bluuebunny/crossref_metadata_2025_split huggingface dataset:
Marked regional heterogeneity in blood flow within a single skeletal muscle at rest and during exercise hyperaemia in the rabbit
Authors: IVERSEN P. O. , STANDA M. , NICOLAYSEN G. 
Published: December 2008

In 1985 both Pendergast et al. and Piiper et al. described a major regional heterogeneity in blood flow within single skeletal muscles both at rest and during exercise. Based on the microsphere method they described large variations in blood flow between muscle samples as large as 1 g each.The aims of the present study were:

To test this notion of regional heterogeneity in microsphere deposition within single skeletal muscles both at rest and during exercise.
To compare the distribution of microspheres with other blood flow tracers.
To test whether or not any heterogeneity was due to vasomotion in small arteries or arterioles.

Microspheres were infused into anaesthetized rabbits over either 10, 30 or 120 s, or 10 min. Exercise was mimicked by tetanic contractions obtained by electrical stimulation of the motor nerves. Three hindleg muscles were divided into samples of 0.25 g each. Regional heterogeneity was expressed as the coefficient of variation corrected for statistical distribution of microspheres (CVc). The CVc at rest was about 0.34. The CVc was unaffected by the various infusion periods and did not change during exercise. Simultaneous infusions of microspheres and 86Rb+ or antipyrine gave high correlations between the two blood flow tracers, with all r values exceeding 0.83 (n= 18).We conclude that the microsphere method provides reliable estimates for regional blood flow within single skeletal muscles. The distribution of blood flow was markedly heterogeneous both at rest and during exercise. The heterogeneity in blood flow was apparently not a result of vasomotion.
α2‐Aclrenoceptor agonist‐mediated inhibition of [3H]noradrenaline release from rat hippocampus is reduced by 4‐aminopyridine, but that caused by an adenosine analogue or co‐conotoxin is not
Authors: HU P.‐S. , FREDHOLM B. B. 
Published: December 2008

The inhibitory effect of an adenosine analogue, R‐PIA, and an α2‐adrenoceptor agonist, UK 14,304, on [3H]NA efflux from field‐stimulated rat hippocampal slices was examined. The effect of 0.1 μm UK 14,304 was mimicked by 30 nM w‐conotoxin and by 10 μM cadmium chloride, inhibitors of N‐ and L‐type Ca2+ channels. R‐PIA (1 μM) had no effect per se, but caused a clear‐cut inhibition after blockade of the pre‐synaptic α2‐receptor by yohimbine.4‐Aminopyridine (4‐AP) caused a dose‐dependent increase in evoked transmitter release. At 30 μM 4‐AP did not affect the actions of ω‐conotoxin or cadmium chloride. The pre‐synaptic effect of R‐PIA was similarly unaffected by 30 μM 4‐AP. The presynaptic effect of UK 14,304 was virtually abolished by 4‐AP (30 μM). The effect of UK 14,304 (0.1 μM) could be partly restored by reducing the Ca2+ concentration during treatment with 4‐AP (22% inhibition compared to 42% with normal Ca2+). The magnitude of increase in evoked [3H]NA efflux by yohimbine (1 μM) was decreased by 4‐AP in a concentration‐dependent manner from 142% increase in controls to 21 % at 100 μM 4‐AP.The present results indicate that NA release is reduced by somewhat different mechanisms by pre‐synaptic α2‐ and adenosine Aj‐receptors. Furthermore, the results indicate that pre‐synaptic Arreceptors on hippocampal NA neurons do not primarily regulate 4‐AP‐dependent potassium channels, but they might act directly on a Ca2+ conductance.
Bistable firing properties of soleus motor units in unrestrained rats
Authors: EKEN T. , KIEHN O. 
Published: December 2008

EMG recordings from single motor units in the soleus muscle were performed in alert unrestrained rats. A cuff electrode around the tibial nerve and subcutaneously placed electrodes in the foot permitted stimulation of afferent fibres. The movements of the rat and the simultaneous EMG activity were displayed together on a video monitor.Most motor units were tonically active for extended periods during quiet standing. During tonic discharge, maintained shifts between stable low (8–12 Hz; quartiles) and high (16–22.8 Hz) frequency ranges were initiated by short‐lasting synaptic excitation of the motoneuron pool by stimulation of la afferents, or inhibition by stimulation of skin afferents. The shifts were not related to gross limb movements. This phenomenon is referred to as a bistable firing pattern. Bistable firing also occurred spontaneously during quiet standing. Typically the firing frequency shifted between a low (9–12.5 Hz) and a high (20–24.5 H) mode. During recordings of simultaneous activity in two units, spontaneous and stimulus‐induced frequency jumps causing maintained changes in firing frequency were regularly seen to occur in one unit, while the frequency in the second unit was unchanged or only phasically influenced.These results demonstrate for the first time a bistable firing pattern during postural activity in the intact animal. The firing pattern closely resembles the bistable behaviour described in spinal motoneurons in reduced preparations, where it is due to the presence of a plateau potential. This suggests that the bistable firing is unexplained by plateau potentials also in the intact animal.
Effects of atrial natriuretic peptide (ANP) on jejunal net fluid absorption in the rat
Authors: PETTERSSON A. , JÖNSSON C.‐O. 
Published: December 2008

The role of atrial natriuretic peptide (ANP) on jejunal net fluid transport was studied in intact rats as well as in rats subjected to a perivascular denervation of the intestinal segment. In rats with intact nerves, an acute volume expansion with 5% albumin (10% of estimated blood volume) decreased jejunal net fluid absorption by approximately 70% compared to control animals not subjected to volume expansion. After a perivascular denervation of the intestinal segment, the acute volume expansion reversed net fluid absorption into a net fluid secretion. In order to reduce the volume expansion‐induced endogenous release of ANP, one group of rats was subjected to a right atrial appendectomy 7 days prior to the experiments. In these animals, the intestinal response to the same 10% volume load was blunted compared to controls. Administration of rat α‐ANP (99–126; 5 μg kg‐li.v.) induced effects similar to those of volume expansion both in rats with intact perivascular nerves as well as in denervated animals. Volume expansion increased mean arterial pressure (MAP) as well as central venous pressure and decreased heart rate (HR) in all groups. When exogenous ANP was administered, a fall in MAP was seen, while HR remained unchanged.In conclusion, these data strongly indicate a physiological role for ANP in jejunal fluid transfer in response to acute volume expansion.
Mechanism of isotonic water transport in glands
Authors: USSING H. H. , ESKESEN K. 
Published: December 2008

Since water and electrolytes pass cell membranes via separate channels, there can be no interactions in the membranes, and osmotic interactions between water and solutes can be expressed as the product of solute flux, frictional coefficient of solute, and length of pathway. It becomes clear that isotonic transport via a cell is impossible. In glands, where cation‐selective junctions impede anion flux between the cells, isotonic water transport is only possible if sodium, after having passed the junction, is reabsorbed in the acinus and returned to the serosal side. Thus it can be recycled via the cation‐selective junction and exert its drag on water more than once. This hypothesis was tested on frog skin glands. Skins were mounted in flux chambers with identical Ringer solutions on both sides. Na channels of the principal cells were closed with amiloride in the outside solution, and secretion stimulated with noradrenaline in the inside solution. Influx and efflux of Na, K and Br (used as tracer for CI) were measured on paired half‐skins during the constant‐secretion phase. Flux ratios for both Na and K were higher than expected for electrodiffusion, indicating outgoing solvent drag. Flux ratios for K were much higher than those for Na. This is in agreement with the concept that Na is reabsorbed in the acinus and K is not.Two independent expressions for the degree of sodium recycling are developed. Under all experimental conditions these expressions give values for the recycling which are in good agreement.
Transport pathways for Na+ and Br‐ (CI‐) in noradrenaline‐stimulated frog skin (Rana temporaria)
Authors: ESKESEN K. , USSING H. H. 
Published: December 2008

Transport pathways for Na+ and Br‐ across noradrenaline‐stimulated frog skin, in which the sodium channels in the apical membrane had been blocked with amiloride, were examined by pre‐steady‐state flux ratio experiments.
To analyse the experiments, equations are derived from which the fluxes through two parallel pathways can be determined if these differ with respect to the flux ratio as well as the mean passage time for the ion in question.
The fluxes of Na+ and Cl‐ were followed over a period of 3 h and it was found that about 1 h after addition of noradrenaline time‐invariant fluxes could be achieved. In that period inward and outward tracer fluxes of Na+ and Br‐ (used as a substitute for Cl‐) were followed during the build‐up of isotope in the tissue until steady‐state fluxes were attained.
The experiments showed that when the Na channels of the capital cells are blocked the glands provide the major pathway for sodium transport across the skin. The efflux of Br‐ can be separated into two components. A fast one through the mitochondria‐rich cells, which is the pathway for passive anion fluxes, and a slower one through the glands. No influx through the slow transport pathway could be detected. In some skins exchange of Br‐ through the mitochondria‐rich cells is revealed. An anion exchange mechanism also appears to be present in the basolateral membrane of the gland cells.
Heterogeneous blood flow distribution within single skeletal muscles in the rabbit: role of vasomotion, sympathetic nerve activity and effect of vasodilation
Authors: IVERSEN P. O. , NICOLAYSEN G. 
Published: December 2008

A major heterogeneous distribution of blood flow has been described on a non‐microvascular level within single skeletal muscles at rest and during exercise hyperaemia both in the dog and in the rabbit.Thde heterogeneity in blood flow distribution could bhd composed of both a steady‐state region‐to‐region variability (spatial) and a time‐dependent variability (temporal) in blood flow to each region. In the present study we estimated their relative contributions to the variations in blood flow within the muscles. Furthermore, we determined whether sympathetic nerve activity contributed to and whether pharmacologically induced vasodilation affected the heterogeneous blood flow pattern.Regional blood flow measurements were based on microsphere infusions into anaesthetized rabbits. Blood flow was determined under both resting conditions and during exercise hyperaemia in regions weighing 0.25 g each within hind leg muscles.Thde coefficient of variation for the spatial variability wahd twice that of the temporal one: 0.32 and 0.16 (mean) respectively. Neither stimulation of the sympathetic nerves, sympathectomy nor vasodilation affected the heterogeneity in blood flow. When exercise hyperaemia was induced, blood flow increased in all regions so that a positive (P &#x006c; 0.05) correlation was present between resting and exercising blood flow values in the individual regions.Although regional variation in vascularization could explain the observations during exercise hyperaemia, we have at present no fully satisfying explanation for the observed regional heterogeneity in blood flow.
Aldosterone secretion during acute metabolic and respiratory alkalosis in the goat
Authors: AUGUSTINSSON O. , JÓNASSON H. , JUNKERGÅRD J. 
Published: December 2008

Received 6 March 1989, accepted 20 April 1989. ISSN 0001–6772. Department of Physiology, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden.Mhdtabolic and respiratory alkalosis were produced in goathd with the primary aim of studying possible influence of a reduced blood hydrogen ion concentration on aldosterone secretion.Metabolic alkalosis was induced by I h i. v. infusion of hypertonic tris(hydroxy‐methyl)aminomethane (THAM) solution. The infusion was associated with a significant reduction in plasma aldosterone concentration (PA). It occurred in the absence of a detectable fall in plasma K or obvious change in plasma renin activity, but simultaneously with a moderate increase in plasma cortisol concentration and a significant reduction of plasma Na concentration. It suggests that changes of the primary aldosterone regulators were not the cause of the fall in PA, but leaves open the possibility that either the decreased blood hydrogen ion concentration as such or THAM‐induced blood hypertonicity reduced the aldosterone secretion.Thde respiratory alkalosis was due to heat polypnoea elicitehd by 2 h exposure of the goats to 45°C. Here, no obvious change in PA was observed during the alkalotic period, which, however, was associated with a rise in plasma K. Increased K stimulation may therefore have masked a possible inhibitory influence of the alkalosis upon the aldosterone secretion.
Renal denervation does not prevent dehydration‐induced natriuresis in sheep
Authors: PARK R. G. , CLEVERS J. , McKINLEY M. J. , RUNDGREN M. 
Published: December 2008

Normal sheep or sheep in which the renal nerves had been extirpated were deprived of water for 2 days in order to determine whether changes in renal nerve activity contribute to natriuresis during water deprivation. Both groups of sheep showed a considerable natriuresis throughout the period of water deprivation and increases in plasma osmolality and plasma Na concentration. Renal denervation, as indicated by the absence of catecholamine fluoresence in kidney sections, was extensive.Phdevious experiments have suggested cerebral involvemenhd in the induction of dehydration‐induced natriuresis. The present results indicate that the efferent pathway mediating this cerebral influence on renal sodium excretion does not involve the renal nerves, suggesting a hormonal mechanism as the likely pathway.,
The enhancement of carbachol‐induced salivary secretion by VIP and CGRP in rat parotid gland is mimicked by forskolin
Authors: LARSSON O. , OLGART L. 
Published: December 2008

Low doses of vasoactive intestinal polypeptide (VIP) and calcitonin gene‐related peptide (CGRP) have been shown to augment the salivary volume secretion evoked by muscarinic receptor agonists or substance P (SP) in rat parotid gland. Since VIP and CGRP are known to activate adenylate cyclase, we have studied whether forskolin, which directly activates this enzyme, can mimic the effects of these peptides on salivary secretion from the parotid gland in anaesthetized (Inactin 0.5 g kg‐1 i. p.) rats. We have also studied the effect of the secretagogues and peptides on glandular blood flow as revealed by the laser Doppler technique.Crbachol (5 nmol kg‐1) and SP (185 pmol kghd‐1) injected i. v. caused a transient increase in parotid blood flow and a decrease in systematic blood pressure concomitant with a salivary secretion of 3.3 ± 0.3 mg(n= 22) and 18.7 ± 1.9 mg(n= 25) respectively. VIP (150 pmol kg‐1) and CGRP (25 pmol kg‐1) also caused a transient increase in glandular blood flow concomitant with a decrease in systemic blood pressure, but no salivary secretion. The glandular blood flow increased by 166 ± 5% and 43 ± 11% for VIP and CGRP respectively. When carbachol was given 20 s after the injection of VIP or CGRP, the secretory response was increased by about 250% and 60% respectively. The adenylate cyclase stimulator forskolin (2.5 pmol kg‐1) produced the same type of response regarding blood flow and systemic blood pressure as VIP and CGRP and potentiated the salivary secretion evoked by carbachol (5 nmol kg‐) by about 100%.Since forskolin can mimic VIP in potentiating salivary secretion, the ability of this peptide to induce CAMP formation in the gland cells may contribute importantly to the stimulation of salivary secretion.,
Effects of pre‐junctional a‐receptor blockade on vascular neuro‐effector characteristics in rats on high sodium intake
Authors: SJÖRLOM‐WIDFELDT N. , NILSSON H. , GUSTAFSSON H. , ELY D. L. , FOLKOW R. 
Published: December 2008

Various in‐vitro studies have indicated a direct attenuating effect of sodium on the affinity of adrenergic α2‐receptors. It has been suggested that ingested sodium in this way might increase blood pressure by reducing the activity of central α2‐receptors and therebl‐ increasing sympathetic discharge. However, such an effect of sodium would also impair the function of peripheral α2‐receptors. In the present study ne have therefore investigated the effect of high sodium intake on the a,‐receptor‐mediated inhibition of the vascular neurogenic response.Male Wistar rats were given 2% NaCl in their drinking water from 4 to 9 weeks of age. Another group receiving plain tap water served as controls. Segments of small branches from the mesenteric artery were mounted in a myograph. Responses to transmural nerve stimulation were determined before and after α2‐receptor blockade with either yohimbine or idazoxan.The response to a continuous nerve stimulation that elicited 30% of maximal contraction was increased 2–3 times after addition of either idazoxan (0.1 μm) or yohimbine (0.3 μm), with no significant difference between sodium‐treated and control rats; if anything the enhancement was slightly greater in the sodium‐treated group. Also, responses to intermittent burst stimulation were increased from 30 to about 80% of maximal response in both rat groups.The results thus indicate that high sodium intake does not affect the inhibitory influence of pre‐junctional α2‐receptors on the vascular neurogenic response.
Characterization of the actions of botulinum neurotoxin type E at the rat neuromuscular junction
Authors: MOLGÓ J. , DASGUPTA B. R. , THESLEFF S. 
Published: December 2008

Botulinum neurotoxin (BoTx) serotype E blocks spontaneous and evoked quanta! release of acetylcholine at the rat neuromuscular junction. Increasing extracellular Ca2+ to 8 mmol l‐1 or substituting Ca2+ with La3+ (0.1 and 1.0 mmol l‐1) or depolarizing the nerve terminals by 20 mmol l‐1 K+ markedly increases miniature end‐plate potential frequency in normal muscle, but in BoTx‐E poisoned preparations none of these ions, with the exception of 1 mmol l‐1 La3+, was able to restore spontaneous quantal transmitter release to levels recorded at unpoisoned junctions. In absolute values the enhancement with La3+ was much less than that reported at normal junctions.Nerve stimulation in the presence of 3,4–diaminopyridine (10–20 μmol l‐1) and high calcium (8 mmol l‐1) evoked multiquantal end‐plate potentials and muscle twitches. We conclude that the neuromuscular block produced by BoTx serotype E is similar to that previously described for BoTx serotype A but differs from that produced by BoTx serotypes B, D and F in not causing desynchronization of nerve impulse‐evoked transmitter release. 3,4–Diaminopyridine might be useful in the treatment of poisoning by BoTx serotype E since it markedly enhanced synchronous transmitter release from poisoned motor nerve terminals.
Water intake and changes in plasma and CSF composition in response to acute administration of hypertonic NaCI and water deprivation in sheep
Authors: RUNDGREN M. , JONASSON H. , HJELMQVIST H. 
Published: December 2008

Water intake and changes in plasma and cerebrospinal fluid (CSF) composition were measured in response to intracerebroventricular (i. e.v.) and intracarotid infusions of hypertonic NaCI solutions and after 48 h of water deprivation in sheep. Significant interindividual differences in dipsogenic sensitivity to i. e.v. NaCI were found, whereas no such differences were observed in response to intracarotid infusion of hypertonic NaCI. In the more sensitive animals, the increase in CSF [Na] at initiation of drinking during i. e.v. infusion did not differ significantly from the increase in plasma [Na] seen at the thirst threshold during intracarotid infusion of 1 M NaCI. The thirst‐eliciting infusions of hypertonic NaCI into the carotid arteries were associated with a small, significant, increase in CSF [Na], which however did not differ from that caused by an i. e. v. non‐dipsogenic ‘control’ infusion of a slightly hypertonic (0.154 M) NaCI solution. Water deprivation for 48 h induced increases in CSF and plasma [Na] similar to those observed at the onset of drinking in response to i. e.v. and intracarotid infusions of hypertonic NaCI. However, the dehydrated animals drank about four times the amount of water consumed in response to the separate treatments with hypertonic NaCI.It is concluded that significant interindividual differences in dipsogenic sensitivity to osmotic stimuli are present in sheep, and that these differences may not necessarily be simultaneously expressed on both sides of the blood‐brain barrier.The thirst‐eliciting effect of intravascular infusion of hypertonic NaCI may be induced without concomitant increase in CSF [Na] and/or osmolality.A simultaneous increase in CSF and plasma [Na] and/or osmolality is suggested to contribute to the conspicuous water consumption seen in response to dehydration compared to that caused by acute administration of hypertonic NaCl.
Cardiovascular and metabolic responses to static contraction in man
Authors: GAFFNEY F. A. , SJØGAARD G. , SALTIN B. 
Published: December 2008

There is substantial controversy regarding muscle blood flow and its regulation during static exercises. Major issues include (1) the relationship between developed force and muscle blood flow, (2) the ability of metabolic vasodilation to overcome neurally mediated vasoconstriction, (3) the time course and magnitude of hyperaemic flow following static exercise and (4) blood flow to the contralateral inactive limb. At rest, 15, 25 and 50% maximal voluntary contractions (MVC) femoral venous flow in four healthy young men (LBF; mean±1 SD) was 0.4 ± 0.3, 1.76 ± 0.65, 0.90 ± 0.32 and 1.06 ± 0.59 l min‐1, and mean arterial pressures (MAP) were 104±13, 140±14, 160 ± 17 and 161 ± 11 mmHg. Thus, LBF does not increase proportionally with increasing levels of MVC, despite increased arterial pressure. Further, during both 25 and 50% MVC, which were held to exhaustion, an elevated limb vascular resistance was encountered towards the end of contraction, which suggests that neurally mediated vasoconstrictor activity overrides local vasodilation.Femoral venous effluent documented perfusion of active muscle during contractions of 15 and 25% MVC, but less so at 50% MVC. Immediately in recovery LBF reached levels of 3–3.5 l min‐1, which corresponded to 150 ml 100 g‐1 min‐1. When both O2 uptake and lactate release during the contractions and in recovery were taken into account, a close correlation between rate of energy turnover and exerted force was found.When MAP was raised by static contraction of the opposite quadriceps, LBF in the inactive leg increased momentarily. Within 1 min vascular resistance became elevated and the blood flow became reduced.