bluuebunny/crossref_metadata_2025_split huggingface dataset:
Thyrotropin‐releasing hormone has stimulatory effects on ventilation in humans
Authors: NINK M. , KRAUSE U. , LEHNERT H. , HEUBERGER W. , HUBER I. , SCHULZ R. , HOMMEL G. , BEYER J. 
Published: December 2008

Thyrotropin‐releasing hormone (TRH) stimulates pituitary thyrotropine synthesis and release and also regulates autonomic nervous system functions by acting as a neuromodulator and neurotransmitter. In experimental animals a stimulation of ventilation by thyrotropin‐releasing hormone was shown when applied at central nervous system sites that affect respiratory motor output. It was the goal of our study to investigate the respiratory properties of thyrotropin‐releasing hormone on basal and stimulated (i. e. CO2‐rebreathing) conditions following systemic thyrotropin‐releasing hormone application in healthy humans. Thyrotropin‐releasing hormone (200 μg, 400 μg intravenous) initiated a rapid short lasting rise of minute volume, ventilatory airflow and alveolar oxygen tension under steady state breathing (P < 0.001). Breathing frequency was less affected, heart rate rose concomitantly (P < 0.001). While breathing with increasing concentrations of carbon dioxide, minute volume was higher under thyrotropin‐releasing hormone than under placebo alone. Further effects (e. g. nausea, dizziness, palpitations) mostly appeared later than respiratory changes and thus may not be responsible for their initiation.Our findings prove systemic thyrotropin‐releasing hormone to be a strong respiratory stimulant in man. Response in respiratory output was also accompanied by central nervous system‐effects (e. g. dizziness, restlessness, augmented vigilance). The mode of thyrotropin‐releasing hormone effects on respiration after peripheral administration is still speculative. An augmented sympathetic output or a direct receptor mediated action at central nervous system sites may be responsible, while a peripheral effect cannot be excluded.
Left ventricular responses to experimental aortic coarctation in growing puppies
Authors: LESKINEN M. 
Published: December 2008

The haemodynamic status of 8 coarctated and 7 sham‐operated beagle puppies was studied by a catheterization technique at rest and during isoproterenol and volume loading at the ages of 7 (I) and 9 (II) months (5 and 7 months after the experimental coarctation).Proximal aortic systolic and pulse pressures were constantly higher in the coarctation group than in the control group (P < 0.05), and the systolic pressure gradient across the coarctation was always significantly higher in the coarctation group [I at rest mean 45 pL 5 (SD) vs 5 pL 4 mmHg, P < 0.001, and after I isoproterenol infusion 56 pL 9 vs 10 pL 6 mmHg, P < 0.001, and after I dextran infusion 58 pL 10 vs 8 pL 7 mmHg, P < 0.001]. The time constant of exponential isovolumic left ventricular pressure fall after the isoproterenol tests was longer in the coarctation group (I 28 pL 8 ms and II, 30 pL 4 ms) than in the control group (I, 21 pL 2, P < 0.05 and II, 19 pL 3 ms, P < 0.005), indicating impaired relaxation. The tension time index during the volume loading tests increased in the coarctation dogs (I, 4150 pL 660 and II, 4080 pL 810 mmHg s min‐1) to higher levels than in the control group (I, 3550 pL 220, II, 2540 pL 1140 mmHg s min‐1, P < 0.05 both). Cardiac output, left ventricular end diastolic pressure, inotropic parameters and heart rate were similar in both groups during the infusions.The results show that the hearts of the young animals exposed to chronic pressure load by aortic coarctation maintained their pump performance well. The changes in left ventricular relaxation may be an early sign of impaired diastolic function.
Neuropeptide Y (NPY): a vasoconstrictor in the eye, brain and other tissues in the rabbit
Authors: NILSSON S. F. E. 
Published: December 2008

The effect of neuropeptide Y (NPY) on uveal vascular resistance was studied in rabbits by direct determination of uveal blood flow from a cannulated vortex vein. Regional blood flows, in the eye, the brain and several other tissues, were measured, with radioactive microspheres, during neuropeptide Y‐infusion in rabbits with and without α‐adrenoceptor blockade.Intravenous infusion of increasing doses of neuropeptide Y caused a dose‐dependent increase in the total uveal vascular resistance. Maximal effect, a 70% increase, was achieved with 120 pmol kg‐1 min‐1. In the microsphere experiments, this dose rate was given i.v. over 10 minutes and blood flow determinations were made before and at 2 and 10 minutes after the start of the infusion. After 2 minutes of neuropeptide Y, there were marked blood flow reductions in the spleen, kidneys, adrenal glands, gastro‐intestinal tract, choroid plexus and pineal and pituitary gland. The effect in the eye was small at 2 minutes, but at 10 minutes local blood flows in the choroid and the ciliary body were decreased by 50% and the iridal blood flow by 30%. Retinal blood flow was not affected by neuropeptide Y. At 10 minutes there were also significant blood flow reductions in the brain, tongue, masseter muscle and several glandular tissues. The effects of neuropeptide Y on local blood flow in rabbits that had been subjected to α‐adrenoceptor blockade were very similar to the effects in the animals without α‐adrenoceptor blockade.The results show that, in the rabbit, neuropeptide Y has marked effects on local blood flows in several tissues, including the eye, and suggest that neuropeptide Y may significantly contribute to the uveal vasoconstriction during sympathetic nerve stimulation.
Oedema‐preventing mechanisms in a low‐compliant tissue: studies on the rat tail
Authors: AARLI V. , AUKLAND K. 
Published: December 2008

The long‐term effect of elevated tail venous pressure (Pv) on interstitial fluid pressure (Pi) and colloid osmotic pressure (COPi) was studied in rats. Measurements were performed on different rats after 1–5 days of congestion, and on a sham operated control group. Two different degrees of venous stasis were obtained by means of graded ligation of tail veins and skin. Moderate degree of ligation (group 1) caused no visual oedema. More extensive ligation (group 2) gave marked oedema already on day 1 and further progression and exudation from the skin during the following 3 days. Tail venous pressure was measured by micropuncture and interstitial fluid pressure by the wick‐in‐needle technique. Interstitial fluid was sampled by a dry wick method, and colloid osmotic pressure was measured with a membrane osmometer.In group 1, Pv had increased from 6.5 to 21.5 mmHg on day 1, and thereafter remained unchanged. Interstitial fluid pressure increased from 3.4 to 16.9 mmHg after ligation and to 19.2 mmHg on day 1. Colloid osmotic pressure fell from 11.7 to 5.8 mmHg. From day 1, both interstitial fluid pressure and colloid osmotic pressure remained largely unchanged.In group 2 rats, tail venous pressure increased to 33.0 and 36.3 mmHg on day 1 and 2 and then fell towards control level during the following 3 days. Interstitial fluid pressure increased to 22.9 and 31.4 mmHg before a rapid decline towards control level. Colloid osmotic pressure was reduced from 11.7 to 5.6 mmHg.We conclude that hydrostatic counterpressure may provide an oedema‐preventing effect of up to about 15 mmHg. Greater acute increase of interstitial fluid pressure lead to exudation and pressure fall. Reduction of colloid osmotic pressure contributed 6–7 mmHg already on day 1.
Influence of some α2‐‐receptor agonists and antagonists on the excitatory non‐adrenergic, non‐cholinergic neurotransmission in the airways of guinea‐pigs in vivo
Authors: JACOBSSON L. , GRUNDSTRÖM N. , ANDERSSON R. G. G. 
Published: December 2008

Neural control of smooth muscle tension in the airways of guinea‐pigs can be subdivided into at least four components: an excitatory cholinergic, an inhibitory noradrenergic, an excitatory non‐adrenergic, non‐cholinergic and an inhibitory non‐adrenergic, non‐cholinergíc component. The existence of α2‐adrenoceptors that modulate the excitatory non‐adrenergic, non‐cholinergic nerve activity has also been demonstrated. The aim of the present study was to investigate the dose‐dependence of the selective α2‐receptor agonists UK 14,304, dexmedetomidine and clonidine on these α2‐adrenoceptors in the airway of guinea‐pigs in vivo.Electrical stimulation of the cervical vagus nerves in anaesthetized guinea‐pigs resulted in a biphasic response in insulllation pressure: an immediate increase due to excitation of cholinergic nerve fibres and a slower, longer‐lasting increase due to activation of the excitatory non‐adrenergic, non‐cholinergic fibres to be studied. The cholinergic compound was abolished by atropine, leaving the excitatory non‐adrenergic, non‐cholinergic component as the sole response recorded during vagal stimulation. UK 14,304 and dexmedetomidine attenuated the response in a dose‐dependent manner, whereas the effect of the partial agonist clonidine was less dose‐related. UK 14,304 and dexmedetomidine reduced the insufflation pressure about 60 and 53% respectively at the highest dose.In conclusion, the neurotransmission in the excitatory non‐adrenergic, non‐cholinergic nerves is attenuated by selective α2‐receptors in a dose‐dependent manner. The present study adds support to earlier observations that the excitatory non‐adrenergic, non‐cholinergic neural system in the airways of guinea‐pigs is modulated by α2‐adrenoceptors.
Cholecystokinin‐stimulated insulin secretion and protein kinase C in rat pancreatic islets
Authors: KARLSSON S. , AHRÉN B. 
Published: December 2008

In isolated rat pancreatic islets, the possible involvement of protein kinase C in cholecystokinin‐8‐stimulated insulin secretion was investigated. In islets exposed for 24 hours to the phorbol ester 12‐O‐tetradecanoyl phorbol 13‐acetate (500 nmol l‐1), a procedure known to down‐regulate islet protein kinase C‐activity, the insulinotropic effect of cholecystokinin‐8 (10‐7 mol l‐1) was partially reduced (by 34 ± 8%, P < 0.001). In contrast the insulinotropic response to acute exposure to 12‐O‐tetradecanoyl phorbol 13‐acetate (10‐6 mol l‐1) was totally abolished (P < 0.001), whereas the insulin response to glucose (8.3 mmol 1‐l) was not affected. In normal islets, the protein kinase C‐inhibitor, staurosporine, inhibited 12‐O‐tetradecanoyl phorbol 13‐acetate‐ and glucose‐stimulated insulin secretion (P < 0.01), but was without effect on cholecysto‐kinin‐8‐stimulated insulin release. Furthermore, in normal islets, cholecystokinin‐8 had no effect on insulin release at a low glucose level (3.3 mmol l‐1). However, at this low glucose level, cholecystokinin‐8 clearly potentiated insulin release induced by acute exposure to 12‐O‐tetradecanoyl phorbol 13‐acetate (lo‐8— 10‐6 mol l‐1, P < 0.001). This potentiating effect was abolished by the removal of extracellular Ca2+.It is concluded that the insulinotropic effect of cholecystokinin‐8 in rat islets is partially mediated by the protein kinase C pathway. Furthermore, the lack of effect of cholecystokinin‐8 on insulin secretion at a low glucose level might be explained by an insufficient activation of protein kinase C under these conditions.
GABA, receptor mediated fast synaptic inhibition in the rabbit brain‐stem respiratory system
Authors: SCHMID K. , BOHMER G. , GEBAUER K. 
Published: December 2008

The involvement of GABA mediated neurotransmission in the central control of respiration was investigated by administration of the specific GABA, receptor agonist muscimol and the specific GABA, receptor antagonist bicuculline into the fourth cerebral ventricle of the rabbit. Cycle‐triggered averaging of the phrenic nerve activity (PNA) was used to quantify drug‐induced changes of the central respiratory pattern. Muscimol reduced the peak amplitude of PNA and increased the duration of the respiratory phases. High amounts of muscimol led to a long‐lasting but reversible central apnea.Bicuculline very effectively blocked the effects of externally applied muscimol. Blockade of intrinsically active GABAergic neurotransmission by bicuculline resulted in a multitude of effects. Peak amplitude of PNA increased whereas the duration of both inspiration and expiration decreased. In this respect, effects of bicuculline and muscimol were complementary. Bicuculline reduced the slope of the inspiratory ramp, increased postinspiratory activity and induced an augmenting type of discharge activity in the last part of expiration resulting in a smooth transition between expiration and inspiration. In some cases the respiratory modulation was completely lost and PNA became perfectly tonic. This ‘apneustic’ type of respiratory pattern could be transformed into rhythmic breathing by increasing the respiratory drive.We conclude that neurotransmission via GABA, receptors is important for the maintenance of respiratory rhythm as well as the generation of normal respiratory pattern.
Dependence of the mean power frequency of the electromyogram on muscle force and fibre type
Authors: GERDLE B. , HENRIKSSON‐LARSÉN K. , LORENTZON R. , WRETLING M.‐L. 
Published: December 2008

The aim of this study was to investigate whether the mean power frequency of the electromyogram of the knee extensors was force and/or muscle fibre‐type dependent. Ten female subjects performed a gradually increasing static knee extension (5 seconds duration) using an isokinetic dynamometer. Electromyogram‐signals were obtained from the vastus lateralis, vastus medialis and the rectus femoris muscles. The torque signal and the three electromyogram signals were recorded on a tape recorder. From the electromyogram recordings the mean power frequency and the signal amplitude were determined. Muscle biopsies were later obtained from the right vastus lateralis and stained for alkaline and acid mATPase for the determination of fibre‐type proportion and areas.Both the mean power frequencies and the signal amplitudes of the three knee extensors were positively torque dependent. Furthermore it was found that the fibre type proportion and the regression coefficient of the torque (%)‐mean power frequency relationship were positively correlated. Also a negative correlation existed between the type‐1 (%) proportion and the intercept of the individual torque (%)‐mean power frequency relationships. In contrast to proposed models of the electromyogram signal no correlation was found between the mean power frequency and the fibre area.
Pulmonary, hepatic and splenic sequestration of technetium‐99m labelled autologous rabbit granulocytes: scintigraphic cell distributions after intravenous and intraarterial injections, exsanguination and intraarterial injection of cells passed through an intermediary host
Authors: FARSTAD B. S. , SUNDREHAGEN E. , OPDAHL H. , BENESTAD H. B. 
Published: December 2008

In man, about half the intravascular granulocytes are not freely circulating, but temporarily sequestered (‘marginated’), so that they cannot be retrieved by bleeding. Where and how the sequestration occurs is not settled and is the subject of the present report. Isolated autologous rabbit granulocytes, labelled with two different 99mTc methods, were reinjected and followed with external scintigraphy.Intraarterial as well as intravenous injection led to rapid accumulation of radioactivity over the lungs. This finding was corroborated and extended by similar experiments, where the labelled cells had firstly been passed through an intermediary rabbit host to remove altered cells, i. e. cells damaged, ‘primed’ (pre‐activated), or activated. In the final autologous host about two thirds of the label rapidly localized to the lungs and liver, and a few per cent to the spleen (which is very small in the rabbit). Even though more than half of the intermediary rabbit's calculated blood volume was removed, the blood sample contained only a few per cent of the rabbit's radioactivity; consequently, many of the labelled leucocytes had marginated during the bleeding. The proportional distribution of radioactivity over lungs, spleen, kidneys, and the rest of the intermediary animal was not markedly changed by this exsanguination, but there was a 4–20% decrease over the liver.Taken together, our findings indicate that normal granulocytes marginate in lungs, liver, and spleen ‐ apparently explicable by the effects of cell size, vessel diameter, cell stiffness (visco‐elastic properties) and size of the arterio‐venous hydrostatic pressure difference. The liver and spleen seemed to play additional roles, since radioactivity over these organs decreased much slower than expected from reported blood half‐times of intact and slightly damaged rabbit granulocytes. This led to a suggestion that macrophages exposed to blood normally phagocytose apoptotically dying granulocytes.
Resiniferatoxin‐, capsaicin‐ and CGRP‐evoked porcine coronary vasodilatation is independent of EDRF mechanisms but antagonized by CGRP(8–37)
Authors: FRANCO‐CERECEDA A. 
Published: December 2008

In the present study the effects of activation of capsaicin‐sensitive C‐fibre afferents by resiniferatoxin and capsaicin as well as the effects of the co‐stored peptides calcitonin gene‐related peptide substance P and neurokinin A on porcine coronary vascular tonein vitrowas investigated.Resiniferatoxin, capsaicin, calcitonin gene‐related peptide and neurokinin A all evoked a sustained, concentration‐dependent vasodilatation of potassium (60 mm)‐precontracted arteries. Substance P also caused vasodilatation of the precontracted arteries but this effect was transient and tachyphylaxis developed rapidly upon repeated administration. Incubation with the calcitonin gene‐related peptide fragment (8–37) did not influence the vascular tone per se but markedly attenuated the dilatory effect of calcitonin gene‐related peptide and totally abolished the vasodilatation induced by resiniferatoxin and capsaicin while leaving the effect of neurokinin A and substance P unaltered. Incubation with methylene blue, an inhibitor of endothelium‐derived relaxing factor mechanisms, which completely blocked the substance P‐evoked vasodilatation, as well as substance P‐tachyphylaxis, did not influence the vasodilator response to resiniferatoxin, capsaicin or calcitonin gene‐related peptide. The neurokinin A‐evoked vasodilatation was most likely mediated through activation of neurokinin 1‐receptors since it remained unchanged in the presence of the neurokinin 2‐receptor antagonist dactinomycin and (Nle10)‐neurokinin A (4–10), which selectively activates neurokinin 2‐receptors, had only a minor dilatory effect on the precontracted arteries.It is concluded that RTX, capsaicin and CGRP share several characteristic features with regard to coronary vasodilatation and the present study provides evidence that cardiac vasodilatation upon activation of C‐fibre afferents by both RTX and capsaicin is mediated by CGRP.
Muscle lactate transport studied in sarcolemmal giant vesicles: dependence on fibre type and age
Authors: JUEL C. , HONIG A. , PILEGAARD H. 
Published: December 2008

Lactate transport was studied in sarcolemmal giant vesicles obtained from rat or rabbit skeletal muscle. With this technique it is possible to obtain quantitative information on sarcolemmal transport characteristics. In equilibrium exchange experiments with 10, 30 and 60 mm lactate, vesicles from ‘red’ rat muscles had a 50% higher lactate transport capacity than vesicles from ‘white’ muscles. Giant vesicles made from rabbit red muscles had a 39% higher lactate transport capacity than vesicles from white muscles. These differences probably reflect a different number of lactate transporters, whereas the lactate affinity in red and white muscles are identical.Lactate transport capacity decreased with age. Sarcolemmal giant vesicles made from 22‐month‐old rats had a 28% lower transport capacity than vesicles from 2‐month old rats. In absolute terms, the initial exchange flux with 30 mm lactate was 92 and 127 pmol cm‐2 sec‐1 for old and young rats, respectively. In supplementary studies in which microelectrode measurements were made in single mouse muscle fibres, it was shown that the cellular acidification rate due to lactate incubation, was 38% lower in fibres from 18‐month old mice than in fibres from 2‐month old mice.
Characterization, localization and actions of endothelins in umbilical vessels and placenta of man
Authors: HEMSÉN A. , GILLIS C. , LARSSON O. , HAEGERSTRAND A. , LUNDBERG J. M. 
Published: December 2008

Endothelin‐like immunoreactivity was observed in the endothelial lining of umbilical vein and artery as well as in the epithelium of the amniotic membrane. High levels of endothelin‐like immunoreactivity (0.4–1.4 pmol g‐1) were detected in human amniotic membrane, umbilical vessels and placenta. The concentration of endothelin‐like immunoreactivity in the amniotic fluid was much higher (77 pmol l‐1) than in umbilical cord plasma (10 pmol l‐1). Characterization by reverse phase HPLC revealed that most of the endothelin‐like immunoreactivity eluted in the position of synthetic endothelin‐1 or oxidized endothelin‐1.Specific, high affinity binding sites for endothelin‐1 were present in placenta and umbilical artery. Endothelin binding sites were also found in cultured smooth muscle cells from the umbilical artery and vein. In the placenta, endothelin‐1 and ‐3 were almost equipotent as competing ligands for endothelin‐1 binding sites, whereas in the umbilical artery endothelin‐3 was much less potent than endothelin‐1. Scatchard analysis of the binding for placental membranes displayed a straight line (r=–0.994) indicating a single class of endothelin receptors with a Kd‐value of 80 pmol l‐1 and Bmax of 113 fmol mg‐1. Endothelin‐1 caused potent contractions of umbilical arteries and veins with threshold effects at 10 pmol l‐1 while endothelin‐3 had no contractile effect up to 10‐7 mol l‐1.It is concluded that endothelin‐1 predominates over other endothelins in umbilical vessels, amnion and placenta, and high levels of endothelin‐1 was observed in foetal circulation and amniotic fluid. Endothelin‐receptors seem to be of different types in placenta (ETB type) and umbilical vessels (ETA type).