bluuebunny/crossref_metadata_2025 huggingface dataset:
The cyclic‐AMP concentration in plasma and in muscle in response to exercise and beta‐blockade in man
Authors: CHASIOTIS D. , HARRIS R. C. , HULTMAN E.
Published: December 2008

At rest the cAMP concentration in (muscle samples of) the quadriceps femoris ranged from 1.55 to 3.00 μmol per kg dry muscle and in plasma from 15.3 to 32.3 nmol per 1. Blockade of the beta adrenoreceptors with propranolol resulted in a significant decrease in the concentration in muscle at rest, the magnitude of the fall being related to the inital level. Similarly in plasma there was a trend towards lower levels of cAMP in those with the highest pretreatment levels, but the overall change was not statistically significant. There was no relation between the concentrations in muscle and plasma, before or after beta‐blockade. Maximum dynamic exercise for 4–8 min resulted in an approximate doubling in the cAMP concentration in both muscle and blood. The increase in plasma was closely related to that in muscle. Beta‐blockade inhibited totally the rise in cAMP in muscle during exercise but was marginally less effective in preventing the increase in blood. No increase in plasma or muscle cAMP levels during 40–70 s isometric contraction were observed.
The effects of Ca2+ and Sr2+ at different modes of activation in the smooth muscle of the rat portal vein
Authors: ARNER ANDERS , LÖVGREN BJÖRN , UVELIUS BENGT
Published: December 2008

The dependence of Ca2+ for different modes of activation has been investigated in the rat portal vein in vitro by evaluating the effects of substituting Sr2+ for Ca2+ in the extracellular fluid. For the spontaneous contractile activity as well as for contractures induced by depolarizing (high‐K+) solution Sr2+ can to a large extent replace Ca2+. Sr2+ is however a poor Ca2+‐substitute for the contractile response induced by α‐stimulation (noradrenaline). The inhibition of spontaneous contractions by β‐stimulation (isoprenaline) is markedly less pronounced in Sr2+ solutions. Available data in the literature suggest that agonist interaction with α‐receptors, in contrast to β‐receptors, is Ca2+ independent. Our results thus suggest that there exists a Ca2+ specific step between the α‐receptor agonist occupancy and membrane excitation.
Structurally based changes of renal vascular reactivity in spontaneously hypertensive and two‐kidney, one‐clip renal hypertensive rats, as compared with kidneys from uninephrectomized and intact normotensive rats
Authors: GÖTHBERG G. , HALLBÄCK‐NORDLANDER M. , KARLSTRÖM G. , RICKSTEN S.‐E. , FOLKOW B.
Published: December 2008

Renal vascular beds from spontaneously hypertensive rats (SHR) at different stages of hypertension, from two‐kidney, one‐clip renal hypertensive rats (RHR) and from uninephrectomized rats (UNR) were in constant‐flow, paired perfusions compared with kidneys from normotensive control rats (NCR) concerning vascular smooth muscle sensitivity to noradrenaline (NA) and resistance vessel reactivity, as reflected by the position, respectively the shape, of the dose‐resistance response curves. None of these kidney variants differed significantly from controls concerning smooth muscle sensitivity to NA during in vitro perfusion. However, both the steepness and maximal pressor responses of the renal resistance curves increased progressively with age in SHR, to become ultimately much enhanced when related to age‐matched controls. It suggests a well preserved smooth muscle contractility and a progressive elevation of the average wall/lumen ratio in the SHR renal resistance vessels. Also the untouched, “high‐pressure” RHR kidneys showed increased vascular reactivity, while it was somewhat reduced in the clipped, “low‐pressure” RHR kidneys and unchanged in the hypertrophied but normotensive UNR kidneys. These results, when combined with other finings concerning renal vascular design (Göthberg & Folkow 1982a), illustrate how the renal resistance vessels readily adapt structurally to hypertension, hypotension, kidney hypertrophy and also with age, and in directions which tend to chronically “autoregulate” glomerular blood supply and filtration.
Intramural blood flow distribution in the small intestine of the cat studied by carbon monoxide uptake and85krypton elimination
Authors: REDFORS S. , SJÖVALL H. , JODAL M. , LUNDGREN O.
Published: December 2008

Carbon monoxide (CO) uptake from the feline small intestine was measured to investigate if it could be used to determine blood flow in the superficial parts of the intestinal mucosa. Several observations were made that substantiated this proposal: 1) Lowering PCOin the intestinal lumen from 100 to 70 kPa did not influence the rate of CO absorption during “resting” blood flow conditions, while the same reduction of lumen PCOresulted in a decreased rate of CO uptake during isoprenaline induced vasodilatation. These observations suggest that CO uptake was flow limited during “rest” and diffusion limited during vasodilation. 2) Lowering perfusion pressure or totally occluding the intestinal vascular supply markedly reduced the rate of CO uptake. 3) The diffusion distance for CO into the tissue was calculated to be 75–225 μm, i. e. CO mainly diffused into the villous tissue. 4) The flow values calculated from the CO measurements were of the same order of magnitude as earlier reported with other techniques (microspheres, indicator dilution method). It was concluded that CO absorption mainly reflected villous blood flow during “resting” and low intestinal blood flow. Total blood flow (venous drop recorder) and muscle layer blood flow (85Kr elimination) were measured simultaneously to CO uptake. From these determinations “resting” blood flow distribution in the small intestine was calculated.
Cardiac output and its distribution through capillaries and A‐V shunts in diving seals
Authors: BLIX A. S. , ELSNER R. , KJEKSHUS J. K.
Published: December 2008

Regional blood flow and cardiac output were determined by distribution of radioactive microspheres injected via catheter into the left ventricle during experimental diving and recovery in juvenile spotted seals (Phoca vitulina largha) and grey seals (Halichoerus grypus). Cardiac output was 9.7 L/min before diving, declined 90% during submersion and increased to 12.1 L/min after 40 s of recovery. Left ventricular myocardial perfusion declined from 179 ± 24 (21) to 25 ± 2 (6) ml/min · 100 g at 2 min submersion, and measured 23 ± 3 (8) after 10 min of submersion. Cerebral cortical flow was reduced from a pre‐dive value of 115 ± 3 (15) to 40 ± 5 (3) and 49 ± 6 (3) at 2 and 5 min of diving, respectively, but increased to 253 ± 14 (4) ml/min · 100 g at 10 min along with elevated PCO2 (84 torr) and lowered pH (7.10) in arterial blood. It remained at that level in recovery. Brain stem perfusion after 10 min submersion was still identical with control, but increased to 275% of control in recovery. Adrenal flow decreased to 34 and 27% of control at 2 and 5 min of diving, respectively. Recovery flow after 10 min of diving was 200% of control. Liver, kidney, fat, skin, and stomach were ischemic throughout the dive. Recovery flow increased slowly in these tissues. Skeletal muscle (M. psoas) was perfused at a low rate. (3 ml/min · 100 g) pre‐dive and was ischemic during diving. Recovery muscle perfusion was variable at different sites (from 5 to 105 ml/min · 100 g). Pre‐dive pulmonary capillary perfusion was 58 ± 8 (9) ml/min · 100 g, decreased to 7 ± 0 (3) ml/min · 100 g after 10 min of submersion, and had increased to 50% of pre‐dive value after 40 s of recovery from a 10 min dive. Conclusions are: (1) previous information from implanted flow transducers was confirmed, (2) detailed data for discrete tissues elaborate the concept of selective redistribution of cardiac output in diving seals, (3) non‐uniform reperfusion contributes to the maintenance of arterial presssure during recovery, and (4) substantial A‐V shunting of cardiac output took place in the first 2–5 min of the dive, when total capillary/nutritive flow was low. Late in the dive, however, CO was routed through systemic capillaries mainly in the cerebral circulation and less than 15% through A‐V shunts.
Effects of alpha‐adrenoceptor agonists and antagonists on insulin secretion, calcium uptake, and rubidium efflux in mouse pancreatic islets
Authors: ISMAIL NABILA A. , EL‐DENSHARY E. S. M. , IDAHL L.‐Å. , LINDSTRÖM P. , SEHLIN J. , TÄLJEDAL I.‐B.
Published: December 2008

Epinephrine, norepinephrine or the more selective alpha‐2 adrenoceptor agonist, clonidine, inhibited insulin release from isolated pancreatic islets of lean mice or obese mice homozygous for the geneob.Clonidine was highly effective at 0.1 μmol/1. In contrast, the preferential alpha‐1 adrenoceptor agonist, phenylephrine, had no or only a modest effect at 10 μmol/1. The effects of norepinephrine or clonidine were counteracted by yohimbine, a preferential blocker of alpha‐2 receptors, but not by prazosine, an alpha‐1 receptor blocker. The glucose‐stimulated uptake of45Ca2+ in the islets was only consistently inhibited by epinephrine. This effect was counteracted by yohimbine. Clonidine had no effect on the release of86Rb+ from preloaded islets. It is concluded that insulin secretion is suppressed by alpha‐2 receptor agonism in the pancreatic beta‐cells and that this effect is mediated by mechanisms other than the transmembrane fluxes of calcium or potassium ions.
Cyclo‐oxygenase inhibition by indomethacin and recirculation following cerebral ischemia
Authors: KÅGSTRÖM ERIK , SMITH MAJ‐LIS , WALLSTEDT LARS , SIESJÖ BO K.
Published: December 2008

In this study we examined the effect of pretreatment with the cyclo‐oxygenase inhibitor indomethacin (10 mg‐kg‐1) on local cerebral blood flow (CBF) in the immediate recirculation period following complete and incomplete ischemia. Ischemia of 15 min duration was induced in lightly anaesthetized and artificially ventilated rats, and local CBF was measured with a 14C‐iodoantipyrine autoradiographic technique after recirculation periods of 5 min. Following complete ischemia indomethacin‐treated animals showed a reduced incidence of perfusion defects of the “no‐reflow” type. Perfused structures had somewhat higher flow rates than in untreated rats. A similar enhancement of immediate reflow was observed following incomplete ischemia provided that the structures in question had been severely ischemic. In structures that suffered only mild ischemia, the drug reduced postischemic CBF. It is concluded that, in the rat brain, cyclo‐oxygenase inhibition does not curtail postischemic reactive hyperemia. Furthermore, the previously reported beneficial effect of indomethacin on brain circulation following complete ischemia seems to be due to an enhancement of immediate reflow, and to amelioration of an initial hindrance to reflow.
Influence of ethanol on systemic and pulmonary hemodynamics in anesthetized dogs
Authors: KETTUNEN R. , TIMISJÄRVI J. , SAUKKO P. , KOSKELA M.
Published: December 2008

Immediate circulatory reactions to acute intragastric ethanol administration were studied by a catheterization technique in spontaneously breathing dogs. Diluted ethanol was given in a dosage of 1 g/kg in test group I (n = 11), and 2 g/kg in group II (n = 10). The control group (n = 14) received only water. The highest blood ethanol concentration was 0.90 ± 0.07 mg/ml (mean ± SE) in group I, and 1.97 ± 0.10 mg/ml in group II. Heart rate and cardiac output increased (p< 0.001), but stroke volume, mean aortic blood pressure and right atrial blood pressure remained practically unchanged. Systemic vascular resistance decreased. Mean pulmonary arterial blood pressure increased markedly in both test groups (p< 0.001) while pulmonary arterial wedge pressure did not change. The pulmonary arterial resistance increased (pxyl 0.01). Changes in respiratory rate or volume and arterial pO2were negligible in group I, but respiratory minute volume decreased in group II. In conclusion, ethanol in concentrations 0.5 to 2.0 mg/ml increased resistance in the pulmonary arterial tree, indicating pulmonary arterial vasoconstriction, but reduced systemic vascular resistance, thus putting a concept of peripheral vasodilation in favour.
Contribution of local blood flow regulation mechanisms to the maintenance of arterial pressure in upright position during epidural blockade
Authors: HENRIKSEN OLE , SKAGEN KNUD , HAXHOLDT OLGA , DYRBERG VIGGO
Published: December 2008

The contribution of local blood flow regulation mechanisms to the maintenance of arterial pressure in upright position was studied in 5 normal subjects. Central sympathetic blockade was induced by epidural anesthesia. Blood flow in anterior tibial muscle in both legs and in brachioradial muscle in one arm was measured by the local133Xe washout technique. Arterial blood pressure was recorded directly from the radial artery. Slow head‐up tilt (about 30°) caused a decrease in blood flow of about 36 % in the dependent legs and in arm remaining at heart level. Arterial pressure decreased by about 10%. Blockade of the local sympathetic veno‐arteriolar “axon reflex” in one leg by injection of phentolamine into the common femoral artery caused a vasodilatation in the ipsilateral muscle, while muscle blood flow did not change in the other leg or arm. Within 20 s after the injection of phentolamine arterial pressure decreased by about 7%. This cannot be explained by a “systemic” effect because injection of phentolamine into the femoral vein did not effect arterial pressure within the first 40 s. Vasoconstriction due to blood‐borne factors is ruled out since preventing the increase in vascular transmural pressure in the leg by inducing counterpressure locally, abolished the vasoconstriction. Thus, the results suggest that the local veno‐arteriolar “axon reflex” together with myogenic mechanisms contribute to the maintenance of arterial pressure in the upright position.
Cerebral circulatory responses to hypercapnia and hypoxia in the recovery period following complete and incomplete cerebral ischemia in the rat
Authors: KÅGSTRÖM ERIK , SMITH MAJ‐LIS , SIESJÖ BO K.
Published: December 2008

In this study we examined the reactions of cerebral vessels to hypercapnia and hypoxia during the recovery period following cerebral ischemia. We used ventilated, lightly anesthetized rats and induced complete ischemia by CSF compression, incomplete ischemia by bilateral carotid occlusion combined with hypotension. After 15 min of ischemia and 60 min of recirculation the animals were rendered hypercapnic or hypoxic for 2–3 min and local CBF was then measured autoradiographically with14C‐iodoantipyrine. Following complete ischemia vascular CO2responsiveness was abolished or attenuated in most structures analysed. However, there was a considerable interstructural heterogeneity. For example, in the cerebellum and the red nucleus flow rates were observed which approached values obtained in hypercapnic control animals, whereas CO2responsiveness was abolished in several cortical areas and hippocampus. The response to CO2following incomplete (“forebrain”) ischemia varied considerably. In the cerebral cortices areas with low flow rates were often mixed with hyperemic zones, and in most structures that had very low flow rates during ischemia, CO2responsiveness was lost or grossly attenuated. Structures that had suffered moderate or only mild ischemia had better retained or completely preserved CO2response. The cerebrovascular reaction to hypoxia was found to be attenuated in most, but not abolished in any of the structures examined. In general, the vascular response to hypoxia was better preserved than that to hypercapnia. Reactivity was similar following complete and incomplete ischemia. As observed during hypercapnia, there were pronounced interstructural variations with considerable increases in flow rates e.g. in the substantia nigra and the cerebellum.
Studies on the mechanisms by which (Gln4)‐neurotensin reduces lower esophageal sphincter (LES) pressure in man
Authors: THOR KJELL , RÖKAEUS ÅKE
Published: December 2008

The mechanisms behind the reduction of lower esophageal sphincter (LES) pressure by (Gln4)‐neurotensin were investigated in 17 healthy volunteers. LES pressure was measured with a continuous pull‐through technique. Intravenous infusion of (Gln4)‐neurotensin (6, 12 or 18 pmol × kg‐1 × min‐1) caused a significant, prompt and dose‐related fall in LES pressure from a mean basal value of 35.2 ± 3.4 mmHg to 29.2 ± 3.0, 27.3 ± 3.5 and 25.9 ± 2.7 mmHg, respectively. Atropine (1 mg) administered as a single i.v. bolus injection did not change the mean pressure significantly. After atropine, the LES pressure response to 12 pmol ± kg‐1 × min‐1 of (Gln4)‐neurotensin was abolished. The increase in LES pressure following a bolus injection of pentagastrin (0.6 μg × kg‐1) was not inhibited by 12 pmol × kg‐1 × min‐1 of (Gln4)‐neurotensin. The concentration of plasma neurotensin‐like immunoreactivity (p‐NTLI) in all experiments was lower than, or in the same order of magnitude as, that obtained postprandially. Thus, the data indicate that reduction of LES pressure by neurotensin may occur postprandially and that this effect seems to involve a cholinergic nervous pathway, rather than being due to a direct myogenic action.
Membrane potential oscillations in enzymatically isolated rat myocardial cells
Authors: LEHTO H. , TALO A. , TIRRI R. , VORNANEN M.
Published: December 2008

Enzymatical isolation was used for preparation of single myocardial cells, contractions of which were mainly of slow phasic type but normal fast contractions also occurred. Membrane potential (MP) changes of these cells were measured by conventional micro‐electrode techniques. Initial MP level of these cells varied between ‐60 to ‐90 mV (74.4 ± 1.9). In the majority of the cells the MP rapidly dropped to ‐20 to ‐40 mV and continued to decline while oscillating. In some cells MP recovered from ‐20 to ‐40 back to a more negative potential, and the MP oscillation was strongest (up to 20 mV) between ‐30 to ‐50 mV. In about 3% of the impalements the MPs did not degenerate at all, but stayed at initial values for several minutes. The MP oscillations were dependent on the MP level and connected to the slow phasic contractions. In connection to the normal fast contractions, two types of action potentials (AP) could be registered. Near ‐50 mV the cells often generated slow APs of duration 200–400 ms and dV/dt < 3 V/s but at higher MP level normal fast APs up to 120 mV (100–300 ms and dV/dt > 40 V/s) were generated. The slow phasic contractions were never connected to either type of AP.
Arterial pressure‐blood flow relations during limb elevation in man
Authors: NIELSEN HENRIK VAGN
Published: December 2008

The effect of local arterial hypotension upon blood flow was studied in 13 healthy humans. Blood flow was measured by the local133Xe washout technique in the calf or foot region. Changes in arterial pressure was achieved by elevation of the leg above heart level, while the subject rested in supine position. In papaverine‐infiltrated subcutaneous tissue, local arterial pressure and blood flow was linearly related. In subcutaneous and skeletal muscle tissue with normal vasomotor tone, blood flow remained constant during a decrease in regional arterial pressure of 30 mmHg—autoregulation of blood flow. Blood flow ceased in vasoparalysed tissue as well as in tissue with normal vasomotor tone, when the local diastolic arterial pressure was reduced to zero. The elevated foot showed signs of vascular ischaemia during these conditions. When the vessels in the ischaemic foot were distended by inflating a femur cuff to a pressure level above the diastolic blood pressure beneath the cuff, the colour of the foot changed into bluish‐red and a substantial blood flow was recorded. It is concluded, that the arteries‐arterioles seemed to be collapsed with blood flow cessation, when the diastolic portion of a pulsatile inflow pressure was reduced to zero. Vascular distension seemed to reopen the arterial‐arteriolar collapse, and during these conditions the vascular bed offered only little resistance to the systolic peak injection.
The significance of liberated cyclooxygenase products for the pulmonary and cardiovascular actions of leukotriene C4in the guinea pig depends upon the route of administration
Authors: DAHLÉN SVEN‐ERIK
Published: December 2008

Leukotriene C4(LTC4), given as an aerosol or by the intravenous route, was at least 100 times more potent than histamine in causing an increase of the tracheal insufflation pressure in pentobarbital anaesthetized artificially ventilated guinea pigs. Indomethacin or meclofenamate enhanced the longlasting bronchoconstriction elicited with aerosols of LTC4, but antagonized the relatively short lived airway response to intravenously injected LTC4. However, by increasing the injected dose of LTC4, a slowly developing but maximal bronchoconstriction could be obtained in the presence of indomethacin. Indomethacin did not affect the airway response to histamine, administered by either route. Intravenous injection of LTC4had little effect on the heart rate, but evoked a biphasic change of the systemic arterial blood pressure. An initial pressor response, which was attenuated but not abolished by indomethacin, was followed by a longlasting reduction of blood pressure. The hypotensive period evoked with higher doses of LTC4occurred earlier and was of greater magnitude in indomethacin treated animals. Thus, LTC4has a potent cyclooxygenase‐independent bronchoconstrictor action in the intact guinea pig, which supports the possibility that LTC4and its metabolites are important mediators of airway anaphylaxis in this animal. Depending upon the route of administration, secondarily released prostaglandins and/or thromboxanes may amplify or reduce the direct pulmonary effects of LTC4.
On the mode of action of the sympathetic fibres on intestinal fluid transport: Evidence for the existence of a glucose‐stimulated secretory nervous pathway in the intestinal wall
Authors: SJÖVALL HENRIK , REDFORS STAFFAN , JODAL MATS , LUNDGREN OVE
Published: December 2008

The effect of sympathetic nerve stimulation or close i. a.infusion of noradrenaline on net fluid transport was investigated on anesthetized cats. In the presence of glucose in the solution perfusing the intestinal lumen the adrenergic mechanisms increased net fluid absorption in normal intestines. Substituting glucose with mannitol in the perfusate abolished this effect of adrenergic stimulation on the net fluid uptake. Furthermore, the effect of noradrenaline on net fluid transport in normal or choleraic intestines was abolished by tetrodotoxin (TTX), a nerve conductivity blocking agent. This suggests that the sympathetic influence is dependent on intraluminal glucose and that noradrenaline exerts its effect mainly via nerves. TTX significantly increased fluid uptake from normal intestines perfused with an isotonic electrolyte solution containing glucose while a considerably smaller effect was seen in intestinal segments perfused with a solution with mannitol. Based on these findings it is proposed that glucose in some way activates intramural nervous reflex(es) in the intestinal wall. According to this hypothesis the enhancement of fluid transport induced by adrenergic stimuli is explained by an inhibition of the glucose‐activated nervous secretion
Substance P and capsaicin‐induced contraction of human bronchi
Authors: LUNDBERG JAN M. , MARTLING CLAES‐ROLAND , SARIA ALOIS
Published: December 2008

Substance P induced a dose‐dependent contraction of human segmental bronchi in vitro with a threshold dose of about 10‐6M. These preparations were obtained from patients undergoing lung tumor surgery. The substance P‐induced contractions were resistant to mepyramine and atropine, suggesting a direct effect on the bronchial smooth muscle. Capsaicin (10‐5M) also induced a slowly developing strong atropine‐resistant contraction of human bronchi in vitro. A rapid tachyphylaxis developed for the response to capsaicin. Both substance P and capsaicin were less potent than acetylcholine and histamine in inducing contractions of human bronchi. This finding may however be partly due to the experimental conditions and both substance P and capsaicin were comparatively much more potent in guinea‐pig preparations. Transmural field stimulation of the bronchial preparations in man resulted in contractions that were largely sensitive to atropine. The presence of capsaicin‐induced bronchial contractions however indicates the existence of a local non‐cholinergic axon‐reflex control of bronchial smooth muscle tone by substance P in man
Influence of lactate accumulation of EMG frequency spectrum during repeated concentric contractions
Authors: TESCH P.A. , KOMI P.V. , JACOBS I. , KARLSSON J. , VIITASALO J.T.
Published: December 2008

One hundred and twenty consecutive maximal leg extensions at a constant angular velocity of 1.5 radians. s‐1 were performed by nine physical education students. Integrated electromyographic (IEMG) activity and power spectrum density function (PSDF) of the EMG were recorded from m. vastus lateralis, m. vastus medialis and m. rectus femoris using bipolar surface electrodes. Muscle biopsies were obtained from m. vastus lateralis before and after exercise. Tissue samples were analyzed for muscle fiber type distribution and lactate and glycogen concentration. Muscle force and IEMG decreased in parallel over the exercise period. Thus, the IEMG/force ratio was unchanged. Mean power frequency (MPF) of PSDF of the three muscles decreased by 10% (p<0.001) during the initial 25 contractions with no further decline during the latter part of exercise. The relative contribution of the highest bandwidth (130–500 Hz) of the PSDF decreased (p<0.001) between the first and final contractions. Muscle glycogen concentration decreased from 85 ± 23 to 68 ± 22 mmol ± kg‐1 w. w.during the exercise. Muscle and blood lactate concentration averaged 12.1 ± 8.8 mmol ± kg‐1 w. w.and 3.8 ± 0.8 mmol ± l‐1, respectively. The relative changes in MPF and in the highest bandwidth were correlated with muscle lactate concentration and fiber type distribution: in individuals with a high proportion of fast twitch muscle fibers and/or the greatest lactate accumulation, MPF and high frequency components of EMG PSDF decreased most markedly. Reductions in muscle force and IEMG are suggested to be partly due to a decreased motor neuron firing rate. It is discussed whether lactate or associated metabolic changes are influencing the motor unit action potential through feedback processes
Mechanism of inhibition of gastric acid secretion by vagal denervation in the rat
Authors: VALLGREN S. , EKELUND M. , HÅKANSON R.
Published: December 2008

Acute bilateral subdiaphragmatic vagotomy in the conscious fistula rat greatly reduced gastric acid secretion, stimulated by the combined intravenous infusion of pentagastrin (10 μg/kg/h), histamine dihydrochloride (3 mg/kg/h) and carbachol (50 μg/kg/h). The reduction of acid output was immediate (within 15 min after vagotomy). The greatly reduced acid response to these secretagogues persisted for at least 8 weeks after vagal denervation (longest time studied). The sudden and dramatic effect of vagotomy on acid secretion is not related to a possible deficiency of either acetylcholine or histamine at the respective receptor site since the combined infusion of gastrin, histamine and carbachol did not prevent the suppression of acid secretion. Since the decline in acid output following vagal denervation was immediate, it probably reflects a sudden inaccessibility rather than loss of muscarinic or H2‐receptors. The acid output obviously depends upon intramural “transducer” systems that respond to and transmit the vagal input. It is likely that the intramural ganglia represent such “transducer” systems. In the absence of a vagal drive these neuronal “transducers” cease to fire and as a result the parietal cells become almost unresponsive to stimuli.
A spin label study on the effect of dibutyryl cyclic AMP on synaptic plasma membranes isolated from rat brain
Authors: HEINONEN ERKKI , GRIPENBERG JOHAN , JANSSON STEN‐ERIK
Published: December 2008

The fluidity of the deep layer of the lipid bilayer and the mobility of sulphydryl (‐SH) groups of synaptic plasma membranes, isolated from rat brain and spin‐labelled with a doxyl derivative of stearic acid and with a nitroxide derivative of maleimide, respectively were studied using electron spin resonance (ESR) techniques. Dibutyryl cyclic AMP (db‐cAMP) and adenosine triphosphate (ATP) had no effect on the fluidity of the deep layer of the lipid bilayer of synaptic plasma membranes. While protein dephosphorylation was inhibited by Zn2+, db‐cAMP together with ATP increased the mobility of‐SH groups above the value obtained with db‐cAMP alone.
Evidence for bicarbonate‐dependent magnesium reabsorption
Authors: HARTMANN ANDERS , LANGBERG HARALD , DIBONA GERALD , KIIL FREDRIK
Published: December 2008

During ethacrynic acid administration about 50% of the filtered load of magnesium is reabsorbed. To examine whether the remaining component of magnesium reabsorption is bicarbonate‐dependent, i. e.varies with factors known to alter passive reabsorption, experiments were performed in anesthetized dogs. During ethacrynic acid administration MgCl2infusion raised the plasma concentration of magnesium (PMg) from 0.64 ± 0.05 to 3.06 ± 0.27 mM and doubled magnesium reabsorption. The infusion of acetazolamide at high PMgreduced bicarbonate reabsorption by 41 ± 3% and magnesium reabsorption by 31 ± 16%. When plasma pH was reduced to 7.04 ± 0.02 and increased to 7.83 ± 0.02 by altering PCO2, at a constant plasma bicarbonate concentration of 31.2 ± 0.8 mM, magnesium and bicarbonate reabsorption were correlated (r=0.82). The infusion of mannitol, which acts by reducing passive solute transport without affecting bicarbonate reabsorption, halved magnesium reabsorption. By combining mannitol and acetazolamide infusions, only 6 ± 4% of the filtered magnesium was still reabsorbed. These results indicate that the reabsorption of magnesium remaining after the infusion of ethacrynic acid and after raising PMgvaries with changes in PCO2and is inhibited by the infusion of acetazolamide and mannitol as expected for bicarbonate‐dependent passive reabsorption.
Effects and distribution of vagal capsaicin‐sensitive substance P neurons with special reference to the trachea and lungs
Authors: LUNDBERG JAN M. , BRODIN ERNST , SARIA ALOIS
Published: December 2008

The origin of substance P (SP)‐immunoreactive neurons in the lower respiratory tract, esophagus and heart of guinea‐pigs was demonstrated by surgical denervation or capsaicin pretreatment with subsequent determination of the tissue levels of SP by radioimmunoassay. In other experiments the effect of vagal nerve stimulation on the SP levels in these tissues was studied. The effects of capsaicin‐sensitive afferents in the respiratory tract mucosa and bronchial smooth muscle was also studied by analysis of vascular permeability to Evans blue and insufflation‐pressure changes. Our present data indicate that all SP nerves in the trachea and lung are afferent and capsaicin‐sensitive. The trachea and stem bronchi receive SP afferents mainly from the right vagus nerve with cell bodies located in both the nodose and jugular ganglia. The SP innervation of the lung seems to have a dual origin: 1. Afferents from both vagal nerves with a crossed type of innervation pattern. 2. A non‐vagal source which consists of about 40% of the SP nerves in the lung. These nerves probably originate from thoracic spinal ganglia. The effects of ether and capsaicin on insufflation pressure and increase in vascular permeability were dependent on the integrity of capsaicin‐sensitive afferents of both vagal and non‐vagal origin. In the guinea pig, systemic capsaicin pretreatment to adult animals seemed to result in irreversible changes in the respiratory tract, while in the rat a successive recovery of the functional response of capsaicin‐sensitive afferents occurred. Different regims of systemic capsaicin pretreatment induced different effects on the cholinergic (atropine‐sensitive) insufflation‐pressure response. Capsaicin pretreatment, using multiple injections over two days, depressed the cholinergic insufflation‐pressure increase, while the cholinergic vagal component was unaffected in animals which received a single dose of capsaicin or local pretreatment with capsaicin on the vagal nerves. The local treatment was more effective with regard to SP depletion in target areas when using alcohol as solvent than when capsaicin was dissolved in paraffin oil, while the functional deficits were similar. The SP nerves in the esophagus were mainly of vagal afferent origin, while the heart atrium seemed to have a dual innervation by both vagal and non‐vagal SP nerves.
Correlation between electrical and mechanical activity in myogenic and neurogenic control of the bovine retractor penis muscle
Authors: SAMUELSON ULF , SJÖSTRAND NILS O. , KLINGE ERIK
Published: December 2008

The electrical and mechanical activity of fine bundles of the bovine retractor penis muscle (rp) were investigated with the sucrose‐gap technique. The main results were: the muscle displayed prominent automaticity. It showed a vigorous and long lasting active response to stretch. Phasic contractions of the rp were associated with electrical firing while tonic contractions were not necessarily correlated to spike activity. Stimulation of excitatory nerves induced excitatory junction potentials (EJP). Single EJPs could elicit spikes and repetitive firing with long lasting contraction. The EJPs were abolished by phentolamine and adrenergic neuron blocking agents. Physostigmine suppressed EJPs while scopolamine and atropine enhanced them and counteracted the effect of physostigmine. This points to an endogenous neurogenic prejunctional muscarinic suppression of the excitatory adrenergic neurotransmission. Inhibitory nerve stimulation could produce an inhibitory junction potential (IJP). However, the inhibitory nerves may also act on the contractile process without an IJP as a necessary step.
Sympathetico‐adrenergic influences on the small intestinal vascular reactions in experimental septic shock
Authors: FALK A. , MYRVOLD H.E. , HAGLUND U.
Published: December 2008

The objective of this study was to explore the vascular reactions in the small intestine and the possible role of sympathetico‐adrenergic influences. The experiments were performed on 23 cats. The small intestinal blood flow was estimated using a drop counting technique. In one series of cats (n=7) the small intestine and the adrenal glands had intact vascular and nervous supply (I), in another series (n=7) the small intestine was sympathetically denervated and the adrenal vessels ligated (II), and in a third series (n=9) the small intestine was innervated but the adrenal vessels ligated (III).The septic state was induced by i. v.infusion of live E.coli bacteria for two hours. The small intestinal blood flow decreased and intestinal blood flow resistance increased in all series within 3 min upon bacterial infusion. The intestinal vasoconstriction was maintained in cats with intestinal denervation as well as in cats with the adrenal vessels ligated, favouring that other humoral factors than catecholamines are involved. During the later phase of bacteremic shock the intestinal blood flow remained in the preseptic range in the series with a denervated small intestine and ligated adrenals as well as in intact cats, but declined gradually and significantly in cats with adrenal ligation only (III).This pattern of reactions favours a local rather than a remote sympathetico‐adrenal influence.
Intradental nerve activity induced by reduced pressure applied to exposed dentine in the cat
Authors: NÄRHI M. , HAEGERSTAM G.
Published: December 2008

In order to study the excitation of intradental nerves by fluid flow in dentinal tubules the following experiments were performed. The fluid flow was caused by reduced hydrostatic pressure applied to the exposed dentine surface of the canine teeth in the anesthetized cat. In one series of 7 cats the intradental nerve activity was recorded by means of electrodes inserted in dentinal cavities. Provided that the pressure was sufficiently reduced and applied to acid‐etched dentine in preparations of sufficient depth, intradental nerve activity of different impulse amplitudes was recorded. The responding pressure sensitive units were found to be sensitized by a brief local application of veratrine and desensitized by potassium chloride. In the second series 26 single functional pulp nerve fibre units were dissected from the inferior alveolar nerve in 7 cats. Nerve impulses were recorded by means of platinum‐iridium wire electrodes. The conduction velocities of the 9 fibres responding to reduced pressure varied from 8.3 to 43.0 m/s. Five of these fibres also responded to elevated pressure. None of the 9 fibres conducting impulses with a velocity below 2 m/s responded to a reduction in pressure. Thus, the present data strongly suggest that intradental nerve endings with myelinated axons are activated by fluid flow in dentinal tubules. Our results support the hydrodynamic mechanism of dentine sensitivity.
A calcium clamp technique in man
Authors: TØRRING O. , SJÖBERG H.‐E.
Published: December 2008

Calcium infusion imply a risk for cardiovascular complications. To avoid the risks, we have developed a new method for calcium infusion in man which can keep ionized calcium concentration in whole blood (WB‐Ca++) in a steady state at a predetermined level. A solution of calcium chloride (Calcii chlor. Nord.), containing 0.117 mmol Ca++/ml water, is infused intravenously by means of an IMED 922H infusion pump. WB‐Ca++ is determined every 5–10 min with a calcium ion‐selective electrode, NOVA 2®.The infusion rate is continuously adjusted. With the same initial infusion rate, 0.31 mmol Ca++/kg b. w./hour, hypercalcemia that is WB‐Ca++ above 1.27 mmol/1 was reached within 10 min in healthy volunteers, 8 females with a mean age of 26 years (range 19–36) and 7 males with a mean age of 29 years (range 25–34).The presettled WB‐Ca++ level, 1.45 mmol/1, was obtained within 25 min and maintained in a steady state for 155 min at 1.45 ± 0.01 mmol/1 (mean ± SE) in the females and at 1.46 ± 0.01 mmol/1 in the males. The range of the individual steady state mean WB‐Ca++ was 1.42 ± 0.02 to 1.49 ± 0.02 mmol/1.No side‐effects of the infusion were noted except for a slight increase in systolic and diastolic blood pressure 60 min after start of the infusion. In conclusion, the calcium clamp technique is safe and suitable for such situations where a presettled easily controlled WB‐Ca++ level is required.
Thresholds of intradental A‐and C‐nerve fibres in the cat to electrical current pulses of different duration
Authors: VIRTANEN A. , NÄRHI M. , HUOPANIEMI T. , HIRVONEN T.
Published: December 2008

Electrical current pulses of quite variable duration have been used in activation of intradental nerves both in human subjects and experimental animals. It seems, however, that little information is available about the effect of pulse duration on the responses of single pulp nerve units. The aim of the present study was to investigate the effect of pulse duration on excitation thresholds of intradental A‐and C‐fibres in the cat. In 12 anesthetized cats 61 C‐and 53 A‐nerve units were identified and recorded. Electrical thresholds were determined with current pulses of different duration from 0.2 to 50.0 ms. The maximal stimulus intensity was 200 μA.Conduction velocities of all recorded units and absolute refractory periods of 20 A‐and 20 C‐units were determined. Intradental A‐and C‐fibres had different strength‐duration properties. With all pulse durations A‐fibres had the lowest thresholds. Part of the C‐fibres did not respond to the shortest current pulses even with the maximum stimulus intensity (200 μA).With 0.2 ms pulses only 31.1% of the recorded C‐fibres could be activated. In some A‐fibres a single current pulse of long duration was capable of inducing several action potentials, when the stimulus intensity was increased suprathreshold. Refractory periods of A‐units were <2.0 ms and those of C‐units 5.0–9.0 ms. It is concluded that in electrical stimulation of teeth duration of current pulses strongly affects responses of single intradental fibre units. With long pulses function of A‐fibres is pronounced because of repetitive firing in some units. These properties of pulp nerves should also be considered, when electrical stimulation is applied to human teeth.
Changes in segmental reflexes following chronic spinal cord hemisection in the cat:
Authors: HULTBORN H. , MALMSTEN J.
Published: December 2008

In a companion paper (Hultborn & Malmsten 1983) it was described that ventral root discharges to stimulation of peripheral nerves became larger on the side of a chronic spinal hemisection (left) than on the other side. In the present paper, based on the same experiments, conditioning of monosynaptic test reflexes was used to study changes of both excitatory and inhibitory effects on specified motoneuronal pools. Conditioning stimulation was given to Ia afferents (reciprocal Ia inhibition, presynaptic inhibition of Ia fibers), high threshold muscle afferents, low and high threshold cutaneous afferents and motor axons (recurrent inhibition). A comparison of the efficacy of conditioning stimuli on the two sides showed that facilitatory effects were larger on the side of hemisection in a clear majority of cases. Inhibition was almost always either more efficient on the side of hemisection or equally efficient on the two sides. In control cats, facilitatory effects tended to be larger on the right side, while the results for inhibitory conditioning generally showed no clear side‐bias. The increase in facilitatory effects after lesions may contribute to symptoms of spasticity.
The cortical and medullary blood flow at different levels of renal nerve activity
Authors: HERMANSSON K. , ÖJTEG G. , WOLGAST M.
Published: December 2008

The effect of (1) renal denervation and (2) stimulation of the renal nerve on the regional renal blood flow were determined by the Rb uptake method. Under control conditions the total renal blood flow was 3.64±0.09 ml·min‐1·g‐1tissue increasing significantly (p<0.02) to 4.39±0.28 ml·min‐1·g‐1after denervation. Upon stimulation of the peripheral portions of the sectioned renal nerves the blood flow decreased almost linearly with the frequency of stimulation reaching 0.99±0.24 ml·min‐1·g‐1at 10 Hz. Utilizing the relation between blood flow and stimulation frequency the control blood flow correspond to a spontaneous activity of 1.5 Hz. As expected the cortical blood flow responded in the same way as for the total renal blood flow. In the renal medulla denervation gave a much more pronounced response where e.g. the inner medullary flow increased from 0.88±0.09 to 1.30±0.16 ml·min‐1·g‐1, i.e. a 50% increase (p<0.05). Stimulation with 2 Hz produced a steep fall in the blood flow, whereafter it decreased linearly with the stimulation frequency reaching 0.11 ml·min‐1·g‐1at 10 Hz stimulation. This demonstrates again that the renal medulla is sensitive to renal nerve activity primarily in the low level range. It should be remarked, however, that the 86‐Rb uptake method reflects the effective blood flow, which might differ from the blood flow in absolute terms. It is concluded that the renal nerve activity influences the blood flow of all regions of the kidney within the entire range 0–10 Hz. The renal medullary blood flow is affected presumably to a greater extent in the low level range around the basal tone. The sympathetic nerves might then also be important with respect to the urine concentration mechanism.
The involvement of the enteric nervous system in the intestinal secretion evoked by cyclic adenosine 3‘,5’‐monophosphate
Authors: EKLUND STEFAN , CASSUTO JEAN , JODAL MATS , LUNDGREN OVE
Published: December 2008

Intestinal fluid secretion was evoked in vivo in rats and cats by introducing dibutyrylcyclic adenosine 3,5‐monophosphate (db‐cAMP) or theophylline, a phosphodiesterase inhibitor, in the intestinal lumen. The intestines were denervated periarterially. It was demonstrated that three compounds of varying chemical structure and with different modes of action on nerves (tetrodotoxin, lidocaine, hexamethonium) decreased the secretory response 60–70%. It is concluded that the secretion induced by increasing the intracellular cAMP concentrations is in part evoked via the enteric nervous system
Functional α1‐adrenoceptors in the rat heart during β‐receptor blockade
Authors: ASK J. A. , STENE‐LARSEN G.
Published: December 2008

In absence of β‐receptor blocking agents, α‐adrenergic inotropic effects could be demonstrated in the rat myocardium for the synthetic α‐agonists phenylephrine and methoxamine, but not for the naturally occurring catecholamines, adrenaline and noradrenaline. Other synthetic α‐agonists were without effects. In the presence of the β‐receptor blocking agent, propranolol or timolol, marked α‐effects were demonstrated for adrenaline and noradrenaline in both the right and left atria and the right ventricle. The results indicate that α‐receptors may be functionally important in the β‐blocked myocardium.
Isometric muscle endurance during acute β‐adrenergic blockade
Authors: TESCH P. A. , KAISER P. , KAIJSER L.
Published: December 2008

Isometric muscle endurance was measured in fourteen physically active men without (placebo) and after acute oral administration of 160 mg propranolol (Inderal®). Quadriceps muscle contractions were sustained at 65% maximum voluntary contraction (MVC) to exhaustion. Muscle biopsies were obtained from m. vastus lateralis at rest for subsequent histochemical analysis for myofibrillar ATPase and amylase‐PAS in order to determine fiber type composition and capillary density. The time to exhaustion was shorter (p< 0.01) during β‐blockade (0.82 ± 0.22) min than placebo (0.90 ± 0.23) min. Changes in endurance time, induced by β‐blockade, were not correlated with any of the muscle morphological or histochemical variables examined. It is concluded that muscular performance is impaired as a result of β‐blockade on muscle tissue irrespective of any concomitant change in central circulation.