bluuebunny/crossref_metadata_2025 huggingface dataset:
Human sympathetic nerve activity to glabrous skin does not increase during simulated diving
Authors: FAGIUS J. , TRAVERSA R.
Published: December 2008

In humans, cardiovascular adjustment to simulated diving causes a marked increase in sympathetic outflow to intramuscular vessels and muscle vasoconstriction. Skin vasoconstriction in the hand also occurs during diving in humans. Skin nerve sympathetic activity (SSA), containing vasoconstrictor signals to glabrous skin, unexpectedly was reduced during diving in a previous study of SSA recorded in the peroneal nerve. SSA was recorded by microneurography in the median nerve in 13 healthy volunteers during simulated diving. Skin blood flow in the hand and one finger was monitored. The typical SSA response, irrespective of duration of diving and water temperature, was an increase during the control period immediately prior to immersion of the face and a sudden reduction of SSA when the face was immersed. The increase in SSA preceding the dive was accompanied by vasoconstriction, which continued during the dive, but re‐dilation regularly occurred before the end of the dive. Inhibition of SSA was not total. Mental arithmetic during diving evoked strong bursts of SSA, similar to those seen normally during mental stress. It is concluded that the true response of SSA to simulated diving is an inhibition of the immediately preceding outflow, in agreement with observations of cutaneous blood flow in animals. The skin vasoconstriction recorded during simulated diving is a consequence of an SSA increase before the procedure, suggested to be a stress response before the forthcoming manoeuvre. The SSA response during simulated diving is the opposite to that of sympathetic outflow to muscle, which emphasizes the diversity of sympathetic regulation of different organ systems.
Is palmar and plantar sweating thermoregulatory?
Authors: KERASSIDIS S.
Published: December 2008

We tested the hypothesis that palmar and plantar sweating has a thermoregulatory role and is mediated by the same thermoregulatory mechanisms that control sweating in the rest of the body surface. In a series of empirical tests involving 34 participants (five of whom exhibited palmar hyperhydrosis), the effect of high environmental temperature on sweating was examined. Wilcott's finding, that effects at the palm are of considerable magnitude, was confirmed only in subjects who were in a state of excitement. In relaxed subjects, the effect of high environmental temperature on palmar and plantar sweating was negligible. We conclude that the palms and soles do not directly participate in thermoregulation.
Reduced oxygen availability during high intensity intermittent exercise impairs performance
Authors: BALSOM P. D. , GAITANOS G. C. , EKBLOM B. , SJÖDIN B.
Published: December 2008

This study examined the influence of reduced oxygen availability on the ability to perform repeated bouts of high intensity exercise on a cycle ergometer. Seven male physical education students performed 10 exercise bouts (of 6 s each), interspersed with 30‐s recovery periods, under hypoxic and normoxic conditions. The hypoxic condition was carried out in a low pressure chamber at 526 mmHg. Subjects were instructed to try to maintain a target pedalling speed of 140 rev min‐1 during each exercise period. The mean power output of the first exercise bout was ˜ 950 W. In both experimental conditions, all subjects were able to maintain the target speed for the first 3 s of each of the 10 exercise bouts. During the last 3‐s interval of each exercise period the target speed was not maintained in both conditions over the 10 sprints. However, the reduction was greater in the hypoxic condition (P < 0.05). Post‐exercise blood lactate accumulation was higher with hypoxia [10.3 (0.7) vs. 8.5 (0.8) mmol 1‐1P < 0.05]. Oxygen uptake, measured during the exercise and recovery periods of sprints 6–9, was lower in the hypoxic condition [3.03 (0.2) vs. 3.19 (0.2) 1 min‐1, P < 0.05], These results indicate that a reduction in oxygen availability during high intensity intermittent exercise results in a higher accumulation of blood lactate and a lower oxygen uptake. The ability to maintain a high power output is impaired.
Nitric oxide‐like activity in guinea pig colon as determined by effector responses, bioassay and chemiluminescence analysis
Authors: IVERSEN H. H. , WIKLUND N. P. , GUSTAFSSON L. E.
Published: December 2008

The role of nerve‐induced release of nitric oxide (NO) as a modulator of neuroeffector transmission was studied in the longitudinal muscle of the guinea pig colon. The biological activity of a vascular relaxing factor released by nerve stimulation was examined in a bioassay cascade system. Furthermore, biochemical measurements of nerve‐induced release of the NO metabolite nitrite (NO2‐) were made with a chemiluminescence technique. Transmural nerve stimulation elicited contractile responses that were partly blocked by atropine and further inhibited after additional application of the tachykinin receptor antagonist CP‐96, 345. The NO‐synthase inhibitorNw‐nitro‐L‐arginine (NOARG) enhanced the nerve‐induced contractions and concomitantly increased the basal degree of contraction (‘tone’). The relaxations obtained by nerve stimulation after treatment with atropine and histamine were inhibited by NOARG. Electrical stimulation of the guinea pig colon released a non‐adrenergic non‐cholinergic (NANC) vascular relaxing factor into the tissue superfusate. The half‐life of this factor down the cascade was the same as that observed with exogenous application of NO NOARG and tetrodotoxin (TTX) inhibited the release of the relaxing factor. During transmural nerve stimulation there was a significant increase in NO/NO2‐release. This increase was inhibited by TTX andNw‐nitro‐L‐arginine methyl ester (L‐NAME). In conclusion, pharmacological analysis as well as bioassay and biochemical measurements suggest that NO is released during nerve stimulation in the guinea pig colon, where it mediates smooth muscle relaxation.
Central control of disynaptic reciprocal inhibition in humans
Authors: CRONE C. , NIELSEN J.
Published: December 2008

The disynaptic pathway from muscle spindle la afferents to motoneurones of the antagonist muscle is one of the best studied pathways in the spinal cord. Early animal studies ‐ mainly in the cat ‐ have provided a detailed knowledge of the pathway itself and of the integration of segmental and supraspinal convergence at the interneuronal level. Although this knowledge was used to formulate hypotheses on the function of the pathway during natural movements, the reduced animal preparation limited the possibilities of testing these ideas. However, such information has more recently been obtained from human subjects by using indirect electrophysiological techniques. In most of these experiments the disynaptic la inhibition was demonstrated as a short‐latency depression of a monosynaptic test reflex (H‐reflex) following a conditioning stimulation of the antagonist nerve. Changes in the size of this depression during voluntary tasks were then taken as evidence of a central regulation of the pathway. It has for example been demonstrated in this way that the brain regulates the la inhibitory interneurones in parallel with their corresponding motoneurones during extension‐flexion movements, but not during co‐contraction of antagonistic muscles. The importance of the central control of the pathway has also been emphasized by the finding of a disordered regulation of its activity in patients with lesions of the brain. This may possibly contribute to the inappropriate co‐contraction of antagonistic muscles observed in some of these patients. It seems reasonable to expect that this kind of experiment in the future may contribute significantly to the knowledge of the central control of spinal motor mechanisms.
The influence of muscarinic and prostaglandic mechanisms on regional cerebral and peripheral blood flows and on the vascular effects of thyrotropin releasing hormone (TRH)
Authors: KOSKINEN L.‐O. D.
Published: December 2008

TRH has pronounced vascular effects. The final transmitter mechnisms of these effects are not fully understood. The present study was conducted in order to elucidate whether these effects are mediated by prostaglandic or muscarinic mechanisms. Muscarinic blockade augmented the vasoconstricting‐ and pressor effect of TRH; vasodilation in the brain was attenuated only in the caudate nucleus. Indomethacin provoked a decrease in regional cerebral blood flow and in the gastric mucosal blood flow. No effect of indomethacin was observed on the vascular effects of TRH. It is concluded that the cerebral vasodilating and peripheral vasoconstricting effects of TRH are not mediated by prostaglandins. Muscarinic mechanisms are involved in the vasodilating effect of TRH only in the caudate nucleus.
A morphometric study of the effect of bilateral cervical sympathetic ganglionectomy on the architecture of pial arteries in spontaneously hypertensive and normotensive rats
Authors: KÅHRSTRÖM J. , NORDBORG C. , HARDEBO J. E. , OWMAN C.
Published: December 2008

The influence of the cranial sympathetic nerves on the architecture of pial arteries in normo‐ and hypertension was examined. For this purpose the effect of bilateral superior cervical ganglionectomy was evaluated in normotensive rats (WKY) and stroke‐prone spontaneously hypertensive rats (SHRSP). The operations were performed at the age of 1 wk, which is just prior to the onset of ganglionic transmission. The length of the inner media contour was measured and the media cross‐sectional area was determined planimetrically, with computerized digitalization of projected photographic images of transversely sectioned pial arteries. Four wk after sympathectomy there was a 20% reduction in media cross‐sectional area and a consequent reduction in the ratio between media area and calculated luminal radius in the major pial arteries at the base of the brain in WKY but not in SHRSP. Conversely, in small pial arteries linear regression analysis showed that in WKY subjected to ganglionectomy the relationship between media cross‐sectional area and luminal radius was significantly larger in arteries with a radius less than 21 μm compared to untreated WKY. No such effect was seen in the corresponding SHRSP vessels. In addition, the cross‐sectional area of the internal elastic membrane (IEM) in the basilar arteries of WKY was measured by means of a computerized image‐analysing system. Mean cross‐sectional area of the IEM was approximately 45% larger following SE than in control animals. The present findings propose a ‘trophic’ role for the sympathetic perivascular nerves in large pial arteries of the rat. The increased media‐radius ratio in the small pial arteries of the WKY following sympathectomy might reflect a compensatory hypertrophy due to reduced protection from the larger arteries against the pressure load. The inability to detect any morphometrically measurable effect of the sympathectomy in the cerebral arteries of SHRSP is probably explained by a marked growth‐stimulating effect of the high pressure load in these animals.
Membrane stretch evoked by cell swelling increases contractile activity in vascular smooth muscle through dihydropyridine‐sensitive pathways
Authors: BÜLOW A. , JOHANSSON B.
Published: December 2008

Effects of the dihydropyridine calcium antagonist felodipine and of calcium reduction were studied on osmotically induced contractile responses in the vascular smooth muscle of the rat isolated portal vein. Previous studies have shown that changes in osmolarity that cause cell swelling are accompanied by increased contractile activity in this smooth muscle (Johansson & Jonsson 1968). A transient enhancement of the contractile activity developed in the portal vein on return to standard Krebs solution after exposure to 60 mM urea. This osmotic response was dependent on extracellular Ca2+ (abolished in Ca2+ free solution+ 0.1 mM EGTA) and was reduced in proportion to the decrease in spontaneous phasic contractile activity when Ca2+ was lowered from the standard 2.5 mM concentration. Felodipine, 3 nM, reduced the spontaneous activity to approximately 50% but showed an even more pronounced inhibitory effect on the osmotic responses which were reduced to less than 20% of control. Other calcium antagonists such as verapamil, 60 nM and diltiazem, 300 nM, were also more effective in inhibiting the osmotic responses than the spontaneous activity. In contrast, the K+ channel opener, pinacidil, 100–200 nM, reduced the spontaneous activity to 50% but had only minor inhibitory effect on the osmotic responses, about 75% still persisting.

It is suggested that stretch of the cell membrane in response to variations in osmolarity induces contractile activity in vascular smooth muscle by mechano‐electrical coupling involving dihydropyridine‐sensitive pathways.
Role of the sympathetic nervous system in cardiac performance during hyperkalaemia in the anaesthetized pig
Authors: O'NEILL M. , PATERSON D. J.
Published: December 2008

Cardiovascular performance was studied in 18 α‐chloralose anaesthetized pigs when arterial potassium ([K+]a) was raised to levels observed in heavy exercise. The effects of hyperkalaemia were then studied during cardiac sympathetic nerve stimulation or during an infusion of noradrenaline. Elevation of [K+]a up to ca. 10 mM caused a progressive decline in cardiovascular performance. However, right cardiac sympathetic nerve stimulation elevated all cardiovascular parameters in the presence of raised [K+]a and offset the negative cardiac effects of hyperkalaemia. Electrical pacing of the right atrium to heart rates (HRs) equivalent to those observed during right cardiac sympathetic nerve stimulation did not offset the depressive effects of hyperkalaemia and, indeed, hastened the decline in cardiovascular performance. Infusion of noradrenaline (1 m̀g kg min‐1 i. v.) during hyperkalaemia caused an increase in all cardiovascular parameters similar to that seen during sympathetic nerve stimulation. After propranolol (0.5 mg kg‐1 i. v.), sympathetic nerve stimulation slightly increased HR, systolic blood pressure (SBP) and dP/dtmax. Elevation of [K+]a occurred more rapidly after propranolol, but the heart was still protected from hyperkalaemia during cardiac sympathetic stimulation. Infusion of noradrenaline elicited arrhythmias in six pigs. Infusion of KCI reduced the incidence of arrhythmias and in some cases abolished them. These findings may be related to how the heart is protected from exercise‐induced changes in potassium and catecholamines.
Influence of coronary venous retroinfusion and vasodilatation on regional myocardial blood flow measurement with microspheres. An analysis of ‘microsphere loss’ from ischaemic and reperfused porcine hearts
Authors: HAGA Y. , NORDLANDER R. , SJÖQUIST P.‐O. , RYDÉN L.
Published: December 2008

The influence of coronary venous retroinfusion and a vasoselective calcium antagonist felodipine on the microsphere loss in a porcine model of myocardial ischaemia and reperfusion was studied.

Sixteen open‐chest pigs underwent 45 min of myocardial ischaemia induced by occlusion of the left anterior descending coronary artery followed by 4 h of reperfusion. Either felodipine (felo‐retro group, 7 nmol kg‐1, n= 6) or the corresponding amount of vehicle (vehicle‐retro group, n= 5) was infused retrogradely into the coronary veins over 30 min, starting 5 min before reperfusion. In a third group, the same amount of felodipine was administered intravenously (felo‐iv group, n= 5). Myocardial regional blood flow was measured with radiolabelled microspheres (ø= 15 μm) injected before ischaemia to investigate a possible loss during ischaemia.

In the felo‐retro group, the apparent blood flow in the ischaemic areas, expressed as a percentage of the corresponding values in the non‐ischaemic areas (%‐flow), were 73±15, 73±11 and 75±19 in the subendocardial, midmyocardial and subepicardial layers, respectively. The corresponding percentage flows were 64±11, 70±11 and 62±9 in the vehicle‐retro group and 75±18, 77±15 and 76±11 in the felo‐iv group. The differences between the groups were not satistically significant.

It is concluded that in this open‐chest preparation microsphere loss observed in the ischaemic and reperfused myocardium is not increased by coronary venous retroinfusion or by a concomitantly administered vasodilative agent like felodipine.
Acute renal denervation causes time‐dependent resetting of the tubuloglomerular feedback mechanism
Authors: THORUP C. , KURKUS J. , MORSING P. , PERSSON A. E. G.
Published: December 2008

Renal effects of acute renal denervation (DNX) were studied in anaesthetized rats. In a first series, whole kidney clearance measurements were made 120 and 240 min after unilateral DNX. At 240 min, urine production was 3.59±0.87 μL min‐1 in control kidneys and 7.74±1.97 μL min‐1 in denervated kidneys. The corresponding values for sodium excretion were 0.56±0.17 and 1.41±0.34 μmol min‐1, potassium excretion 0.48±0.08 and 0.97±0.37 μmol min‐1 and glomerular filtration rate (GFR) 0.83±0.08 and 1.05±0.16 mL min‐1, respectively. In a second series, tubuloglomerular feedback (TGF) characteristics were determined with the stop‐flow pressure (Psf) technique. With increasing time, the sensitivity of the TGF mechanism diminished in denervated rats, as indicated by an increased turning point (TP). TP was significantly increased 2 h after DNX from 19.1±1.13 in control to 25.9±1.10 nL min‐1. TP was further increased 4 h after DNX to 37.3±3.12 nL min‐1. However, the maximal TGF response to increased flow in the late proximal tubule was not altered. But, Pst was significantly higher in DNX rats than in the controls (47.4±1.01 vs. 43.0±1.53 mmHg) in spite of a lower blood pressure (107±2.9 vs. 119±2.2 mmHg). We conclude that intact renal nerves are essential for the setting of the TGF sensitivity and hence the regulation of GFR
Natriuresis obtained by intracerebroventricular infusion of hypertonic NaCI in rats with papillary necrosis.
Authors: JACOBSSON E. , SJÖQUIST M.
Published: December 2008

Raising the sodium concentration in the third cerebral ventricle increases renal sodium, potassium and water excretion. The identification and characterization of the factor(s) mediating the centrally evoked natriuresis would be greatly facilitated if the exact intrarenal effector site were known. We have assessed the importance of inner medullary structures for the effects of CNS stimulation by examining its ability to alter renal excretion in rats with papillary necrosis, induced 2 d earlier with 2‐bromoethylamine hydrobromide (BEA), 250 mg kg‐1 body wt i. v. Male Lewis x DA rats were divided into a BEA‐treated group (n = 6) and a control group receiving vehicle alone (n = 6). In contrast to the white papillae normally seen, the papillae of BEA‐treated animals were bright red and showed a clear line of demarcation at their base. The rats were anaesthetized i. p. with Inactin (120 mg kg‐l body wt). Artificial cerebrospinal fluid (CSF) was infused (520 nL min‐1) via a cannula into the left lateral ventricle. After 45 min CSF containing 1 M NaCl was used. Stimulation of the control rats with hypertonic CSF increased urine flow rate five‐fold (5.4± 0.8 to 27.1±6.1 μL min‐1), Na excretion 23‐fold (0.4±0.1 to 7.6±1.8 μmol min‐1) and K excretion fourfold (0.6±0.18 to 3.8±O.5 pmol min‐1). When the concentration mechanisms were damaged with BEA, the basal excretion rates of water and Na increased. The natriuretic response to ICV stimulation was severely impaired in these rats, but the kaliuretic effect was sustained. In conclusion, the natriuretic effect of ICV stimulation with hypertonic CSF is dependent on an intact renal inner medulla, which is not the case for the less pronounced kaliuretic response. Thus, either the juxtamedullary nephrons possess marked natriuretic responsiveness, not present in the cortical ones, or the responsiveness lies mainly in the papillary collecting ducts. However, it cannot be excluded that a disturbance of salt balance contributes to the observations.
Thyroid hormone regulation of myosin heavy chain isoform composition in young and old rats, with special reference to IIX myosin
Authors: LARSSON L. , MÜLLER U. , LI X. , SCHIAFFINO S.
Published: December 2008

The effects of 4 weeks of thyroid hormone (3,5,3′‐triiodothyronine, T3) treatment on the myosin heavy chain (MHC) composition were compared in the slow‐twitch soleus and the fast‐twitch extensor digitorum longus (EDL) muscles from young (3–6 months) and old (20–24 months) male albino rats. Four MHC isoforms were separated on silverstained 6% sodium dodecyl sulphate polyacrylamide gel electrophoresis. According to immunoblotting experiments with specific MHC monoclonal antibodies, the four MHCs corresponded to types I, IIB, IIX and IIA. In the soleus, the type I MHC content was higher in the old than in the young animals, and the type IIA content lower. Type IIX myosin was observed in some young control soleus, but not in old ones. After T3 treatment, the content of type I MHC decreased substantially in both young and old animals and that of type IIA increased. After T3 treatment, type IIX myosin was observed in both young and old animals, with a slighty higher IIX myosin content in old age, but the age‐related different in the contents of types I and IIA was diminished. In EDL, the type IIX MHC content was significantly higher in the old animals, at the significantly by T3 treatment in EDL, either in young or old animals. In conclusion, an age‐related motor unit transformation is observed in both the slow‐twich soleus and the fast‐twitch EDL and the capacity for MHC isoform switching in response to T3 treatment is not impaired in old age.
Excitation and contraction in atrial and ventricular myocardium of the guinea‐pig
Authors: ÁSGRÍMSSON H. , JÓHANNSSON M. , ARNARDÓTTIR S. Á.
Published: December 2008

Several parameters of excitation‐contraction coupling were compared in two types of muscle, using thin strips from the left atria and papillary muscles from the right ventricles of guinea‐pigs. (1) The duration of the action potential and twitch is much longer in ventricular than in atrial muscle. (2) Mechanical restitution can usually be described by a monoexponential function in ventricular and biexponential function in atrial muscle. (3) Post‐extrasystolic potentiation, when related to the steady state force, is greater in ventricular muscle. (4) When priming with paired‐pulse stimulation, mechanical restitution can be studied after the short interval and after the long interval. In atrial muscle, mechanical restitution is very similar after the short and long intervals but in ventricular muscle they are different in size. (5) Ryanodine (10‐6 M) can decrease the steady state force to about 10% of control in atrial but only to about 35% in ventricular muscle. Ryanodine (10‐8 M) causes the slow phase of restitution in atrial muscle to disappear but in ventricular muscle only increases the rate of mechanical restitution. (6) Ca‐antagonists (Cd2+ 0.2 mM) can decrease the steady state force to zero in atrial and ventricular muscle. Ca‐antagonists, in low concentrations (Cd2+ 0.01 mM), mainly affected the fast phase of mechanical restitution. (7) The recirculation fraction of calcium was about 0.64 in atrial and 0.27 in ventricular muscle.

The findings are discussed in the light of known ultrastructural differences between atrial and ventricular myocardium.
Carbachol‐induced increase in inositol trisphosphate (IP3) content is attenuated by adrenergic stimulation in the isolated working rat heart
Authors: MARTINUSSEN H. J. , WALDENSTRÖM A. , RONQUIST G.
Published: December 2008

The interrelated responses of concomitant adrenergic and muscarinic receptor stimulation on second messengers and mechanical activity in the isolated perfused working rat heart were studied. The hearts were perfused with Krebs‐Henseleit buffer in a modified Langendorff apparatus. The hearts were perfused with noradrenaline (10‐6mol L‐1,n= 20), with carbachol (3 times 10‐7mol L‐1n= 11) or with noradrenaline plus carbachol (n= 20) in the above‐mentioned concentrations. The hearts were frozen at 20 s, 30 s and 40 min after addition of noradrenaline and noradrenaline plus carbachol and at 20 s and 40 min after addition of carbachol. Five hearts were freeze‐clamped directly after preperfusion and another five hearts after 40 min of perfusion and used as controls. Myocardial cAMP increased at 20 s and 40 min after noradrenaline perfusion. In contrast to this cAMP was unchanged at 20 s and decreased at 40 min after perfusion with noradrenaline plus carbachol. IP3content increased after 20 s of carbachol‐ and after 40 min of noradrenaline perfusion (P< 0.05). However, noradrenaline plus carbachol did not induced any significant increase in IP3content after 20 s and 30 s, but after 40 min a decrease below basal level was found (P< 0.05). Noradrenaline stimulation attenuated muscarinic agonist induced IP3formation. A reciprocity existed in that noradrenaline induced IP3formation was attenuated by carbachol. No direct relationship was observed between the IP3response and contractility, also valid for cAMP. Hence, a significant increase in contractility was found in spite of a blunted cAMP response probably not accounted for by an anα1‐adrenergic effect alone.
Intravenous lipid infusion results in myocardial lipid droplet accumulation combined with reduced myocardial performance in heparinized rabbits
Authors: HEXEBERG S. , HESSEVIK I. , HEXEBERG E.
Published: December 2008

The question addressed in this study was whether a relation between myocardial lipid droplet accumulation and depressed myocardial function existed following intralipid infusion for 45 min in open chest, anaesthetized rabbits. One group of rabbits (n = 8) received intralipid infusion whereas a control group (n = 8) received sodium chloride. Local myocardial performance was obtained by sonomicrometry and the fractional volume of myocardial lipid droplets was measured by morphometric methods. The fractional volume of lipid droplets was 0.667 ± 0.1160% in the intralipid group compared with 0.318 ± 0.080% in the control group (P < 0.03). Cardiac output and stroke volume fell 26% (P < 0.0001) and 34% (P < 0.000), respectively, as a result of intralipid infusion. However, myocardial blood flow obtained by radiolabelled microspheres remained unchanged. Local myocardial function was reduced for both segments after intralipid infusion; maximal systolic shortening was reduced from 15.63 ± 1.45 to 12.07 ± 1.55% (P < 0.002) in the circumferential segment and from 9.46 ± 1.17 to 7.40 ± 0.53% (P < 0.05) in the longitudinal segment. The end‐diastolic length of the circumferential segment was reduced by 3% (P < 0.05) after intralipid infusion. The reduced end‐diastolic length of circumferential segments together with unchanged left ventricular end‐diastolic pressure might indicate reduced left ventricular end‐diastolic compliance. We conclude that acute intralipid infusion in rabbits results in myocardial lipid droplet accumulation and depressed local myocardial function.
Fluid and protein secretion from ferret submandibular and parotid glands in response to sympathetic nerve stimulation or administration of sympathomimetics.
Authors: TOBIN G. , MIRFENDERESKI S. , ÅHSTRÖM T. , EKSTRÖM J.
Published: December 2008

Electrical stimulation of the sympathetic innervation evoked secretion of submandibular and parotid saliva. By changing the mode of stimulation from a continuous to an intermittent one the fluid response increased and glandular blood flow improved. The volumes from the submandibular glands were larger than those from the parotid glands and further, the protein concentration of submandibular saliva was higher than that of parotid saliva. Adrenaline, isoprenaline and phenylephrine evoked larger fluid responses from submandibular than from parotid glands. However, the fluid response was small compared to the parasympathetic one. Substance P‐evoked saliva was used as carrier for protein released by sympathetic nerve stimulation or administration of adrenaline and isoprenaline. In vitro tissues of submandibular and parotid glands responded to adrenaline with a dose‐dependent release of protein. Taken together, the analytical pharmacology performed in vivo and in vitro, and including the antagonists phentolamine, dihydroergotamine, propranolol and metoprolol, showed that in submandibular glands, α(α1)adrenoceptors were predominantly involved in fluid secretion and β(β1)‐adrenoceptors predominantly involved in protein secretion. In parotid glands, fluid secretion seemed solely to depend on α(α1)‐adrenoceptors, while β(β1)‐adrenoceptors seemed almost solely involved in protein secretion.
Influences of time intervals between meals and total food intake on resting metabolic rate in rats
Authors: MUNCH I. C.
Published: December 2008

Resting metabolic rate was measured in rats receiving single or double food portions every day or every other day, adding up to the same total food intakes. Starving rats were also measured. At two different total food intakes, there were no differences between the rats that were fed a meal every day and those fed a double meal every other day. Thus, the time interval between meals does not determine the extent of the metabolic depression. Also, the resting metabolic rates of rats fed various reduced food regimens are very similar to each other and to the resting metabolic rate of starved rats. The results of this study thus indicate that metabolic depression during starvation and severe caloric restriction in rats is an initially uniform response that modulates itself late in the starvation or restriction period in accordance with the total food intake.
Electrical field stimulation of rat mesenteric small arteries: force and free cytosolic calcium during neurogenic contractions and mechanisms of non‐neurogenic relaxations
Authors: JENSEN PETER E.
Published: December 2008

The effect of transmural electrical field stimulation (TEFS) of rat mesenteric small arteries was studied. Stimulation parameters were selected to cause tetrodotoxin (TTX) sensitive contractions. In arteries precontracted with PGF2αin the presence of phentolamine, TTX insensitive relaxation could be induced by TEFS. The relaxing effect of TEFS required higher stimulation amplitude and duration than the contractions. Thus, by appropriately choosing stimulation parameters, contractile responses could be elicited which were little affected by any relaxing effect, while contractions were abolished by TTX at any stimulation conditions in the present study.

The contractions were abolished by cold storage and almost completely inhibited by phentolamine. Thus, contractions were neurogenic and primarily caused by noradrenaline. At low frequencies, TEFS caused phentolamine sensitive increases in free cytosolic calcium with no contractions. At higher frequencies, there was a further increase in free cytosolic calcium, associated with contraction. Only at high frequencies, noradrenaline from nerves caused sensitization of the contractile filaments to free cytosolic calcium as during stimulation with exogenous noradrenaline.

The relaxations were associated with decreases in free cytosolic calcium and were probably non‐neurogenic since they were resistant to TTX, cold storage, capsaicin, and repeated stimulation. Furthermore, relaxations were almost completely abolished by increasing extracellular potassium to 40 mM or by adding tetraethylammonium chloride or 4‐aminopyridine. Relaxations were also reduced by ouabain and potassium free conditions.
Physiological characteristics of two extreme muscle compartments in gastrocnemius medialis of the anaesthetized rat
Authors: De RUITER C. J. , De HAAN A. , SARGEANT A. J.
Published: December 2008

Rat medial gastrocnemius (GM) muscle is a compartmentalized muscle. The functional properties and fibre type composition of the most proximal and most distal compartment were studied in in situ preparations. The proximal compartment contained predominantly fast twitch oxidative fibres. The distal compartment was mainly composed of fast twitch glycolytic fibres. With the use of two small electrodes placed around the primary nerve branches, both compartments could be separately stimulated within the same muscle. The length‐force relationship was less broad and maximal twitch and tetanic forces were obtained at lower muscle lengths for the proximal compartment. The differences (mm) were 0.9 ± 0.2 and 1.2 ± 0.2 for maximal twitch and tetanic force (120 Hz) production, respectively (P < 0.001). The shortening velocity for maximal power production was lower (P < 0.001) for the proximal compartment (proximal: 57.1 ± 2.7 mm s‐1, distal: 73.1 ± 3.0 mm s‐1). During a standard fatigue test the fatiguability was significantly lower for the proximal compared with the distal fibres. Our findings suggest that the proximal compartment is likely to be activated in vivo during activities requiring relatively low power outputs for longer time periods. In contrast the distal compartment is probably recruited only during high power demanding short lasting activities. The presented model makes it possible to study fatigue related changes in power production of the ‘red’ and ‘white’ areas of the GM separately in a way that is probably meaningful with respect to in vivo function.
Both gravity and non‐gravity dependent factors determine regional blood flow within the goat lung
Authors: MELSOM M.N. , FLATEBØ T. , KRAMER‐JOHANSEN J. , AULIE A. , SJAASTAD Ø. V. , IVERSEN P. O. , NICOLAYSEN G.
Published: December 2008

Distribution of pulmonary blood flow has traditionally been regarded as determined by gravity. This view has been challenged recently by reports describing marked gravity‐independent distribution of flow. These reports were based on experiments in which local blood flow was measured by methods that have not been thoroughly evaluated. In the present study, we showed that in the goat lung regional trapping of i. v. infused microspheres (Ø= 15 um) correlated to endothelial uptake of a simultaneously i. v. infused diamine (r = 0.99, region size ˜ 1.5 cm3, dry weight ˜ 40 mg). This indicates that the deposition of microspheres reflects true regional pulmonary blood flow. Using the microsphere method, we found a marked gravity‐independent heterogeneity in blood flow (coefficient of variation ˜ 40%) in the awake goat. We could find no pattern related to anatomy that could account for this variability. We re‐examined the influence of gravity by analysing the distribution of pulmonary blood flow in anaesthetized goats both in prone and supine positions. The dorsal to sternal distribution of flow appeared to be inverted when the animals were turned from prone to supine recumbency, indicating that gravity influenced the distribution of pulmonary blood flow along this axis. However, along the gravitational axis, distribution of blood flow varied considerably from lung to lung. It appears that in awake goats the distribution of pulmonary blood flow is the result of several different determinants.
Cerebral reactive hyperaemia and arterial pressure in anaesthetized goats
Authors: GARCIA J. L. , FERNANDEZ N. , GARCIA‐VILLALON A. L. , MONGE L. , GOMEZ B. , DIEGUEZ G.
Published: December 2008

The effects of arterial pressure on cerebral reactive hyperaemia were studied in anaesthetized goats measuring electromagnetically middle cerebral artery flow and performing arterial occlusions of 5–30 s. Under normotension (mean arterial pressure, MAP = 11± 0.3 kPa), reactive hyperaemia (peak hyperaemic flow to control flow and repayment to debt ratios) increased, and cerebrovascular resistance during peak hyperaemic flow decreased, as ischaemia duration lengthened; the virtual maximal changes were obtained after 20 s ischaemia. During hypertension by aorta constriction (MAP = 18 ± 0.7 kPa) or by i. v. infusion of noradrenaline (MAP = 19 ± 0.8 kPa) middle cerebral artery flow did not change significantly and cerebrovascular resistance increased 25 and 46%, respectively (P< 0.05). During both types of hypertension reactive hyperaemia was over 50% higher, and the decrement in cerebrovascular resistance during peak hyperaemic flow was also higher, than under normotension. During hypotension by constriction of the inferior vena cava (MAP = 5 ±.5 kPa) or by i. v. infusion of isoproterenol (MAP = 6±.5 kPa), middle cerebral artery flow decreased 35% or did not change, and cerebrovascular resistance decreased 41 and 45 %, respectively (P< 0.05). In these conditions, reactive hyperaemia and the decrement in cerebrovascular resistance during peak hyperaemic flow were reduced SOY, and it was similar in both types of hypotension. The absolute levels of cerebrovascular resistance obtained during peak hyperaemia were similar during normotension, hypertension and hypotension. Thus, arterial pressure is a main determinant of postocclusive cerebral reactive hyperaemia, and myogenic mechanisms may be of significance in determining the early stage of cerebral reactive hyperaemia after brief ischaemias. Adrenergic mechanisms might be of minor significance in this type of cerebral reactive hyperaemia.
Ethanol inhibits NMDA‐induced toxicity and trophism in cultured cerebellar granule cells
Authors: Wegelius K. , KORPI E. R.
Published: December 2008

In cerebellar granuleCellcultures, glutamate and N‐methyl‐D‐aspartate (NMDA) caused either neurotoxic or trophic effects, depending on the developmental stage of the neurones. Ethanol (100 mM) partly inhibited delayed neurotoxicity induced by the excitatory amino acids (25μM glutamate for 15 min or 100/tM NMDA for 30 min) assessed 24 h after the incubations in mature cultures in the absence of Mg2t. Glycine (5 μM) potentiated the toxicity of glutamate and the ethanol inhibition, and was routinely added in these experiments. The viability of neurones in the presence of 25 mM K+and 0.8 mM Mg2twas not impaired when maintained in 40–50 mM ethanol for the whole culture period of 7 days. However, ethanol almost completely inhibited the trophic effects of NMDA on developing cultures in 12.5 mM Kμ0.8 mM Mg2+medium. Glutamate (25 μM) and NMDA (100μM) potently induced45Ca2+uptake by granule cells from day 2 in vitro onward. Sixty‐five per cent of the 15‐min45Ca2finflux induced by glutamate and 80% of that induced by NMDA were inhibited by ethanol (100 mM). MK‐801 (a non‐competitive antagonist of NMDA receptors; 100 nM) completely inhibited the toxic and trophic actions of glutamate and NMDA, as well as the45Ca2+influx induced by NMDA, but only 80% of the45Ca2finflux induced by glutamate. These results show that the toxic and trophic actions of glutamate are mediated mainly by Ca2+influx through NMDA receptors. Both of these actions and the underlying Ca2+influx are significantly inhibited by ethanol at pharmacological concentrations (< 100 mM), although the mechanisms of inhibition still need further study.
Atrial natriuretic peptide and its mRNA in heart and brain of vasopressin‐deficient Brattleboro rats
Authors: ARJAMAA O. , TASKINEN T. , KANERVO A. , VUOLTEENAHO O. , LEPPALUOTO J.
Published: December 2008

To understand the secretion and synthesis of atrial natriuretic peptide we measured immunoreactive atrial natriuretic peptide from plasma, heart tissues and brain areas, and ANP mRNA was determined from heart auricles and ventricles of vasopressin‐deficient Brattleboro rats (DI) and from desmopressin treated Brattleboro rats (DI + DDAVP). Long‐Evans rats (LE) served as controls. DI + DDAVP rats were given for 3 days sc. injections of 0.5/g l‐desamino‐8‐D‐arginine vasopressin in 1 ml. saline twice a day. The rats were housed in single metabolic cages and urinary output and water intake were measured daily. All the body and organ weight parameters were similar in the three groups when the rats were killed. No change was seen in the plasma ANP level between the groups. The right ventricle of DI + DDAVP rats had significantly (P < 0.05) higher concentration of ANP than LE rats (15.8 + 4.4 vs. 3.4 + 0.6 ng mg“1tissue). The left ventricle of DI and DI+DDAVP had significantly (P < 0.05) lower amounts of ANP mRNA than LE rats (0.5 ± 0.2 vs. 1.3 + 0.2 and 0.5 + 0.1 vs. 1.3 + 0.2 arbitrary units). In the hypothalamus, the ANP concentration was significantly (P < 0.05) lower both in DI and in DI + DDAVP rats than in LE rats (9.3 ±1.3 vs. 14.5 ±±1.6 and 6.1+0.6 vs. 14.5 ± 1.6 pg mg‐1tissue).

To conclude, although the water intake and urinary output of DI rats were changed towards normal with desmopressin treatment, the heart ventricular and hypothalamic ANP did not parallel the change. Desmopressin increased the ANP concentration in the right ventricle of DI rats. Thus the correction of the complete vasopressin deficiency‐does not appear to associate with synthesis or release of atrial natriuretic peptide in heart or hypothalamus.
Nitric oxide regulates coronary blood flow at various coronary arterial pressures in intact porcine hearts
Authors: OFFSTAD J. , NAESS P. A. , AKSNES G. , TØNNESSEN T. , ILEBEKK A. , KIRKEBØEN K. A.
Published: December 2008

Nitric oxide (NO) is known to regulate basal coronary blood flow (CBF). The objective of the present study was to examine the importance of NO in CBF regulation at various coronary arterial pressures (CAPs) in vivo.

Experiments were performed in 11 open‐chest pentobarbitone sodium anaesthetized pigs. CAP was reduced in steps by a hydraulic occluder on the mid left anterior descending coronary artery (LAD) before and after a 5‐min intracoronary infusion of the inhibitor of NO synthesis, A‐nitro‐L‐arginine (NOARG, 30 /imo\ min“1). CAP was recorded and NOARG infused through a catheter inserted into the LAD just distal to the occluder. CBF was measured by Doppler flowmetry on the LAD.

NOARG significantly reduced CBF by 11±4, 20 ± 5, 10 ± 3, 15 ± 4, 19 ± 2, 25 ± 4 and 25 ± 5 mL min‐1 100 g‐1 (mean ± SE) at CAPs of 30 (n = 6), 40 (n = 9), 50 (n= 9), 60 (n = 9), 70 (n = 9), 80 (n = 8) and 90 (n = 6) mmHg, respectively. These decrements were not statistically different, but the percentage reductions in CBF after infusion of NOARG were significantly greatest at the lowest CAPs. The slight haemodynamic alterations induced by NOARG could not explain the reductions in CBF. Thus, the reductions in CBF after infusion of NOARG were caused by inhibition of a continuous NO release from the coronary endothelium.

Coronary NO contributes significantly to CBF at all CAPs between 30 and 90 mmHg. The pronounced reduction in CBF during NO inhibition at the lower CAPs indicates an important vasodilating role of intact endothelium in a region supplied by a stenosed coronary artery.
Endothelium‐dependent rhythmic contractions induced by cyclopiazonic acid, a sarcoplasmic reticulum Ca2+‐pump inhibitor, in the rabbit femoral artery
Authors: OMOTE M. , MIZUSAWA H.
Published: December 2008

The vascular responses to cyclopiazonic acid (CPA), an inhibitor of the Ca2+‐ATPase in the sarcoplasmic reticulum, were investigated in the rabbit femoral artery, suspended in an organ chamber for isometric tension recordings. CPA produced rhythmic contractions in the femoral artery which had been contracted with phenylephrine. CPA, however, did not induce the rhythmic responses in endothelium‐denuded arteries.NG‐nitro‐L‐arginine methyl ester and methylene blue, inhibitors of the formation and the action of nitric oxide, respectively, failed to antagonize the CPA‐induced rhythmic contractions in the phenylephrine‐contracted artery. In contrast, the CPA‐induced rhythmic contractions were abolished by charybdotoxin, a Ca2+‐activated K+channel antagonist, but not by glibenclamide, a blocker of the ATP‐sensitive K+channel. Nifedipine also inhibited the CPA‐induced rhythmic contractions in the endothelium‐intact artery and relaxed the endothelium‐denuded artery treated with CPA. These results indicate that the CPA‐induced rhythmic contractions in the phenylephrine‐contracted rabbit femoral artery may be attributed to the periodic inactivation of the voltage‐dependent Ca2+channel, presumably regulated by the Ca2+‐activated K+channel. The activation of the K+channel by CPA might occur only when the endothelium is present.
Influence of cerebrovascular sympathetic, parasympathetic, and sensory nerves on autoregulation and spontaneous vasomotion
Authors: MORITA Y. , HARDEBO J. E. , BOUSKELA E.
Published: December 2008

The effect of removal of cerebrovascular sympathetic, parasympathetic or sensory nerve on brain cortical blood flow and spontaneous vasomotion during changes in systemic blood pressure was studied by laser‐Doppler flowmetry in anaesthetized rats. Selective section of sympathetic fibres along the internal carotid artery markedly affected the ability to autoregulate, as measured in microvessels of the middle cerebral arterial territory. Removal of the parasympathetic nerves tended to reduce the ability to autoregulate, whereas no significant influence was found after sensory denervation. Following the denervations, spontaneous vasomotion was not significantly affected in frequency or amplitude.
Electrophysiological study of blink reflex in humans: differences in mental and supraorbital nerves
Authors: JÄÄSKELÄINEN S.K.
Published: December 2008

In order to find an explanation for the discrepancy between previous reports on the consistency of the blink reflex response with stimulation of the mental nerve, the habituation of the blink reflex was studied with stimulation of the supraorbital and mental nerves in 14 healthy adults. A series of eight electrical stimuli was delivered to the distributions of the nerves on each side at frequency rates of 1.0, 0.5, 0.2 and 0.1 Hz. The latencies and peak‐to‐peak amplitudes of the ipsilateral late blink reflex components (R2i) were measured. The habituation phenomenon was analysed by means of multivariate analysis of the amplitudes, the nerve and frequency effects were determined by means of a repeated measures analysis of variance model. The blink reflex showed more pronounced amplitude attenuation of the consecutive responses with stimulation of the mental than the supraorbital nerve at rates of 0.5 and 0.2 Hz, and marginally so also at 0.1 Hz. For the supraorbital nerve, habituation could be demonstrated with stimulation frequencies of 1.0 and 0.5 Hz, while for the mental nerve a statistically significant habituation phenomenon was found even with the lowest repetition rate of 0.1 Hz. The greater tendency of the mental nerve blink reflex to habituate is obviously one reason why it has previously sometimes been considered too inconsistent to be useful in clinical practice. For the recording of the supraorbital nerve blink reflex, a 10 s interval between stimuli is adequate, whereas longer interstimulus intervals may have to be adopted to obtain consistent blink reflex responses with stimulation of the mental nerve.