bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of NPPB on chloride (CI) transport in distal colon of potassium (K+) adapted rats
Authors: VERON D. , MARTIN R. S. , ESCOBAR E. , TUFARO D. , VISCONTI P. , TEZON J. G. , ARRIZURIETA E. E. 
Published: December 2008

Secondary hyperaldosteronism enhances the rate of K secretion in distal colon, at least in part, through the stimulation of Na+‐K+‐Cl‐ cotransport across the basolateral membrane. To maintain a constant intracellular Cl‐ activity an increase in Cl‐ transport out of the cell must be assumed. We explored, under amiloride 10‐4 M and short circuited conditions, conductive pathways for Cl‐ exit in the distal colon of K+‐adapted rats by means of a putative Cl‐ channel blocker, NPPB (5‐nitro‐2(3‐phenyl‐propylamino‐benzoate. Results prior to NPPB showed an increase in JClras after K+ loading from 5.84 + 0.66 to 8.33 ±0.86 and JCl8m from 4.77 ±0.55 to 8.16±0.96/μEq h“1 cm”2 (P < 0.001), when compared with controls. Net fluxes were not different between groups. Luminal NPPB in K+ adaptation resulted in a decrease of JClsm, from 7.85 ±1.5 to 6.69 ± 1.5 μEq h‐1 cm‐2 (P < 0.05). There were no changes in both unidirectional Cl‐ fluxes in controls under luminal NPPB and in potential difference (V) and short‐circuit current (I‐.) under any condition. Finally, K+ adaptation resulted in an increase of luminal cyclic AMP (cAMP) concentration (0.09 ±0.02 to 0.20 ±0.03 pmol 100 μ‐1, P < 0.05), when compared with control rats.The data may suggest a transcellular recycling of Cl‐ and an activated NPPB inhibitable serosal to mucosal Cl‐ pathway on luminal membrane in the K+ adapted state, possibly mediated by an increase in cAMP production.
Prolonged bleeding time during nitric oxide inhalation in the rabbit
Authors: HOGMAN M. , FROSTELL C. , ARNBERG H. , SANDHAGEN B. , HEDENSTIERNA G. 
Published: December 2008

During a study on the modulatory effect of inhaled nitric oxide (NO) on the airway, we observed an increased bleeding tendency. Therefore, we studied bleeding time and blood rheology in rabbits during inhalation of 3, 30 and 300 parts per million (ppm) NO. The rabbits were intubated during neurolept anaesthesia and were ventilated mechanically. The bleeding time was significantly increased after 15 min of inhalation of 30 ppm NO, from 51 + 5 to 72 + 7 s (mean + SEM, P < 0.001, n= 7). However, there were no changes in haematocrit, whole blood or plasma viscosity, erythrocyte aggregation tendency, or erythrocyte deformability. Inhalation of 3 ppm NO increased bleeding time from 46+11 to 59 + 8 s (n.s., n= 4) and 300 ppm NO from 48 + 12 to 78 + 17s(P<0.05, n= 4).In another group of rabbits mean arterial pressure (MAP) was monitored using NO inhalation. A non‐significant decrease was seen with 3 ppm and 30 ppm NO, from 63 + 2 to 59 + 3 mmHg (n= 6) and from 65 + 2 to 61 + 1 mmHg (n= 6) respectively. Inhalation with 300 ppm NO decreased MAP from 62 + 3 to 55 + 2 mmHg (P < 0.05, n= 6). We conclude from these data that inhalation of NO, 30 ppm or more exerts systemic effects.
Interferon‐induced class II expression at the spongiotrophoblastic zone of the murine placenta is linked to fetal rejection and developmental abnormalities
Authors: VASSILIADIS S. , TSOUKATOS D. , ATHANASSAKIS I. 
Published: December 2008

Type II interferon is known to induce a plethora of gene expression involved in the humoral and cellular immunity. One of the multiple sites of action of γ‐IFN is the fetoplacental unit, where its role has not yet been clearly defined. We have previously shown in vitro that γ‐IFN may induce expression of class II MHC antigens on the spongiotrophoblast layer of the murine placenta, which under physiological conditions is negative for these antigens. Indeed, the absence of class II antigens from the placenta could be part of a mechanism evoked by fetal tissues to escape a host vs. graft reaction. In the present study we show that intraperitoneal in vivo administration of low doses of recombinant γ‐IFN to pregnant females specifically induces class II antigens on the spongiotrophoblast zone, increases fetal abortion, causes retardation of eye development in the fetuses and decreases fetal weight. This treatment also affects the maternal pathology as we witness a prominent hypersplenism in the mother accompanied by low levels of haematocrit, elevated IgG production and decreased granulocytic and thrombocytic counts. These results are specifically linked to the pregnant state of the mother, since virgin females do not develop any of the above abnormalities.Our results not only point to a new dimension in γ‐IFN's role during pregnancy, but may be of clinical importance for prophylaxis since administration of γ‐IFN to a pregnant female may lead to abortion, fetal abnormalities or cause haematologic disorders to the mother.
Participation of prostaglandins and bradykinin in the effects of angiotensin II and converting enzyme‐inhibition on sympathetic neurotransmission in vivo
Authors: SCHWIELER J. H. , KAHAN T. , NUSSBERGER J. , HJEMDAHL P. 
Published: December 2008

We investigated the mechanism(s) by which angiotensin converting enzyme (ACE)‐inhibition and angiotensin (Ang) II influence peripheral sympathetic neurotransmission in canine gracilis musclein situ, with a‐adrenoceptors either intact or irreversibly blocked by phenoxybenzamine. ACE‐inhibition by ramiprilat reduced, and subsequent infusion of Ang II (30 ng kg‐1min‐1i.v.) markedly increased arterial plasma Ang‐(1–8)octapeptide levels, basal muscle perfusion pressures and mean arterial pressure. Local intra‐arterial bolus injection of Ang II caused marked vasoconstriction followed by vasodilation. This vasoconstrictor response was enhanced and the ensuing vasodilation was abolished following prostaglandin synthesis inhibition by diclofenac. The vasoconstrictor response to low frequency (0.5 Hz) sympathetic nerve stimulation was also enhanced by diclofenac. The nerve stimulation‐evoked noradrenaline (NA) overflow was reduced by ramiprilat when a‐adrenoceptors were blocked (‐ 11 ± 3 %,P <0.05), but increased when a‐adrenoceptors were intact (+ 28± 14%,P <0.05). During ACE‐inhibition, effective bradykinin receptor antagonism by HOE 140 reduced stimulation‐evoked NA overflow irrespective of a‐adrenoceptor blockade (i.e. by 25 ± 5 and 20 ± 3% in the absence and presence of a‐adrenoceptor blockade, respectively,p< 0.01). Diclofenac increased stimulation‐evoked NA overflow in the absence of a‐adrenoceptor blockade (+ 19 ± 4%,P <0.05). I.v. infusion of Ang II failed to enhance stimulation‐evoked NA overflow both before and after diclofenac.In conclusion, the results support the ideas that local formation of Ang II and bradykinin facilitate, and of prostaglandins inhibit NA release, and that ACE inhibition influences sympathetic neurotransmission through all of these mechanisms in skeletal musclein situ;the net result depends on the degree of prejunctional a‐adrenergic feedback inhibition. Circulating Ang II may enhance the local formation of vasodilatory prostaglandins, but does not seem to modulate NA release even after prostaglandin synthesis inhibition in this model. Our data suggest that circulating Ang II may not reach the perivascular sympathetic nerves to a significant extent in skeletal musclein vivo.
Lymphatic transport and organ uptake of gelatin and hyaluronan injected into the rat mesentery
Authors: ØSTGAARD G. , HELLEVIK T. , REED R. K. , SMEDSRØD B. 
Published: December 2008

The metabolic pathways of denatured collagen (gelatin) and hyaluronan were studied by injecting labelled macromolecules into the mesentery of rats. The label, [125I]tyraminecellobiose is trapped intracellularly after endocytosis, allowing localization of the site of uptake. Mesenteric and thoracic lymph was sampled for 6 h in anaesthetized rats. Separate rats were investigated after an awake period of 6 or 24 h. About 30% of the gelatin remained at the site of injection and of the remaining activity 1.7% was recovered in lymph, 11 yo in the liver and 15% in the kidneys, whereas 3 h after an intravenous injection of gelatin > 70% was recovered in the liver. The change in preferable site of uptake from the liver to the kidney was attributed to local degradation in the mesentery as confirmed by chromatography of tissue extracts and lymph.Following hyaluronan injection and 6 h lymph sampling approximately 30% was left at the site of injection and of the remaining activity 5.7% was recovered in lymph. After an awake period of 6 or 24 h, 30% was regained in the liver. The recoveries in other organs were negligible and mesenteric lymph nodes seem quantitatively unimportant in the uptake of hyaluronan or gelatin from lymph or blood.The liver has a central role in intestinal hyaluronan metabolism, while denatured collagen is more prone to local degradation with remote uptake shared between the liver and the kidney.
Pitfalls in the interpretation of spectral analysis of the heart rate variability during exercise in humans
Authors: CASADEI B. , COCHRANE S. , JOHNSOTON J. , CONWAY J. , SLEIGHT P. 
Published: December 2008

The recent use of spectral analysis of the R‐R interval variability to assess the autonomic drive during exercise has produced inconsistent results. The purpose of this study was to assess whether the spectral components of the R‐R interval variability reflect different mechanisms at rest and during exercise.Autoregressive spectral analysis of the electrocardiographic and breathing signals was performed in 11 healthy young men at rest and during incremental cycle ergometry. The amplitude of respiratory sinus arrhythmia, i.e. the absolute power of the high frequency spectral component, fell at the onset of exercise, consistent with a reduction in cardiac vagal activity. Conversely, the normalized power of the high frequency component, (i.e. the percentage of R‐R interval variance due to the respiratory sinus arrhythmia) increased with increasing work rates. The low frequency spectral component of the R‐R interval variability, which when expressed in normalized units is believed to reflect cardiac sympathetic activity, was no longer detectable in severe exercise when the adrenergic drive is known to be elevated.In conclusion, autoregressive spectral analysis of the R‐R interval variability does not adequately reflect the autonomic changes that occur during incremental exercise. In particular, the evidence indicates that as the cardiac vagal tone falls with increasing levels of exercise, a greater percentage of the residual power of the high frequency component may be due to non‐neural mechanisms.
Sympathetic regulation of fructose secretion in the seminal vesicle of the guinea‐pig
Authors: SJÖSTRAND N. O. , HAMMARSTORÖM M. 
Published: December 2008

Fructose secretion of everted guinea‐pig seminal vesicles was studiedin vitro. Carbachol produced dose dependent increase in fructose secretion. The effect was blocked by scopolamine but not by hexamethonium, mecamylamine, tetrodotoxin or previous denervation. High concentrations of acetylcholine also increased fructose secretion. This response was not augmented by physostigmine. Methoxamine reduced secretion. Methoxamine, terbutaline, clonidine and vasoactive intestinal peptide counteracted carbachol. Field stimulation produced increased secretion that was not blocked by autonomic drugs, tetrodotoxin or previous denervation. Stimulation of the hypogastric nerve produced frequency dependent increase in fructose secretion. The effect was blocked by tetrodotoxin and scopolamine but not enhanced by physostigmine. If the hypogastric nerve was stimulated close to the seminal vesicle the response was unaffected by hexamethonium but proximal stimulation was blocked. After chronic proximal denervation of the hypogastric nerve, stimulation close to the seminal vesicle produced enhanced response. Destruction of the peripheral ganglia at the base of the seminal vesicle abolished the response. Sections showed that most secretory nervesenter the organ at its base. Phentolamine or yohimbine but not prazosine or propranolol or guanethidine enhanced the secretory response to distal hypogastric nerve stimulation. Tyramine counteracted the response but after reserpinization it was enhanced by tyramine.It is concluded that the secretory cells of the guinea‐pig seminal vesicle have a sympathetic secretomotor innervation by short cholinergic neurones with a preganglionic supply via the hypogastric nerve. Inhibitory α1and β2‐adrenoreceptors are present on the cells but neurogenic adrenergic inhibition of the secretion is essentially prejunctional and due to activation of inhibitory α2‐receptors on the secretomotor nerves.
Interdigestive gastroduodenal manometry in humans. Indication of duodenal phase III as a retroperistaltic pump
Authors: BJÖRNSSON E. S. , ABRAHAMSSON H. 
Published: December 2008

To elucidate the specific function of the three phases (I‐III) of the migrating motor complex (MMC) by manometry, detailed analysis of individual pressure waves in the proximal duodenum was performed. Twenty healthy subjects (10 men and 10 women of whom 11 were tube‐naive) underwent computerized manometry for 5 h during fasting followed by 45 min after a meal using an 8‐channel water perfused catheter. Three recording points were in the antrum, three in the proximal duodenum (2 cm apart), one in the distal duodenum and one in the proximal jejunum. In all subjects at least one phase III (median 2) was observed during the 5‐h fasting recording. In the proximal duodenum the mean proportion of retrograde pressure waves, out of all propagating waves, was significantly increased in the last part of phase III (85 ± 9%, mean, SE), compared with early phase III (6 ± 5%), late phase II (5 ± 4%) and the feeding phase (10 ± 5%), irrespective of gender or previous tube‐experience. The median length of the MMCs was 108.5 min. There was no statistically significant difference between men and women or between tube‐naive and tube‐experienced subjects for the duodeno‐jejunal motility indices of phase II and phase III, nor for duration or migration of phase III. The postprandial motility index of the small intestine was increased compared with the interdigestive late phase II, particularly in the jejunum (P < 0.02).The last part of the duodenal interdigestive phase III in healthy subjects shows the feature of a retroperistaltic pump. This cyclic sequence of retropropagation coincides with the reported rapid alkalinization of the duodenal bulb and the gastric antrum occurring in early antral phase I.
Prostaglandins and corticosterone in the oviparous female lizard, Podarcis sicula sicula, during reproduction
Authors: GOBBETTI A. , ZERANI M. , BELLINI‐CARDELLINI L. , BOLELLI G. F. 
Published: December 2008

The in vitro effects of prostaglandin F2α (PGE2α) and prostaglandin E2 (PGE2) on corticosterone release by ovarian follicles, corpora lutea (CL), and interrenals were studies in the female lizard, Podarcis sicula sicula, during reproduction. Follicles and CL were divided according to their different development stages: follicles: pre‐vitellogenic, early‐vitellogenic, mid‐vitellogenic and fully‐grown; CL: CL 1 (unshelled eggs in the oviducts), CL2 (shelled eggs in the oviducts), CL3 (eggs laid 6 h previously) and CL4 (eggs laid 48 h previously). Interrenals were divided according to the reproductive stages: pre‐vitellogenesis, vitellogenesis, ovulation, post‐ovulation, and post‐deposition.PGF2α release was highest in fully‐grown follicles and PGE2 in early‐vitellogenic follicles, corticosterone was highest in pre‐vitellogenic and lowest in early‐vitellogenic follicles. PGE2 decreased corticosterone in pre‐vitellogenic, mid‐vitellogenic and fully‐grown follicles. PGE2α release was highest in CL4, and PGE2 in CL1 and CL2, CL3. In interrenals, PGE2α release was highest and PGE2 lowest during ovulation, corticosterone was highest in CL4. PGF2α increased and PGE2 decreased interrenal corticosterone during vitellogenesis, ovulation, and post‐ovulation. In the plama, PGF2α levels were highest and PGE2 lowest during ovulation, corticosterone was highest during ovulation.These results suggest that corticosterone, modulated by PGF2α and PGE2α, is implied in the reproductive processes with different roles. In fact this steroid could favour ovulatory and luteolytic processes. In addition the hypothesis of an anti‐vitellogenic role of corticosterone in discussed.
Ovarian levels of epidermal growth factor receptor mRNA in the rat‐a postovulatory decrease
Authors: ASSARSSON B. , NILSSON I. , SELSTAM G. 
Published: December 2008

Members of the epidermal growth factor (EGF) family have many different effects on ovarian cells including a strong inhibition of estradiol‐17β production. An increased binding of the EGF family to its receptor is seen at the time of ovulation. The aim of the present study was to measure the mRNA levels of the EGF receptor in the preovulatory follicle and to see if the levels are still high after functional luteolysis.The mRNA of the EGF receptor was measured in whole ovaries, follicles and corpora lutea. Pregnant mare serum gonadotrophin (PMSG) stimulated rats were used to get denned follicles. To achieve luteolytic corpora lutea on day 11, the adult female pseudopregnant rat model was used. Determination of the EGF receptor mRNA was performed with solution hybridization analysis, using a 768 bp long probe of the human EGF receptor (2318–3085).A two‐fold increase in the mRNA levels of the EGF receptor was registered between 09.00 and 21.00 h during the proestrus day in the preovulatory follicle. Concurrently, serum estradiol‐17β levels decreased from 420 ± 65 to 79 ± 6 pM. High levels of EGF receptor proteins in the preovulatory follicle were verified by immunohistochemistry. The levels of EGF receptor mRNA was decreasing from 25.4 ± 4.4 fmol mg‐1 in the corpus luteum on day 1 to 7.6 ± 9.9 fmol mg‐1 on day 11. Thus, the high amounts of EGF receptor in the ovary during the late preovulatory period might be involved in the regulation of ovarian estradiol‐17β production.
Skeletal muscle metabolism during short duration high‐intensity exercise: influence of creatine supplementation
Authors: BALSOM P. D. , SÖDERLUND K. , SJÖDIN B. , EKBLOM B. 
Published: December 2008

Seven male subjects performed repeated bouts of high‐intensity exercise, on a cycle ergometer, before and after 6 d of creatine supplementation (20 g Cr H2O day‐1). The exercise protocol consisted of five 6‐s exercise periods performed at a fixed exercise intensity, interspersed with 30‐s recovery periods (Part I), followed (40 s later) by one 10 s exercise period (Part II) where the ability to maintain power output was evaluated. Muscle biopsies were taken from m. vastus lateralis at rest, and immediately after (i) the fifth 6 s exercise period in Part I and (ii) the 10 s exercise period in Part II. In addition, a series of counter movement (CMJ) and squat (SJ) jumps were performed before and after the administration period.As a result of the creatine supplementation, total muscle creatine [creatine (Cr) + phosphocreatine (PCr)] concentration at rest increased from (mean + SEM) 128.7 (4.3) to 151.5 (5.5)mmolkg_1 dry wt (P < 0.05). This was accompanied by a 1.1 (0.5) kg increase in body mass (P < 0.05). After the fifth exercise bout in Part I of the exercise protocol, PCr concentration was higher [69.7 (2.3) vs. 45.6 (7.5) mmol kg“‘ dry wt, P < 0.05], and muscle lactate was lower [26.2 (5.5) vs. 44.3 (9.9) mmol kg”1 dry wt, P < 0.05] after vs. before supplementation. In Part II, after creatine supplementation, subjects were better able to maintain power output during the 10‐s exercise period (P < 0.05). There was no change in jump performance as a result of the creatine supplementation (P > 0.05).These findings show that enhanced fatigue resistance during short duration high‐intensity exercise following creatine supplementation is associated with a greater availability of PCr and a lower accumulation of lactate in the muscle. The finding that jump performance was not enhanced suggests that short‐term creatine feeding does not influence peak power output.
The migrating motor complex‐the motor component of a cholinergic enteric secretomotor programme?
Authors: MELLANDER A. , ABRAHAMSSON H. , SJÖVALL H. 
Published: December 2008

The role of cholinergic nerves in the cyclic activation of interdigestive motility and secretion was studied in 23 healthy volunteers. Net fluid transport in a distal duodenal segment and the release of pancreaticobiliary secretions into the duodenal lumen, were measured with a triple lumen perfusion technique. Interdigestive motor activity was recorded with a low‐compliance pneumohydraulic system, and the transmural potential difference (PD) was measured as an on‐line marker of electrogenic anion secretion. Transport parameters were related to the migrating motor complex (MMC) in the control situation and after the administration of atropine (0.01 mg kg‐1 body wt, i.v.).The early part of the MMC cycle was characterized by low motor activity, low release of bile and pancreatic juice into the duodenal lumen, a slightly lumen positive transmural PD, and a non‐significant net fluid absorption (‘absorptive mode’)‐ Under control conditions, motor activity and pancreaticobiliary secretions subsequently increased and there was a shift in net fluid transport and transmural PD in the secretory direction (‘secretory mode’). Furthermore, there was a significant correlation between contraction frequency, a more lumen negative PD, and the magnitude of net fluid secretion. After the administration of atropine, the secretory mode was abolished, but there was still a significant correlation between contraction frequency and transmural PD.In conclusion, cholinergic neurones seem to mediate the shift from the absorptive to the secretory mode in the human distal duodenum. The antisecretory effect of atropine may be the result of inhibition of motilin release, reduced activation of tension‐sensitive intramural secretory pathways, or blockade of cholinergic neurones to the secreting epithelium.
Prostacyclin aerosol and inhaled nitric oxide fail to reverse pulmonary vasoconstriction induced by thromboxane analogue in dogs
Authors: WELTE M. , ZWISSLER B. , HABLER O. , KLEEN M. , MESSMER K. 
Published: December 2008

Inhalation of either prostacyclin (PGI2) as an aerosol or nitric oxide (NO) has been shown to elicit selective pulmonary vasodilation during hypoxic pulmonary vasoconstriction in dogs. Hypoxia may produce cardiovascular changes confounding interpretation of drug effects. Therefore, we investigated the effects of PGI2‐aerosol and inhaled NO (50 p.p.m.) on pulmonary pressure‐flow relationships (P/Q_plots) during thromboxane analogue (U46619) induced pulmonary vasoconstriction.In eight anaesthetized dogs infusion of U46619 (0.33 ± 0.18 μg kg_1min‐1) increased the slope (3.5 ± 1.1 to 8.4 ± 1.7 mmHg L‐1min‐1,P <0.001) and the intercept (4.4±2.3 to 10.2 ± 4.6 mmHg,P <0.01) ofP/Qplots indicating pulmonary vasoconstriction. Inhalation of both aerosolized PGI2solution (10μgmL‐1) and NO (50 p.p.m.) reduced neither the slope nor the intercept of theP/Q_plots. Increasing the concentration of the aerosolized PGI2solution to 50 μg mL‐1:(n= 3) did not enhance the effect on pulmonary circulation but systemic vascular resistance fell by 23%. Oxygenation and intrapulmonary shunt remained unchanged during both PGI2‐aerosol and inhaled NO. The failure of PGI2‐aerosol to induce pulmonary vasodilation indicates that during aerosolization PGI2‐concentrations at receptor sites on pulmonary vessels were insufficient to surmount U46619 induced vasoconstriction; this notion is supported by unchanged arterial plasma concentrations of the PGI2degradation product 6‐keto‐PGFlα. Considering that NO inhaled at comparable concentrations in sheep reversed U46619 induced pulmonary vasoconstriction, species differences may account for the failure of both PGI2‐aerosol and NO to dilate pulmonary vessels in dogs.