bluuebunny/crossref_metadata_2025_split huggingface dataset:
The influence on the breathing pattern in man of moderate levels of continuous positive and negative airway pressure and of positive end‐expiratory pressure during air and CO2 inhalation
Authors: ELLINGSEN I. 
Published: December 2008

The purpose of this study was to determine in man the effect on the breathing pattern of continuous positive (CPAP), continuous negative (CNAP) and positive end‐expiratory (PEEP) airway pressure during air breathing and CO2 inhalation. Six subjects were exposed to CPAP, CNAP and PEEP 0.5 kPa, while five subjects were exposed to CPAP and CNAP 0.8 kPa.End‐expiratory lung volume increased during CPAP 0.8 kPa and decreased during CNAP 0.8 kPa. CPAP induced more extensive changes in the ventilatory pattern, and the changes in each parameter were larger than observed during CNAP and PEEP at the same pressure level. In contrast to previous reports we found the effect of CO2 inhalation combined with the effect of pressure breathing to be not stronger than additive. Even moderate CPAP induced alveolar hyperventilation with marked reduction in arterial PCO2 (PaCO2) when breathing air. With increasing fraction of CO2 in the inspiratory gas, the difference in PaCO2 between CPAP and no CPAP disappeared. PEEP also affected the breathing pattern in that it induced an increase in mean inspiratory flow and mean expiratory flow and a reduction in inspiratory duration. Occurrence of ventilatory pauses depended on whether mouthpiece or facemask was used. CPAP and CNAP did not influence the occurrence of pauses, while PEEP prolonged post‐expiratory pauses.We conclude that CPAP, CNAP and PEEP induce active ventilatory responses in man and that strong mechanisms are involved during CPAP since PaCO2 is markedly reduced.
Occurrence and effects of endothelin in guinea‐pig cardiopulmonary tissue
Authors: FRANCO‐CERECEDA A. , MATRAN R. , LOU Y.‐P. , LUNDBERG J. M. 
Published: December 2008

Endothelin‐like immunoreactivity (‐LI) was present in the guinea‐pig cardiopulmonary tissues with the associated autonomic neural supply. The highest levels were found in the stellate ganglion (15 pmol g‐1) followed by the vagus nerve, pulmonary artery, lung and right atrium of the guinea‐pig. Endothelin I, but not endothelin III, induced an increase in contractile force and frequency followed by an atropine‐resistant inhibition of right atrial contractility at higher concentrations. Exposure to endothelin I caused a pronounced, long‐lasting coronary vasoconstriction as revealed by a decrease in perfusate outflow. In addition, both heart and contractile force were attenuated. Guinea‐pig bronchi in vitro contracted upon exposure to endothelin I and III, but only endothelin I caused contraction of pulmonary arteries. The C‐terminal hexapeptide of endothelin I did not influence right atrial, bronchial or pulmonary artery contractility. Endothelin I increased the mean arterial pressure and insufflation pressure and decreased the heart rate in the guinea‐pig in vivo.In conclusion, endothelin‐LI is present in the cardiovascular, respiratory and nervous tissues of the guinea‐pig and endothelin induces strong coronary and pulmonary vasoconstrictor effects. The effects on atrial contractile force and frequency are concentration‐dependent with stimulation at lower and inhibition at higher concentrations. Based on the diversity in response to endothelin III in the bronchi compared to atrium and pulmonary artery, it may be suggested that different receptor populations exist in bronchial and cardiovascular muscle, although the cellular localization and forms of endothelin present in guinea‐pig cardiopulmonary tissue remain to be established.
Inhibitors of lipoxygenase increase the ovulation rate in the in‐vitro perfused luteinizing hormone‐stimulated rabbit ovary
Authors: HELLBERG P. , HOLMES P. V. , BRÄNNSTRÖM M. , OLOFSSON J. , JANSON P. O. 
Published: December 2008

In order to determine whether leukotrienes, products of the lipoxygenase pathway, are involved in ovulation, pairs of rabbit ovaries were treated with the lipoxygenase inhibitors nordihydroguaiaretic acid (NDGA) and caffeic acid (CA) while being perfused in vitro. The control ovaries from each rabbit received luteinizing hormone (LH) (1.5–2.25 μg ml‐1) while the contralateral ovaries were treated with LH + NDGA (100μM) or LH + CA (100 μM). The numbers of ovulations from both the LH + NDGA‐ and LH + CA‐treated ovaries were significantly higher (P < 0.05) than from their respective LH‐stimulated controls. Treatment with NDGA alone in the perfusate did not cause any ovulation, while CA alone caused one ovulation from one of six ovaries perfused. Ovarian tissue levels of prostaglandins after 7 h of perfusion with LH + NDGA or with LH alone showed that, in five of the six ovaries perfused in this group, the tissue levels of PGE2, 6‐keto‐PGFlα and PGF2α were higher in the presence of NDGA. The mean differences were significant (P < 0.05) for prostacyclin but not significant (P > 0.05) for PGE2 and PGF2α.Our interpretation of the findings is that, when used for blocking the lipoxygenase pathway, NDGA and CA increase the substrate availability for the cyclo‐oxygenase pathway of arachidonic acid metabolism, resulting in a net increase in prostaglandins. The increased ovarian levels of prostaglandins, especially prostacyclin, may cause the observed increase in ovulation rate. Consequently, although the leukotrienes may be involved in the mechanism of ovulation in the rabbit, their effects appear to be less pronounced than those of prostaglandins.
Variations in left ventricular volume alter myocardial oxygen consumption more at low than at high inotropy
Authors: ANDERSEN F. R. , ILEBEKK A. , KIIL F. 
Published: December 2008

Variations in left ventricular (LV) wall tension during changes in LV end‐diastolic volume significantly affect myocardial oxygen consumption (MVO2). In the present study we examined if the reduction in M VO2) per beat accompanying a decline in LV end‐diastolic volume at constant LV systolic pressure (LVSP) is dependent on the level of myocardial inotropy. In six anaesthetized open‐chest pigs, the blood volume was expanded by i. v. infusion of a Ringer solution. At constant heart rate (by atrial pacing) and LVSP (by adjustments of a proximal aortic snare), LV end‐diastolic volume was reduced in steps by withdrawals of blood. This procedure was performed at high inotropy (during a continuous intracoronary infusion of isoproterenol, 0.40 ± 0.08 μg min‐1), and at low inotropy (after i. v. injection of 3.4 ± 0.2 mg propranolol).LVSP was about 25 mmHg higher at high than at low inotropy. The fall in LV tension was therefore greater during blood volume reductions at high than at low inotropy because the fall in LV end‐diastolic volume was almost identical and was initiated from the same level at both high and low inotropy. Nevertheless, the slope of the MVO2/LV end‐diastolic volume relationship was significantly (P < 0.05) less steep at high (1.26 ± 0.30 μmol 100 g ‐1 mm‐1) than at low inotropy (2.06 ± 0.48 μmol 100 g‐1 mm‐1). MVO2 per beat fell by only 0.79 ± 0.17 μmol 100 g‐1 (from 6.03 ± 0–4±5 μmol 100 g‐1 = 13.8 ± 3.1%) at high inotropy compared with 1.21 ± 0.19 μmol 100 g‐1 (from 3.79 ± 0.29 μmmol 100 g‐1 = 30.5 ± 3.4%) at low inotropy.The greater reduction in MVO2 per beat at low inotropy was associated with a reduction in LVdP/dt of 24 ± 4%, whereas LVdP/dt remained unchanged at high inotropy. Thus, the changes in MVO2 per beat and LVdP/dt were closely correlated (r = 0.94), and because the reduction in contractility was present only after propranolol administration it appeared to be induced by mechanisms other than variations in β‐adrenergic stimulation.
Actions of endothelin on isolated corpus cavernosum from rabbit and man
Authors: HOLMQUIST F. , ANDERSSON K.‐E. , HEDLUND H. 
Published: December 2008

The effects of endothelin, a vasoconstrictor peptide produced by vascular endothelial cells, were investigated in isolated rabbit and human corpus cavernosum (CC). Preparations from both rabbit and man were potently contracted by endothelin in a concentration‐dependent manner. The contractions developed slowly, could not be reversed despite frequent washings, and were only partly inhibited by the Ca2+ channel blocker nimodipine. Even in Ca2+‐free medium containing the chelator EGTA a small contractile component persisted. In rabbit CC, the contractions in Ca2+‐free medium were not affected by nimodipine, the Ca2+‐channel agonist BAY K 8644, or by depletion of intracellular Ca2+ stores sensitive to noradrenaline (NA) and caffeine, but were almost abolished by the protein kinase C inhibitor H7. In both rabbit and man, carbachol and vasoactive intestinal polypeptide concentration‐dependently relaxed preparations contracted by endothelin. The relaxations induced by carbachol were antagonized by atropine. Endothelin enhanced concentration‐dependently the contractions induced by exogenously applied NA in rabbit CC. The enhancement was more pronounced at low concentrations of NA.This study shows that endothelin potently contracts isolated penile erectile tissue. The contraction seems to be mediated mainly by influx of Ca2+ through the cell membrane, which partly occurs through a pathway other than voltage‐operated calcium channels. However, involvement of other mechanisms cannot be excluded. The results suggest that endothelin can play a role in penile erectile mechanisms.
Myelin basic protein stimulates insulin and glucagon secretion from rat pancreatic islets in vitro and in vivo
Authors: KOLEHMAINEN E. , KNIP M. , LEPPÄLUOTO J. 
Published: December 2008

The effect of myelin basic protein on insulin and glucagon secretion from rat pancreatic islets was studied in vivo and in vitro. The myelin basic proteins isolated from bovine, human and rat brains all stimulated insulin secretion in a similar fashion. In a static incubation of isolated pancreatic islets, myelin basic protein at doses of 15.6–250 μg in a 0.5‐ml reaction volume (1.7 times 10‐8 to 2.7 times 10‐5 M) significantly stimulated hormone release. Maximal stimulation, obtained at the 250‐μg dose, was 6.5‐fold greater than control for insulin secretion and 6.7‐fold greater than control for glucagon secretion. In the case of glucagon no saturation was observed, but saturation was obvious for insulin release at doses of myelin basic protein of 62.5–250μg, larger doses causing permeabilization of the islet membranes as indicated by leakage of acid phosphatase. At a 100‐μg dose the time course of insulin secretion induced by myelin basic protein indicated a fast initial release, and after the first 2 h only a little more insulin was released. At the lower doses of myelin basic protein (11 and 33μg) the secretion rate was nearly constant after the first hour. Significant stimulation of glucagon release by myelin basic protein was seen after 60 min, the rate of release being roughly constant at 33‐and 100‐μg doses thereafter. At the 11‐μg dose significant stimulation of hormone release was observed only after a 4‐h incubation. Lowering the temperature from 37 to 27 and 20°C reduced both basal and stimulated hormone secretion, the extent of stimulation over the basal level remaining the same at all temperatures only for insulin secretion at a dose of myelin basic protein of 100 μg.A dose of 10 mg myelin basic protein injected intravenously into anaesthetized rats resulted 15 min after injection in a circulating concentration of myelin basic protein of 34.7 μg ml‐1 (1.7 times 10‐6 M) as measured by our radioimmunoassay. It stimulated insulin secretion (P < 0.01), having no significant effect on plasma glucagon levels.Since myelin basic proteins have been shown to display fusogenic properties in cell‐free membrane systems, we propose that myelin basic protein exerts its hormone‐releasing effect by aggregating and fusing the hormone‐containing vesicles to the cell plasma membranes.
Effects of magnesium on isolated human fetal and maternal uteroplacental vessels
Authors: SKAJAA K. , FORMAN A. , ANDERSSON K.‐E. 
Published: December 2008

The effects of Mg2+were studied in human umbilical arteries, stem villous arteries and maternal intramyometrial arteries. The vessels were dissected and mounted in organ baths, and isometric tension was recorded. In all fetal preparations investigated, Mg2+(0.5–6.0 mM) in a concentration‐related way decreased pD2values for prostaglandin F2αresponses. The maximum response to prostaglandin F2awas depressed in umbilical arteries, but remained unaffected in stem villous artery preparations. In stem villous arteries pretreated in Ca2+‐free medium, increasing concentrations of Mg2+markedly depressed the response to Ca2+after stimulation with K+ or prostaglandin F2αsuggesting that Mg2+inhibited transmembrane calcium influx and interfered with intracellular calcium effects. In both stem villous and intramyometrial arteries, increasing concentrations of Mg2+increased EC50values for responses to K+, whereas Emaxvalues were unaffected. Mg2+produced relaxation of agonist‐induced contractions by up to 60% in stem villous arteries and up to 40% in intramyometrial artery preparations. The relaxant effect of Mg2+did not seem to be mediated through the endothelium or through changes in the synthesis of prostanoids, since endothelial disruption and treatment with indomethacin left the responses to Mg2+unaffected.Relaxation of vessels important for resistance regulation in the human uteroplacental vascular bed may be of benefit when uteroplacental blood flow is impaired, and the present results support the established use of magnesium sulphate in the treatment of pre‐eclampsia.
Contractile effects of endothelin‐I and localization of endothelin binding sites in rabbit lower urinary tract smooth muscle
Authors: GARCIA‐PASCUAL A. , LARSSON B. , ANDERSSON K.‐E. 
Published: December 2008

In isolated rabbit bladder and urethral smooth muscle, endothelin‐1 caused concentration‐related, slowly developing contractions that were difficult to wash out. Relative to contractions induced by K+ (124 mM), contractions in bladder preparations reached a higher amplitude than in urethral preparations. There was a marked tachyphylaxis to the effects of the peptide. The endothelin‐l‐induced contractions were not significantly affected by phentolamine or indomethacin in the urethra, or by scopolamine or indomethacin in the bladder. Incubation for 30 min in a Ca2+‐free solution abolished the endothelin‐l‐induced contractions. Nifedipine did not affect the actions of endothelin‐1 in the urethra but had a marked inhibitory action on its effects in the bladder. In the presence of endothelin‐1, Ca2+‐induced contractions were significantly blocked by nifedipine in the bladder but not in the urethra.Urethral preparations at resting tension responded to electrical stimulation by tetrodotoxin‐sensitive, frequency‐dependent contractions sensitive to α‐adrenoceptor blockade. Pretreatment with endothelin‐1 (10‐9′ M) produced a significant increase in the nerve‐induced contractions but had no significant effect on contractions induced by exogenous noradrenaline. Endothelin‐1 did not affect spontaneous or stimulation‐induced efflux of 3H‐labelled noradrenaline in urethral smooth muscle. Preparations contracted by endothelin‐1 were frequency‐dependently relaxed by electrical stimulation. The peptide had no significant effect on the responses induced by electrical stimulation in the bladder preparations.In both bladder and urethra, [125]endothelin‐l binding sites were found mainly in the outer longitudinal muscle layer, in vessels and in the submucosa. The highest density of binding sites appeared to be in vessels and the outer muscle layer in both types of muscle.The results suggest that in the rabbit both bladder and urethral smooth muscle contain binding sites for endothelin. The peptide has contractant effects dependent on extracellular calcium in both types of tissue, but voltage‐operated calcium channels seem to involved in activation only of bladder smooth muscle. The functional importance of endothelin‐1 in the rabbit lower urinary tract remains to be elucidated.
Measurement of hepatic protein synthesis in unrestrained mice‐evaluation of the ‘flooding technique’
Authors: LUNDHOLM K. , TERNELL M. , ZACHRISSON H. , MOLDAWER L. , LINDSTRÖM L. 
Published: December 2008

Controversy exists regarding the validity of various techniques for estimating rates of protein synthesis in viva. In the present report, we have compared estimates of hepatic protein synthesis in normal mice with a pulse labelling of [1‐14C]leucine and calculated hepatic protein synthetic rates in a conventional two‐pool model and in a five‐pool compartment analysis. Results obtained with pulse labelling were also compared to those obtained in animals receiving a flooding dose of 1.5 μmol L‐phenylalanine and 0.4 μCi [U‐14C]phenylalanine per gram of body weight or 1.0 μmol L‐leucine and 0.4, μCi [I‐14C]leucine per gram of body weight. Estimates of protein synthesis were calculated with plasma free amino acid, liver acid‐soluble fraction and acylated tRNA specific radioactivities as being representative of the precursor pool for protein synthesis.Rates of hepatic protein synthesis obtained with pulse labelling and either leu‐tRNA or acid‐soluble fractions of liver leucine as the precursor for protein synthesis gave similar results (37 pL 5 vs 42 pL 5% per day) in a two‐pool model, but disagreed in a fivepool model (37 pL 5 us 6 pL 2% per day). Estimates based on plasma enrichment in leucine were only one fifth of values obtained with tRNA in labelling experiments. When the plasma pool with tracer amino acids was used to indicate the precursor labelling of protein synthesis, values obtained with the flooding dose of either phenylalanine or leucine agreed with those obtained with pulse labelling and enrichment in tRNA (30 pL 3 nmol min‐1 us 28 pL 4 nmol min‐1); with however no agreement when the enrichment in the liver mixed tissue pool was used (76 pL 5 nmol min‐1). Complete equilibration of the amino acid pools did not occur despite flooding.Therefore, the flooding technique may only represent an approximate method to measure protein synthesis in vivo, although it gives absolute values that agree well with results from labelling techniques based on tRNA enrichment provided the plasma pool is used as the precursor enrichment.
Effects of weaning on plasma levels of prolactin, oxytocin, insulin, glucagon, glucose, gastrin and somatostatin in sows
Authors: ROJKITTIKHUN T. , UVNÄS‐MOBERG K. , EINARSSON S. , LUNDEHEIM N. 
Published: December 2008

The effect of total weaning (all piglets were weaned at 35 days of lactation) and fractionated weaning (the heavier half of the litter was weaned on day 33 of lactation and the remainder 2 days later) on plasma levels of prolactin, oxytocin, insulin, glucagon, glucose, gastrin and somatostatin in primiparous sows was studied. Twelve crossbred sows were grouped into six pairs according to farrowing date and litter size. The litter of one sow in each pair was weaned in two stages (treatment), and the other was conventionally weaned (control). Blood samples were collected via a permanent jugular vein catheter every 3 hours from 9 a. m. to 9 p. m. from day 31 of lactation until the third day of final weaning.In response to total weaning (studied in the six control sows), plasma prolactin, glucagon and gastrin decreased significantly, whereas plasma insulin and somatostatin significantly increased. Basal concentrations of plasma oxytocin and glucose remained unchanged after weaning. Fractionated weaning did not result in any significant differences in the hormonal and glucose levels as compared with the total weaning. The possible role of prolactin in modulating insulin, glucagon and glucose concentrations as well as the possibility that oxytocin affects gastrin and somatostatin levels following weaning are discussed.
Potential‐dependent potassium currents in the rapidly adapting stretch receptor neuron of the crayfish
Authors: RYDQVIST B. , PURALI N. 
Published: December 2008

The outward current was analysed in the rapidly adapting stretch receptor neuron of the crayfish Pacifastacus leniusculus with a two‐micropipette potential clamp technique and K+‐selective microelectrodes in an attempt to establish if the properties of this current could explain the difference in adaptive behaviour compared to the slowly adapting receptor. A fast activating outward current carried by K+ was revealed. The time constant of activation (tn) was dependent on potential and had a mean value of 0.5 ms at potential steps to 0 mV. Activation followed a second‐order process according to the Hodgkin‐Huxley model. The potential dependence of activation (n∞) followed by a sigmoid curve n∞= l/{l + exp[(E —En)/a]} with a half maximal activation potential En= ‐44 mV and a = ‐13 mV.When long pulses were applied the outward potassium current decreased with two time constants, one that was potential independent (0.2 s) and one that was potential dependent (2–8 s). The latter could be explained by accumulation of K+ in the extracellular space of the neuron. The potential dependence of inactivation followed a sigmoid function k∞= 1/{1 +exp[(E —Ek)/+ a]} with Ek= ‐36 mV and a = 13 mV. The inactivation properties are different from those of the classical fast transient (IA) current. The transport system for the outward potassium current during depolarizing potential steps in the rapidly adapting stretch receptor is similar to the current found in the slowly adapting receptor neuron. However, the activation is faster and seems to occur at potentials more negative than in the slowly adapting receptor. These differences can contribute to but not entirely explain the difference in adaptive behaviour between the slowly and rapidly adapting receptor.
The effects of hypobaric hypoxia (50.6 kPa) on blood components in guinea‐pigs
Authors: OSADA H. 
Published: December 2008

One hundred and five male (Hartley) guinea‐pigs weighing 350–380 g and 30 splenectomized guinea‐pigs were exposed to simulated hypobaric hypoxia of 50.6 kPa (equal to an altitude of 5486 m) for 14 days. The partial pressure of oxygen was set at half that at sea level.The white blood cell count increased significantly on day 3 of the simulated high altitude experiment but returned to normal on day 7, whereas the red blood cell count increased continuously. To study the effect of high altitude exposure on platelets, the platelet count in the splenectomized group was compared to that in a non‐splenectomized group. Investigation of the resistance of red blood cell membranes to osmotic pressure under hypobaric conditions revealed a shift of the onset of haemolysis in the hyperosmotic direction.These findings may help to increase our understanding of the biochemical mechanisms of adaptation to hypobaric hypoxia.