathrm{s}}^{\ensuremath{-}1}$ as the lower limit for the diffusion of single Au atoms on the $\mathrm{Si}(111)\ensuremath{-}(5\ifmmode\times\else\texttimes\fi{}1)\ensuremath{-}\mathrm{Au}$ ordered phase.

In order to understand the functional significance of Na,K-ATPase subunits as well as their isoenzymes, a precise subcellular localization of these in the myocyte is a crucial prerequisite. Cytochemical, immunofluorescence, preembedding immunogold and horse radish peroxidase-diaminobenzidine methods, demonstrated alpha 1 isoenzyme immunoreactivity on the sarcolemma, T-tubules and the subsarcolemmal cisterns of the adult cardiac myocytes. Cytochemically, ouabain resistant Na,K-ATPase precipitate was localized only in the subsarcolemmal cisterns and junctional sarcoplasmic reticulum. For alpha 2 isoenzyme, immuno-reactivity was demonstrated on the sarcolemma as well as in all areas of the myocytes in particularly a close proximation to the sarcoplasmic reticulum and microsomes. For alpha 3 isoenzyme, only a weak insignificant signal was noted on the sarcolemma, intercalated disc and sarcoplasm. It is suggested that cytochemical ouabain resistant precipitate present in subsarcolemmal cisterns and junctional sarcoplasmic reticulum represent alpha 1 isoenzyme of Na,K-ATPase. A differential as well as unique localization of alpha subunit isoenzymes of Na,K-ATPase in specific structures of cardiac myocytes may suggest importance in physiological function at these sites.

Adriamycin, an effective anticancer chemotherapeutic agent, causes an insidious and delayed cardiotoxicity. Different subcellular abnormalities including calcium transport changes in the sarcolemma (SL) as well as downregulation of the adrenergic system have been shown to be associated with the development of this cardiomyopathy. Since both of these activities are influenced by phospholipid methylation, effects of adriamycin on the three catalytic sites of SL phosphatidylethanolamine N-methyltransferase were examined. Rats were administered with a cumulative dose of adriamycin (15 mg/kg) over 2 weeks and examined after 3 weeks. Vehicle injected animals served as controls. Dyspnea, high mortality rate, ascites and decrease in aortic and left ventricular systolic pressure, as well as increase in left ventricular end diastolic pressure were seen in the adriamycin group. Myocardial cell damage typical of adriamycin cardiomyopathy, i.e. sarcotubular swelling, vacuolization and myofibrillar drop-out, was also apparent. Total methyl group incorporation into SL phosphatidylethanolamine using radiolabeled S-adenosyl-L-methionine as the donor was significantly depressed in the 3 week group at catalytic sites II and III. Decreased production of methylated intermediates, phosphatidyl-N-monomethylethanolamine and phosphatidyl-N,N-dimethylethanolamine as well as phosphatidylcholine (PC) was seen. Depression of phosphatidylethanolamine N-methylation was also noticed when SL, isolated from untreated hearts, was exposed in vitro to different concentrations (10, 100 and 1000 microM) of adriamycin. Inhibition of phosphatidylethanolamine N-methylation appears to be mediated by adriamycin-induced increase in the oxidative stress and may contribute in the pathogenesis of subcellular changes associated with this cardiomyopathy.

Cardiovascular effects of estrogens and particularly that of estradiol involve protection of the heart against ischemia. These effects were believed to be mainly indirect, mediated via changes in the blood and blood vessels. In the present paper a direct action of estradiol on the heart is demonstrated. Estradiol stimulates (p0.001) the Na,K-ATPase activity of cardiac sarcolemmal membranes by stimulating in an allosteric manner, the activation of the enzyme by potassium. The latter activation involves also an increase in affinity to potassium of the potassium binding sites on the enzyme molecule, but remains without any effect on the capacity and KD value of specific ouabain binding to the Na,K-ATPase. Estradiol is also antagonizing the depression of Na,K-ATPase activity that may be caused by ischemia and it is stimulating (p0.01) the ouabain-sensitive uptake of 86Rb into the heart cells. Our results indicate, that in addition to the known indirect effects of estradiol on the heart, the hormone also stimulates the activity and improves the kinetics of interaction of cardiac sarcolemmal Na,K-ATPase with ATP as well as with Na+ and K+ ions. This direct action may also account for the cardioprotective effects of estradiol.

During the period between 1963 and 1988, 343 patients were operated due to aortic coarctation. 14 patients (4%) were necessarily reoperated for late postoperative complications. In 3 cases (0.8%) reoperation was indicated due to the development of aneurysm in the region of primary operation of aortic coarctation. The development of aneurysm is prevalently predisposed by Vosschulte's indirect aortoplastic operation by the use of a synthetic patch. In the remaining 11 patients (3.2%) the reoperation was indicated owing to the development of recoarctation. Today recoarctation concerns children which were operated under the age of two. The most important moment favourable for the recoarctation development is the secondary constriction of the repaired region in consequence of the coarctation listel fibroid tissue and owing to the incapability of the anastomosis to grow. The perspective rests on using new suture material and combined techniques. Late postoperative complications which follow operations performed due to aorta coarctation remarkably augment the peri and postoperative mortality. Three cases out of the given group of 14 patients terminated by exitus (21%). Hence, it is necessary to remove all moments of predisposition creating a condition favourable for the development of recoarctation and aneurysm. (Tab 2, Fig. 1, Ref. 14.).

Contact sites are created by fusion of the inner and outer mitochondrial membrane. They represent a dynamic microcompartment for creatine kinase activity. In this microenvironment the active sites of creatine kinase, oxidative phosphorylation, and ADP/ATP transport interact during basal and stimulated metabolism. Electron microscopic studies showed that the occurrence rate of contact sites was changing according to the energy state of the mitochondrion (Biermans et al., 1989). The aim of this study was to stimulate the metabolism of the rat heart by extracellular calcium and to investigate the formation of contact sites and creatine kinase activity. Isolated rat hearts were perfused with Krebs-Henseleit solution containing 1.6 mmol Ca. After 15 min stabilization the hearts were subjected to 0.6, 0.9, 1.8, 2.2, 2.6, or 3.6 mmol Ca for a period of 15 min. Stimulation of the isolated rat hearts with increasing calcium concentrations was physiologically manifested by enhanced dp/dt and LVP values. A higher frequency rate of mitochondrial contact sites was observed and these were associated with higher creatine kinase activity. We suppose that induction of contact site formation is related to the functional activity of the Ca stimulated rat heart and thus efficient production and transport of energy is provided. (Tab. 1, Fig. 6, Ref. 18.).

The authors analyze 50 patients with endarterectomy of the coronary arteries during the periods of 1972-1974 and 1988-1990. The results of endarterectomy of the right and left coronary artery provide evidence of its justification in indicated cases whereby contrary to some departments the results of endarterectomy of the left coronary artery are comparable with endarterectomy of the right coronary artery.

Under physiological conditions different parts of the heart reveal superspecialization of the myocardium reflected by biochemical, functional, structural and histochemical differences, which are even more pronounced under pathological conditions. Postischemic reperfusion, Ca paradox and injury caused by reactive oxygen species were found to result in transmurally unhomogenous damage of the ventricular wall. In the present experiments isolated perfused rat hearts were subjected to damage by the above mechanism and a different vulnerability of defined parts of the heart was observed. Activities of glycogen phosphorylase, SDH, beta-HBDH, and LDH were studied histochemically in both ventricles, the atria and the specialized conductive system of the heart. Marked decreases of activities were observed in the ventricular muscle. The enzyme activities were less decreased in the atrial muscle. Conductive fibres were the least affected tissue in this respect. The differential changes were most sensitively reflected by glycogen phosphorylase. The differences in transmural distribution of damage were shown to be dependent on a complex of specific factors such as intramural pressure gradient, transmural pressure, end-diastolic intraventricular pressure, differences in transmural vessel distribution, transmural hematocrit differences, blood flow, perfusate volume, and endothelial injuries of different origin. It can be concluded that differences in ultrastructure as well as in enzyme activities in different parts of the heart reflect functional, structural and metabolic heterogeneity of the different functional parts of the heart muscle.

Activation of an intracellular calcium-calmodulin complex may play an important role in myocardial injury induced by ischemia and reperfusion. Chlorpromazine and trifluoperazine, calmodulin inhibitors, were used to enhance myocardial preservation by preventing harmful effect of intracellular calcium accumulation. The experimental model used one-hour LAD coronary occlusion and subsequent two-hour reperfusion in 70 dogs divided into four groups. Reperfusion alone significantly increased regional myocardial blood flow and left ventricular enddiastolic pressure and significantly reduced infarct size, dp/dt max, V max, mean aortic pressure, cardiac index and index of left ventricular minute work. Phenothiazines, applied at the 30th minute of occlusion significantly reduced infarct size, left ventricular enddiastolic pressure and index of systemic resistance and significantly increased dp/dt max, V max, cardiac index and regional myocardial blood flow in ischemic and border zones. The physiological results tightly correlated with the biochemical results and ultrastructural findings. The present study suggests that phenothiazines can improve cardiac performance and preservation of myocytes by preventing calcium stimulatory effect on degradative enzymes and may represent a potential clinical tool in modifying myocardial injury induced by ischemia and reperfusion.

Polyclonal specific antisera to beta-receptors were prepared by immunization of rabbits with beta-receptors isolated from a dog myocardium according to Becker et al. (1988). Cryostat sections of the dog heart were fixed in paraformaldehyde in PBS, and incubated with polyclonal antisera to beta-receptors. Sections were then washed and incubated in peroxidase-labelled anti-rabbit antibody. After visualization of the tissue-bound peroxidase with diaminobenzidine, sections were dehydrated in graded alcohols and mounted in Canada balsam. The results demonstrate specific reaction of antibodies on the myocyte sarcolemma.

The fine structural alteration and histochemical changes of the cardiac conduction system were studied in dogs and rats using various models of ischemic and reperfusion injury. The role of Ca2+ overload and reactive oxygen species (ROS) per se were also investigated. In all models of injury the activity of glycogen phosphorylase (histochemical indicator of the early ischemic changes) was present in nodal and conducting cells, although it was markedly diminished or absent in surrounding contractile muscle. Fine structural ischemic alterations progressed more slowly in conducting cells in comparison with working myocardial cells. Changes induced by Ca2+ paradox or ROS were reversible in conducting tissue in contrast to working myocardial tissue. The observations support the concept that conducting cells are more resistant to ischemia and also to reperfusion related injury than contractile myocardial cells.

The role of ischemia itself, calcium overload and of reactive oxygen species (ROC) in reperfusion injury of the heart was characterized from the physiological, biochemical and morphological point of view. Experiments were performed on isolated rat hearts (Langndorff preparation), perfused at constant pressure of 65 Torr and 37 degrees C. The effect of ischemia was studied on the model of 30 min normothermic global ischemia with consequent 30 min reperfusion. Calcium overload and damage by ROS were modelled by Ca(2+)-paradox (3 min Ca(2+)-depletion followed by 10 min Ca(2+)-repletion) and by intraaortal bolus application of ROS-generating system (H2O2 + FeSO4) respectively. Evaluation of functional and biochemical parameters revealed that the changes in electrical activity, accumulation of lactate and the loss in total adenine nucleotides content in heart tissue may be well applied to characterize the participation of the above mechanisms on total reperfusion damage to the heart. Histochemically detected different patterns of distribution of enzyme activities also allow to distinguish between alterations caused by different factors of reperfusion injury.

Today it is accepted that estrogens mitigate the consequences of ischemic heart disease. Preliminary experiments revealed an increase in heart sarcolemmal (Na+ + K+)-ATPase activity after application of estradiol in vivo. It is also well known the key role of latter enzyme for heart function. The facts mentioned above indicate that estradiol may act on the heart just via modulation of the (Na+ + K+)-ATPase activity. In present paper it is confirmed that 17-beta-estradiol stimulates the activity of sarcolemmal (Na+ + K+)-ATPase by allosteric manner, particularly by increasing positive cooperativity between the K(+)-binding sites of the enzyme. This effect is manifested by enhancement in functional capacity of the sodium pump in sarcolemma. Stimulatory effect of estradiol is bound to integrated myocytes: neither is it manifested in isolated sarcolemma in vitro nor exhibits any influence on the affinity of binding sites for cardiac glycosides or on total capacity of the sarcolemma to bind ouabain. Basing on the data obtained it was assumed that estradiol acts on the (Na+ + K+)-ATPase not directly but by means of a mediator released within the myocyte.

The model of calcium paradox was used to test the effect of the calcium entry blocker Diltiazem (concentration 4.0 mumol.l-1) and of the calmodulin inhibitor Trifluoroperazin (concentration 1.0 mumol.l-1). Application of each preparation resulted in improved cardiac function manifested by restoration of the electrical and contractile activity and by increased coronary flow. Both Diltiazem and Trifluoroperazin exerted a protective effect on the preservation of enzymatic activities and of ultrastructure in conditions of impaired calcium homeostasis.

Specific features of myocardial damage induced by overload and the very action of reactive oxygen species were analyzed and characterized. The experiments were performed on the isolated perfused heart of the rat (according to Langendorff). Overload of the heart by calcium ions was studied on the model of calcium paradox; damage of the heart by reactive oxygen species was induced by a single application of a free radicals generating system. Functional, biochemical, and ultrastructural parameters were studied. Several of the examined parameters (lactate accumulation, drop of total adenine nucleotides, transmural heterogeneity in the histochemical reactivity of enzymes) are of a certain value in recognizing the participation of individual factors involved in reperfusion induced damage of the myocardium.

Experiments using a cytochemical method showed the presence of a specific precipitate of the adenylate cyclase (AC) reaction on the sarcolemma and in the subsarcolemmal cisternae and junctional sarcoplasmic reticulum in rat cardiomyocytes. The localization of AC in the given organelles draws attention to the mutual association between Ca2+ ions and cAMP in the modulation of cardiac contractions. Trifluoperazine (TFP) and chlorpromazine (CHP) are known as phenothiazine derivatives inhibiting cellular enzymatic processes dependent on calmodulin and Ca2+. AC is one of these enzyme systems. The administration of TFP and CHP (both in a dose of 0.1 and 3 mmol.1(-1)) did not affect the cytochemical localization of the enzyme. Quantitative determination of 125I-cAMP by RIA showed that CHP inhibited AC activity in both concentrations. TFP, on the other hand, did not inhibit AC activity in 0.1 mmol.1(-1) concentration and actually stimulated its activation in 3 mmol.1(-1) concentration. The different action of the phenothiazine derivatives on AC activity can be attributed partly to the different affinity of TFP and CHP for calmodulin and partly to interaction of the inhibitor-calmodulin complex with the phosphodiesterase (PDE) system.

The protective effect of calcium entry blockers can be studied advantageously on the model of the calcium paradox, particularly on the basis of the preservation of haemodynamic and biochemical parameters as well as on the structure of the myocardium (Meno et al. 1984). Our aim in this study was to test the protective effect of the recently developed Czechoslovak drug diltiazem (LACHEMA) under conditions of the Ca2+ paradox.

The Ca paradox resulted in marked inhibition, up to disappearance, of histochemically studied enzyme activities (SDH, LDH, beta-HBDH, phosphorylase and ATPase) in the subepicardial layer of the myocardium. In the subendocardial region there was only a small decrease. These transmural differences correlated well with ultrastructural changes. It is assumed that the heterogeneity in transmural distribution of injury is the result of transmural differences in coronary flow.

The differential rate of synthesis of penicillinamidohydrolase (penicillin acylase -- EC 3.5.1.11) was studied in Escherichia coli growing in some chemically defined media and in a complex medium. The enzyme is synthesized at a constant rate only during the exponential phase of growth of cells. Its synthesis is induced most effectively (with respect to quantity) by phenylacetic acid. The induction lag of the enzyme synthesis in a medium with acetate corresponds to two generation times. The highest rate of the enzyme synthesis is reached in a medium containing phenylacetic acid as the only source of carbon and energy. The enzyme synthesis is fully repressed by an increased concentration of dissolved oxygen in the medium, even when Escherichia coli is cultivated in the medium with phenylacetic acid as the only carbon and energy source.

The authors have experimentally verified the theoretically deduced relation for the concentration of bacteria in the individual vessels of a multistage continuous system arranged so as to enable—at suitably chosen retention times in the individual vessels—the study of even rapidly occuring changes in the bacterial culture. Moreover, such system permits to compare the development of the batch and continuous culture. It has been demonstrated that according to the chosen retention times any section of the growth curve, the individual phases of which are spacially separated in the individual vessels can be reproduced in the continuous system.

During batch cultivation ofEscherichia coli in a medium deficient in inorganic phosphate, the growth curve after exhaustion of phosphate is linear. Results obtained in batch cultivation were used for deriving expressions for bacterial growth at a constant rate in a single-and multi-stage continuous system. It was found experimentally that the theoretical relations derived are satisfactory.

Normothermic, 3 min lasting perfusion of isolated rat heart with Krebs-Ringer-Henseleit solution in which Ca was replaced by EDTA, followed by successive perfusion of Ca2+ containing medium resulted in structural and metabolic derangement of myocardial cells; this could be demonstrated electronmicroscopically and histochemically. Unlike in ischemia, Ca paradox left the enzymes LDH, SDH, beta-HBDH as well as alpha-glucan phosphorylase and ATP-ases better preserved in the subendocardial layer of the left ventricle. Ultrastructural analysis of this phenomenon showed good correlations with the histochemical findings. A large portion of cardiomyocytes in the subendocardial layer showed only slight changes. On the other hand, myocytes in the subepicardial layer were severely injured and all characteristics of the calcium paradox were present including hypercontraction bands with fusion of myofilaments, extrusion and accumulation of oedematous mitochondria containing electron dense material intracristally, sarcolemmal ruptures, separation of intercalated discs etc. The better preservation of the subendocardial region in experiments with calcium paradox could be explained by inadequate perfusion of this layer with Ca2+ free medium due to transmural anatomical inhomogeneity of the capillary supply, resulting in a better protection of these myocytes from Ca paradox. The heterogeneity in transmural distribution of injuries is a multifactorial phenomenon. In addition to factors such as intramural pressure gradient, transmural pressure, enddiastolic intraventricular pressure etc., the most important factors in both types of injuries should be regarded the amount of vascular supply, blood flow and perfusate volume.

Left descending coronary ligation was performed on 70 dogs and divided into four groups. I. group - permanent occlusion (5 dogs 60 min, 5 dogs 120 min, 5 dogs 180 min), II. group - 15 dogs (60 min occlusion + 120 min reperfusion), III. group - 20 dogs (60 min occlusion, 15 mg Chlorpromazine [CPR], reperfusion 120 min), IV. group - 20 dogs (60 min occlusion, 2 mg Trifluoperazine [TFP] + 120 min reperfusion). CPR or TFP were administered 30 min after the ligation. Effect of drugs was quantified on tetrazolium stained gross sections and studied from physiological, biochemical and ultrastructural points of view. Results reveal that treatment of animals with phenothiazines revealing calmodulin inhibitory action, considerably improved the ultrastructure of myocytes in area at risk and allowed for recovery at least 60 per cent of injured myocytes after restoration of reflow. Ultrastructural findings tightly correlate with physiological and biochemical results.