bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isometric and Concentric Performance of Electrically Stimulated Ankle Plantar Flexor Muscles in Intact Rat
Authors: Willems Mark E. T. , Stauber William T. 
Published: May 2004

SUMMARYThe relationship between muscle force and ankle position during isometric and pre‐loaded slow concentric contractions (angular velocity, 0.52 rad s−1; range of motion, 1.22 rad) and the recovery of isometric force following concentric contractions at different velocities were determined for electrically stimulated plantar flexor muscles in intact rats. Pre‐loaded refers to the isometric contraction which immediately precedes the concentric contraction. Ankle position was controlled by a dynamometer and force was recorded under the sole of the foot. The peak isometric force (19.2 N) was nearly constant at all ankle positions (range of motion, 1.57 rad). The muscle length and distal fibre length of gastrocnemius medialis at ankle positions between 0.79 rad and 2.01 rad were increased by 12.6% and 20.3%, respectively. During slow concentric contractions, the force progressively decreased (23.1 ± 2.1%); the force decreased by only 6.3 ± 0.9% during sustained isometric contractions of similar duration (3400 ms). The recovery of isometric force following concentric contractions with similar stimulation frequencies (80 Hz) was velocity dependent (i.e. more rapid at higher velocities). It is concluded that pre‐loaded slow concentric contractions of the plantar flexor muscles in intact rats do not follow the same relationship as that of isometric force and ankle position. Our results in intact rats show that the force output of electrically stimulated ankle plantar flexor muscles measured under the sole of the foot can be used to study the physiological properties of skeletal muscle working in situ.
The Role of Na+−H+ Exchange in Fluid and Solute Transport in the Rat Efferent Ducts
Authors: Hansen L. A. , Clulow J. , Jones R. C. 
Published: May 2004

SUMMARYIn vivo microperfusion techniques were used to investigate the role of Na+‐H+ exchange in the efferent ducts of the rat. Individual efferent ducts were perfused with a Krebs‐Ringer bicarbonate solution (KRB) containing 0, 1, 3, 5 or 7·5 mM amiloride. Concentrations of 1‐5 mM amiloride inhibited fluid reabsorption from the efferent ducts in a linear dose‐dependent manner with an apparent Km of 3 mM. Inhibition was maximal at 5 mM with reabsorption reduced by about 70%. The effects of amiloride were completely reversible and there was little effect of amiloride on luminal osmolality and concentrations of Na+, Cl− or K+. It is concluded that Na+‐H+ exchange is one of the principal mechanisms responsible for fluid and electrolyte reabsorption in the efferent ducts and offers a means by which the efferent ducts are able to achieve flow‐dependent, autoregulated fluid reabsorption.
Comparison of Step and Ramp Voltage Clamp on Background Currents in Guinea‐Pig Ventricular Cells
Authors: Spindler A. J. , Noble S. J. , Noble D. 
Published: May 2004

SUMMARYIsolated cardiac ventricular myocytes from guinea‐pig were used to investigate the effect of voltage clamp protocols on background Na+ current (ib.Na) and inward rectifier current (iK1). Using long (4 s) clamp pulses and very long step clamps, the i‐V relations showed that removal of Na+ reduces the amplitude and shifts the voltage dependence of iK1 (Spindler et al. 1998). Ramp clamps, however, gave more complicated results, with slower ramps more often giving the same results as steps and pulses. Both iK1 itself and, during faster ramps, other currents show hysteresis, so masking the steady‐state changes. Using pulses, TTX had no effect on steady‐state current. Small differences occurred in the ramps, but even at fast ramp speeds the effects are very much smaller than in Purkinje tissue. Only part of ib,Na is TTX sensitive and the effect does not occur in all cells.
Mechanically Induced Potentials in Fibroblasts from Human Right Atrium
Authors: Kamkin A. , Kiseleva I. , Wagner K. D. , Lammerich A. , Bohm J. , Persson P. B. , Günther J. 
Published: May 2004

SUMMARYIt has been shown that cardiac fibroblasts of the human heart are electrically non‐excitable and mechanosensitive. The resting membrane potential of these cells is ‐15.9 ± 2.1 mV and the membrane resistance is 4.1 ± 0.1 GΩ. Rhythmic contractions of the myocardium associated with stretch of the surrounding tissue produce reversible changes in the membrane potential of cardiac fibroblasts. These mechanically induced potentials (MIPs) follow the rhythm of myocardial contractions. Simultaneous recording of the action potential of cardiomyocytes and MIPs of cardiac fibroblasts demonstrates a delay of 40.0 ± 0.4 ms after the action potential before the appearance of the MIP. Contraction produces a MIP which is more positive or more negative than the reversal potential ‐ the membrane potential due to current injection at which the MIP reverses its direction. Regardless of the initial orientation of the MIP, intracellular polarization increases the amplitude towards the reversal potential if the background MIP had depolarized the membrane or away from the reversal potential if the initial background MIP had hyperpolarized the membrane. Artificial intracellular polarization changed the amplitude but not the frequency of the MIP. The pool of electrically non‐excitable mechanosensitive cells, which change their electrical activity during contraction and relaxation of the heart, may play a role in the mechano‐electrical feedback mechanism which has to be taken into account in the normal function of the heart as well as in pathological processes.
Sweat Ethanol Concentrations are Highly Correlated with Co‐Existing Blood Values in Humans
Authors: Buono Michael J. 
Published: May 2004

SUMMARYThis study compared the concentration of ethanol, both absolute and relative to water content, in sweat and blood. Ten male volunteers consumed approximately 13 mmol (kg body weight)−1 of ethanol. Blood and sweat samples were collected approximately 1, 2 and 3 h following ingestion. Sweat was collected following pilocarpine iontophoresis using an anaerobic technique that prevented ethanol evaporation. In addition, the water content of sweat and blood samples was determined. The correlation between sweat and blood ethanol, expressed in mmol l−1, was r= 0.98. The slope of the relationship was 0.81. When corrected for the water content in each sample, and expressed as mmoles per litre of water, the correlation remained very high (r= 0.97) while the slope increased to 1.01. These results suggest that rapid and complete equilibrium of ethanol occurs across the sweat gland epithelium.
Role of Nitric Oxide in Indomethacin‐Induced Gastric Mucosal Dysfunction in the Rat
Authors: Gürbüz Vildan , Alican Inci , Yegen Berrak Ç. , Bozkurt Ayhan , Oktar Berna , Haklar Goncagül , Yüksel Meral , Kurtel Hizir 
Published: May 2004

SUMMARYThe present study was undertaken to explore the role of nitric oxide (NO) in the pathogenesis of experimental non‐steroidal anti‐inflammatory drug (NSAID)‐induced gastropathy. We assessed the role of NO inhibition and donation in indomethacin‐induced gastric mucosal dysfunction. The stomach was perfused with vehicle (control) for 20 min, followed by indomethacin (10 mg ml−1 in 1.25% sodium bicarbonate, pH 8.4) for 120 min. NG‐nitro‐l‐arginine methyl ester (l‐NAME, 5 and 10 mg kg−1, i.v. bolus), l‐arginine, D‐arginine (100 mg kg−1i.v. bolus, 10 mg kg−1 h−1, 2 h infusion) and the NO donor glyceryl trinitrate (GTN) were given at the same time (20, 40 and 80 μg kg−1 min−1, 15 min infusion) as perfusion with indomethacin was started. Epithelial permeability was quantified by measuring blood‐to‐lumen clearance of 51Cr‐labelled EDTA. Indomethacin caused a 20‐fold increase in 51Cr‐EDTA leakage compared with that of the control group. Treatment with l‐NAME or l‐arginine did not affect the indomethacin‐induced alterations in mucosal permeability. Administration of GTN (20 μg kg−1 min−1) significantly reduced the indomethacin‐induced mucosal dysfunction. By contrast, higher doses of GTN (80 μg kg−1 min−1) exacerbated epithelial dysfunction induced by indomethacin. Elevated levels of carbonyls and myeloperoxidase (MPO) observed after indomethacin administration were significantly reduced, to the control values, when GTN (20 μg kg−1 min−1) was administered along with indomethacin. These data suggest that NO from exogenous sources can exert a dual action on the integrity of the gastric mucosa challenged by indomethacin. Low doses of GTN can prevent mucosal dysfunction induced by indomethacin, while higher doses of GTN may exacerbate the increases in epithelial permeability.
Identification of Calcium‐Activated Potassium Channels in Cultured Equine Sweat Gland Epithelial Cells
Authors: Huang Yu , Ko Wing‐Hung , Chung Yiu‐Wa , Wong P. Y. D. 
Published: May 2004

SUMMARYThe patch‐clamp recording technique was used to examine the properties of the K+ channels in cultured equine sweat gland epithelial cells. With symmetric K+ solutions (140 mM), a single population of K+ channels was identified with a slope conductance of 187 pS and a reversal potential of around 0 mV. The channel was selective for K+ over Na+. Channel activity was increased by membrane depolarization. A 10‐fold increase in [Ca2+]i produced an approximate 60 mV negative shift in the open state probability (Popen)‐voltage curve. Externally applied tetraethylammonium ions (TEA+) caused a rapid and flickery block of the channel and reduced the unitary current amplitude. TEA+ bound to the blocking site with stoichiometry of 1:1 and with a dissociation constant (Kd) of 186 ± 27 μM at +40 mV. A weak voltage dependence of Kd was observed. Iberiotoxin (100 nM) reduced Popen but had no effect on single‐channel conductance. Neither glibenclamide (10 μM) nor intracellular adenosine 5′‐triphosphate (ATP, 1 mM) altered channel activity. In addition, ATP, when applied extracellularly, transiently activated the channel by increasing Popen. Channel activity was low around the resting membrane potential in the intact epithelia, indicating that these channels might not contribute to the resting K+ conductance. However, the channel could be activated in a regulated manner. The K+ channels may play a role in transepithelial fluid secretion in sweat gland.
Molecular Modelling of the Biosynthesis of the Rna‐Editing Enzyme Apobec‐1, Responsible for Generating the Alternative forms of Apolipoprotein B
Authors: Scott James , Navaratnam Naveenan , Carter Charles 
Published: May 2004

SUMMARYWe discovered in 1987 that the shorter form of apolipoprotein B (B48) synthesized in the intestine is due to the action, previously unrecognized in mammalian cells, of an mRNA‐editing process, and more recently we demonstrated that this was due to a specific enzyme (APOBEC‐1) with cytidine deaminase activity. We show here, by sequence alignment, molecular modelling and mutagenesis, that APOBEC‐1 is a cytidine deaminase, responsible for editing apoB mRNA, and that is related in crystal structure to the cytidine deaminase of Escherichia coli (ECCDA). The two enzymes are both homodimers with composite active sites formed with loops from each monomer. In the sequence of APOBEC‐1, three gaps compared with ECCDA match the size and contour of the minimal RNA substrate. We propose a model in which the asymmetric binding of one active site to the substrate cytidine which is positioned by the downstream binding of the product uridine and that this helps to target the other active site for deamination.
Effect of Extracellular Cations on the Inward Rectifying K+ Channels Kir2.1 and Kir3.1/Kir3.4
Authors: Owen J. M. , Quinn C. C. , Leach R. , Findlay J. B. C. , Boyett M. R. 
Published: May 2004

SUMMARYThe effects of Ba2+, Mg2+, Ca2+ and Na+ as blocking ions were investigated in 90 and 10 mM extracellular K+ solutions on the cloned inward rectifying K+ channel Kir2.1 expressed in Xenopus oocytes. Some data were also obtained using another inward rectifying K+ channel Kir3.1/Kir3.4. The addition of Ba2+ caused a concentration‐, voltage‐ and time‐dependent block of both channels. Decreasing the extracellular K+ concentration augmented the block. The data suggest that Ba2+ blocks the channels by binding to a site within the channel pore and that the electrical binding distance, δ, of the site is significantly different for Kir2.1 and Kir3.1/Kir3.4 (∼ 0·38 and ∼ 0·22, respectively). Mg2+ and Ca2+ caused an instantaneous concentration‐ and voltage‐dependent block of both channels. With Kir2.1, decreasing the K+ concentration augmented the block. The voltage dependence of the block was less than that of Ba2+ (δ, ∼ 0·1), indicating a more superficial binding site for these ions within the channel pore. The affinity of the channels for Mg2+ and Ca2+ was ∼ 1000‐fold lower than that for Ba2+. Addition of Na+ resulted in a concentration‐, voltage‐ and time‐dependent block of Kir2.1, similar to that observed with Ba2+. The competition between the blocking cations (for Kir2.1: Ba2+, Mg2+, Ca2+; for Kir3.1/Kir3.4: Ba2+) and extracellular K+ suggests that the binding sites for the blocking cations may be sites to which K+ binds as part of the normal passage of K+ through the channels. It is possible that under normal physiological conditions naturally occurring extracellular cations may partly block the two inward rectifying K+ channels.
Breast Growth and the Urinary Excretion of Lactose During Human Pregnancy and Early Lactation: Endocrine Relationships
Authors: Cox David B. , Kent Jacqueline C. , Casey Tammy M. , Owens Robyn A. , Hartmann Peter E. 
Published: May 2004

SUMMARYBreast volume and morphology of eight subjects were measured before conception and at intervals throughout pregnancy until 1 month of lactation. Breast volume before conception ranged from 293 to 964 ml. At the end of pregnancy the volume of breast tissue had increased by 145 ± 19 ml (mean ±s.e.m., n= 13 breasts, range 12‐227 ml) with a further increase to 211 ± 16 ml (n= 12 breasts, range 129‐320 ml) by 1 month of lactation. Urinary excretion of lactose increased at 22 weeks of pregnancy, signalling the capacity of the breast to synthesize lactose at this time. During pregnancy, both the change in breast volume and the change in cross‐sectional area of the areola were related to the concentration of human placental lactogen in the plasma. The growth of the nipple and the rate of excretion of lactose were related to the concentration of prolactin in the plasma. During the first 3 days after birth, the rate of excretion of lactose was related to the rate of excretion of progesterone. There was no relationship between the growth of the breast during pregnancy and the amount of milk produced at 1 month of lactation.
Breast Volume and Milk Production During Extended Lactation in Women
Authors: Kent Jacqueline C. , Mitoulas Leon , Cox David B. , Owens Robyn A. , Hartmann Peter E. 
Published: May 2004

SUMMARYQuantitative measurements were made of relative breast volume and milk production from 1 month of lactation until 3 months after weaning, and the storage capacity of the breasts was calculated. The increase in breast tissue volume from before conception until 1 month of lactation was maintained for the first 6 months of lactation (means ±s.e.m.) (190·3 ± 13·1 ml, number of breasts, nb= 46). During this period of exclusive breast‐feeding, 24 h milk production from each breast remained relatively constant (453·6 ± 20·1 g, nb= 48), and storage capacity was 209·9 ± 11·0 ml (nb= 46). After 6 months, breast volume, milk production and storage capacity all decreased. There was a relationship between 24 h milk production and the storage capacity of the breasts, and these both appeared to be responding to infant demand for milk. At 15 months of lactation, the 24 h milk production of each breast was substantial (208·0 ± 56·7 g, nb= 6), even though the breasts had returned to preconception size. This was associated with an apparent increased efficiency of the breast (milk production per unit breast tissue) after 6 months, which may have been due to redistribution of tissues within the breast. The possible causes of the decrease in breast volume are discussed.
Comparison of Microvascular Filtration in Human Arms with and without Postmastectomy Oedema
Authors: Stanton A. W. B. , Holroyd B. , Mortimer P. S. , Levick J. R. 
Published: May 2004

SUMMARYOedema is caused by impaired lymphatic drainage and/or increased microvascular filtration. To assess a postulated role for the latter in postmastectomy oedema, filtration was studied in the forearms of 14 healthy subjects and 22 patients with chronic, unilateral arm oedema caused by surgical and radiological treatment for breast cancer. A new non‐contact optical device (the Perometer) and a conventional mercury strain gauge were used simultaneously to record forearm swelling rates caused by microvascular filtration during applied venous congestion. Filtration rate (FR) per 100 ml tissue was measured over 10‐15 min at a venous pressure of 30 cmH2O, a pressure reached in the dependent forearm (FR30), and then at 60 cmH2O (FR60). Apparent filtration capacity of 100 ml soft tissue (CFCa) was calculated from FR60 ‐ FR30/30, after adjustment for bone volume. The Perometer and strain gauge gave similar results in normal and oedematous arms. Mean CFCa in healthy subjects was (3·8 ± 0·4) × 10−3 ml (100 ml)−1 cmH2O−1 min−1, close to literature values. In the patients, FR30 was 47% lower in the oedematous forearm than in the opposite, unaffected forearm (P= 0·04). FR60 showed a similar trend but did not reach significance (P= 0·15). The values of CFCa of (2.2 ± 0.5) × 10−3 ml (100 ml)−1 cmH2O−1 min−1 in the oedematous arm and (2.8 ± 0.5) × 10−3 ml (100 ml)−1 cmH2O−1 min−1 in the unaffected arm were not significantly different (P= 0.47). When differences in arm volume on the two sides were taken into account, the total fluid load on the lymphatic system of the oedematous forearm was (411.0 ± 82.2) × 10−3 ml min−1 at 30 cmH2O and (1168 ± 235.6) × 10−3 ml min−1 at 60 cmH2O, similar to the normal side, namely (503.7 ± 109.3) × 10−3 ml min−1 and (1063 ± 152.0) × 10−3 ml min−1, respectively (P >= 0·50). The filtration capacity of the entire oedematous forearm (CFCa scaled up by total soft tissue volume), (25.4 ± 6.2) × 10−3 ml cmH2O−1 min−1, was not significantly greater than that of the normal forearm, (18.3 ± 2.6) × 10−3 ml cmH2O−1 min−1 (P= 0.40). The results indicate that no major change occurs in the microvascular hydraulic permeability‐area product of the forearm, or in the total filtration load on the lymph drainage system during dependency, in the arm with postmastectomy oedema compared with the normal arm. This argues against a significant haemodynamic contribution to postmastectomy oedema.
Insulin Sensitivity, Clearance and Release in Kininogen‐Deficient Rats
Authors: Damas Jacques , Bourdon Victor , Lefebvre Pierre J. 
Published: May 2004

SUMMARYInsulin sensitivity of kininogen‐deficient rats was compared with that of normal rats using euglycaemic hyperinsulinaemic glucose clamping. Anaesthetized animals were infused with 2‐50 mU kg−1 min−1 of insulin and the glucose infusion rates needed to maintain euglycaemia were determined. Maximum glucose uptake, insulin sensitivity index and insulin clearance were reduced in kininogen‐deficient rats. Captopril increased the amount of glucose needed to maintain euglycaemia during infusion of 2 and 10 mU kg−1 min−1 of insulin in normal rats, but had no effect in kininogen‐deficient rats. Anaesthetized rats of both strains were given an intraperitoneal injection of glucose and the evolution of blood glucose was followed for 120 min. The peak increase was higher in kininogen‐deficient rats. Similar larger increases in blood glucose were observed after glucose injection in normal rats previously treated with HOE 140, a bradykinin B2 receptor antagonist. After glucose injection, plasma insulin increased in both groups of rats but reached lower levels in kininogen‐deficient animals. These results suggest that bradykinin is involved not only in the clearance of glucose and insulin by the tissues during insulin infusion but also that bradykinin can affect the release of insulin after a glucose load.
The Relaxant Effects of Parathyroid Hormone(1‐34) and Parathyroid Hormone‐Related Protein(1‐34) on Ovine Reticulo‐Ruminal Smooth Muscle in Vivo
Authors: Care A. D. , Abbas S. K. , Harmeyer J. , Boivin R. 
Published: May 2004

SUMMARYThe motility of the reticulo‐rumen has been measured in trained, conscious sheep using inflated balloons temporarily introduced to selected regions of that forestomach. The frequency and amplitude of the contractions of the reticulum and both the A and B waves of contraction of the rumen were measured under the same conditions before, during and after the administration of an i.v. bolus of either parathyroid hormone (PTH(1‐34)) or PTH‐related protein (PTHrP(1‐34)) followed by its i.v. infusion. These two peptides are known to share a common receptor in other organs, e.g. the kidney. In this study they both showed an inhibitory effect on reticulo‐ruminal motility. The effect of PTHrP(1‐34) on the rate of ruminal blood flow was also examined and a significant reduction observed, after a transient increase. The secretion of endogenous PTH(1‐34) was stimulated by a 32 % reduction in the plasma calcium ion concentration induced by an i.v. infusion of sodium citrate. Associated with this were significant reductions in reticulo‐ruminal motility, e.g. the reduction in the mean amplitude of the reticular contractions reflected the reduction in plasma calcium ion concentration. When the PTH(1‐34)/PTHrP(1‐34) receptor was blocked with [Asn10,Leu11,D‐Trp12]PTHrP(7‐34) before and during the induction of hypocalcaemia, all but one of the parameters of reticulo‐ruminal motility were normalized. Indeed, by the day following the administration of this blocking agent, all these parameters had returned to their normal range. It is concluded that stimulation of the PTH(1‐34)/PTHrP(1‐34) receptor in reticulo‐ruminal smooth muscle reduces the motility of this tissue and may play a role in the depression of motility of the digestive tract which is characteristic of clinical milk fever in the dairy cow.