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Zoznam článkov

General Physiology and Biophysics


Volume 24, 2005, No. 2

Content:


  Changes in ultraweak photon emission and heart rate variability of epinephrine-injected rats
Y Yoon 1), J Kim, B Lee, Y Kim, S Lee, K Soh

1)Biomedical Physics Laboratory 25-414, School of Physics, Seoul National University, Seoul 151-747, Republic of Korea. dr94@mulli.snu.ac.kr.


Ultraweak photons which are spontaneously emitted from a living body may be applicable as a non-invasive tool to characterize the physiological state of the living body. We investigated changes in the intensity of ultraweak photon emission, body temperature and the cardiovascular autonomic activity induced by epinephrine injection to rats. A high dose of epinephrine can make changes to the cardiovascular autonomic activity or body temperature. Photon emission of the dorsal part, rectal temperature and heart rate variability (HRV) were measured from eight Sprague-Dawley rats. The intensities of photon emissions for saline injections, which were used as a control, decreased from 13042 ± 71 counts/min at the start of measurements to 8709 ± 915 counts/min at 1 h after the injections. In the case with epinephrine injections, the intensity of photon emission reduced slowly from 13361 ± 354 counts/min to 11040 ± 433 counts/min. Rectal temperature increased in both saline- and epinephrine-injected rats, but one hour after the injections the temperature in the epinephrine case was slightly higher than that in the saline case. The standard deviation of the QRS wave complex interval (RR interval) increased from 1 to 4 (p < 0.05) and the spectral ratio of the low frequency component to the high frequency component in the HRV data LF (0.19 ∼ 0.74 Hz) / HF (0.78 ∼ 2.50 Hz) decreased from 0.81 to 0.26 (p < 0.05) in the case of epinephrine injection while no change was found in the case of saline injection. Thus, ultraweak photon emission was closely related to the cardiovascular autonomic activity.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 147-159.

 
  Interactions between tricyclic antidepressants and phospholipid bilayer membranes
Z Fišar 1)

1)Department of Psychiatry, 1st Faculty of Medicine, Charles University, Ke Karlovu 11, 120 00 Prague 2, Czech Republic. zfisar@lf1.cuni.cz.


Participation of electrostatic and other noncovalent interactions in the binding of tricyclic antidepressants (TCAs) to the lipid bilayers was estimated from pH-dependencies of imipramine, desipramine, amitriptyline and nortriptyline binding to the lipid bilayers prepared from different phospholipids, both electroneutral and acidic. The binding was studied using a radioligand binding assay. It was found that the membrane phospholipid composition and methylation of the acyl side chain of TCA has a decisive effect on participation of particular noncovalent interactions in the binding. Apparent high-affinity binding of TCAs to the phosphatidylcholine or phosphatidylethanolamine membranes are achieved mainly by incorporation of uncharged drug molecules into the hydrophobic core of the bilayers. Van der Waals forces and hydrophobic effect are responsible for this binding. Both charged and uncharged drug molecules bind to phosphatidylserine membranes, therefore coulomb- or ion-induced dipole interactions play a role in these binding. Different spatial distribution of charged residues within the interface causes different electrostatic interactions between charged TCAs and vesicles formed from phosphatidylserine and phosphatidylinositol. The data supports the hypothesis under which TCAs could have effect on affective disorders partially via binding to the lipid part of the membrane and following changes of lipid-protein interactions.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 161-182.

 
  Effect of neonatal streptozotocin and thyrotropin-releasing hormone treatments on insulin secretion in adult rats
Z Bačová 1), M Najvirtová, O Krizanova, S Hudecova, Š Zórad, V Štrbák, J Benický

1)Institute of Experimental Endocrinology, Center of Excellence, Slovak Academy of Sciences, Vlárska 3, 833 06 Bratislava 37, Slovakia. zuzana.bacova@savba.sk.


Neonatal STZ (nSTZ) treatment results in damage of pancreatic B-cells and in parallel depletion of insulin and TRH in the rat pancreas. The injury of B-cells is followed by spontaneous regeneration but dysregulation of the insulin response to glucose persists for the rest of life. Similar disturbance in insulin secretion was observed in mice with targeted TRH gene disruption. The aim of present study was to determine the role of the absence of pancreatic TRH during the perinatal period in the nSTZ model of impaired insulin secretion. Neonatal rats were injected with STZ (90 µg/g BW i.p.) and the effect of exogenous TRH (10 ng/g BW/day s.c. during the first week of life) on in vitro functions of pancreatic islets was studied at the age 12–14 weeks. RT-PCR was used for determination of prepro-TRH mRNA in isolated islets. Plasma was assayed for glucose and insulin, and isolated islets were used for determination of insulin release in vitro. The expression of prepro-TRH mRNA was only partially reduced in the islets of adult nSTZ rats when compared to controls. nSTZ rats had normal levels of plasma glucose and insulin but the islets of nSTZ rats failed to response by increased insulin secretion to stimulation with 16.7 mmol/l glucose or 50 mmol/l KCl. Perinatal TRH treatment enhanced basal insulin secretion in vitro in nSTZ animals of both sexes and partially restored the insulin response to glucose stimulation in nSTZ females.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 181-197.

 
  The effects of nitric oxide synthase – versus lipoxygenase inhibition on coronary flow and nitrite outflow in isolated rat heart
V Jakovljevic 1), D Djuric

1)Department of Physiology, Faculty of Medicine, Svetozara Markovića 69, P.O.Box 124, 34000 Kragujevac, Serbia and Montenegro. drvladakg@yahoo.com.


The aim of this study was to assess the changes of coronary flow (CF) and nitrite outflow under inhibition of nitric oxide synthase (NOS) by Nω-nitro-L-arginine monomethyl ester (L-NAME) or lipoxygenase (LOX) induced by nordihydroguaiaretic acid (NDGA) in isolated rat heart. The hearts of male Wistar albino rats (n = 18, age 8 weeks, body mass 180–200 g) were retrograde perfused according to the Langendorff’s technique at gradually increased constant coronary perfusion pressure (CPP) conditions (40–120 cm H2O) which induced flow-dependent nitric oxide (NO) release (nitrite outflow). The experiments were performed during control conditions, in the presence of NO synthesis inhibitor L-NAME (30 µmol/l) or nonspecific LOX inhibitor (NDGA, 0.1 mmol/l) which were administered separately or in combination. CF varied in autoregulatory range from 4.12 ± 0.26 ml/min/g wt at 50 cm H2O to 5.22 ± 0.26 ml/min/g wt at 90 cm H2O. In autoregulatory range, nitrite outflow varied from 2.05 ± 0.17 nmol/min/g wt at 50 cm H2O to 2.52 ± 0.21 nmol/min/g wt at 90 cm H2O and was strictly parallel with CPP/CF curve. The autoregulatory range of CF was significantly extended (40–100 cm H2O, 2.22 ± 0.12 ml/min/g wt and 2.90 ± 0.25 ml/min/g wt, respectively) under the influence of L-NAME. Hemodynamic effects were accompanied by significant decrease in nitrite outflow after L-NAME administration (0.56 ± 0.11 nmol/min/g wt at 40 cm H2O to 1.45 ± 0.14 nmol/min/g wt at 100 cm H2O). NDGA affected CF in the range of CPP 40–70 cm H2O only (from 42 % at 50 cm H2O to 12 % at 90 cm H2O, respectively) with no significant changes in nitrite outflow. When L-NAME was applied in combination with NDGA vs. NDGA only, CF was significantly reduced (from 34 % at 50 cm H2O to 50 % at 90 cm H2O, respectively) with parallel changes in nitrite outflow (from 40 % at 50 cm H2O to 51 % at 90 cm H2O, respectively). The results showed that CF and nitrite outflow could be decreased under L-NAME administration. Nonselective LOX inhibitor (NDGA) decreased control values of CF only at lower values of CPP but did not change nitrite outflow indicating antioxidant properties of NDGA. In addition, L-NAME decreased the effects induced by NDGA on CF and nitrite outflow indicating the role of NO.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 199-207.

 
  Mitochondrial alterations induced by 532 nm laser irradiation
P Kaššák 1), T Przygodzki, D Habodászová, M Bryszewska, L Šikurová

1)Division of Biomedical Physics, Faculty of Mathematics, Physics and Informatics, Comenius University, Mlynská Dolina F1, 842 48 Bratislava 4, Slovakia. pkassak@yahoo.com.


Mitochondrial alterations were monitored after low power green laser (532 nm, 30 mW) irradiation in the case of whole cells (B-14) and isolated mitochondria (from Wistar rat heart). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium-bromide (MTT) assay products were significantly higher (by 8%) in irradiated B-14 cells as compared to non-irradiated controls. Mitochondrial transmembrane potential of B-14 cells, measured by means of a fluorescent probe 3,3'-dihexyloxacarbocyanine iodide (DiOC6(3)), significantly increased (by 13%) after exposure to green laser irradiation. Another MTT assay was used for isolated mitochondria suspensions in order to examine the effect of green laser irradiation on stimulation of processes related to oxidative phosphorylation. It revealed 31.3%-increase in MTT assay products in irradiated mitochondria as compared to controls. Laser irradiation of isolated mitochondria suspension did not significantly change 1,6-diphenyl-1,3,5-hexatriene (DPH) fluorescence anisotropy, indicating that mitochondrial membrane fluidity was not affected by laser light. Fluorescence emission spectra of irradiated as well as non-irradiated mitochondria suspensions showed fluorescence maximum at 635 nm, corresponding to emission of Protoporphyrin IX, which was significantly lower (by 20.7%) in irradiated sample.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 209-220.

 
  Effect of long-term administration of antidepressants on the lipid composition of brain plasma membranes
Z Fišar 1), M Anders, E Tvrzická, B Staňková

1)Department of Psychiatry, 1st Faculty of Medicine, Charles University, Ke Karlovu 11, 120 00 Prague 2, Czech Republic. zfisar@lf1.cuni.cz.


The connection between changes in lipid pattern in brain plasma membranes and long-term administration of therapeutically effective doses of antidepressants has not been sufficiently demonstrated so far. Therefore, we analyzed effect of antidepressants that differ in pharmacological selectivity on membrane lipid composition in the rat brain tissue. Laboratory rats were given desipramine, maprotiline, citalopram, moclobemide or lithium for a 4-week period. We observed a significant decrease in phosphatidylethanolamine representation after administration of maprotiline, citalopram and moclobemide when compared with controls. Membrane cholesterol content was decreased after desipramine administration and increased after citalopram or lithium treatment. Electroneutral phospholipids were decreased after the administration of all tested antidepressants except for desipramine. Decrease in phosphatidylserine was found following long-term administration of maprotiline or desipramine; relative representation of phosphatidylinositol was reduced after lithium treatment. Statistically significant negative correlation between cholesterol and electroneutral phospholipids was discovered. Membrane microviscosity evaluated by fluorescence anisotropy of membrane probes was only slightly decreased after desipramine and increased after citalopram administration. Hypothesis was supported that changes in brain neurotransmission produced by antidepressants could be, at least partially, associated with adaptive changes in membrane cholesterol and phospholipids.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 221-236.

 
  Effect of two distinct stressors on gene expression of the type 1 IP3 receptors
O Krizanova 1), R Kvetnansky, D Jurkovicova

1)Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Vlárska 5, 833 34 Bratislava, Slovakia. olga.krizanova@savba.sk.


Inositol 1,4,5-trisphosphate (IP3) is one of the second messengers, which triggers calcium release from intracellular pools via IP3 receptors. Previously we have shown that single immobilization stress increased gene expression of both, the type 1 and type 2 IP3 receptors (IP3R1 and IP3R2, respectively). In this study we evaluated whether long-term exposure to softer stressor (cold exposure to 4°C) can affect the response to single immobilization stress. We examined modulation of the type 1 IP3 receptor gene expression by each stressor separately, and then in their combination. Rats were immobilized for 30 min and 120 min and were decapitated immediately or 3 h after immobilization. Cold stress was performed by exposure of animals to 4°C temperature for 1, 7 and 28 days. To determine the effect of both stressors in combination, animals exposed to cold for 28 days were afterwards exposed to immobilization for 120 min and decapitated 3 h after the end of stressful stimulus. Our results verify that single immobilization increases the IP3R1 gene expression in left atria of rat heart, while cold stress elevates the level of gene expression only after the exposure to cold for 7 days. The exposure to cold for 28 days did not increase the gene expression of the type 1 IP3 receptor compared to control. Application of both stressors (28 days of cold exposure followed by 120 min of immobilization with subsequent 3 h rest) showed the tendency of increased IP3R1 gene expression compared to absolute, nonstressed control, but level of the type 1 IP3 receptor mRNA was significantly lower compared to mRNA levels of solely immobilized animals. Thus, cold exposure affects the response of the gene expression of the type 1 IP3 receptor to immobilization stress.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 237-246.

 
  On the derivation of the Kargol's mechanistic transport equations from the Kedem–Katchalsky phenomenological equations
G Suchanek 1)

1)Institute of Physics, Swietokrzyska Academy 15, 25-406 Kielce, Poland. suchaneg@pu.kielce.pl.


In the present article, it was demonstrated that – by starting from the so-called adjusted Kedem–Katchalsky (KK) phenomenological equations (Suchanek et al. 2004), i.e. the equations: Jv = LpΔP − LpDΔΠ. JD = −LDpΔP + LDΔΠ it is possible to derive practical transport equations (for the volume flow and the solute flow) in the form of the Kargol´s mechanistic transport equations (Kargol and Kargol 2000, 2001, 2003a,b,c, 2004; Kargol 2002). On this basis, it has been found that the KK thermodynamic formalism for membrane transport (practical equations) is in general identical with the mechanistic equations for membrane transport.

General Physiology and Biophysics. Volume 24, 2005, No. 2: 247-258.