bluuebunny/crossref_metadata_2025 huggingface dataset:
Acute volaemic changes modify the gastroduodenal resistance to the flow of saline in anaesthetized dogs
Authors: SANTOS A. A. , XAVIER‐NETO J. , JR. A. T. SANTIAGO , SOUZA M. A. N. , MARTINS A. S. , ALZAMORA F. , ROLA F. H.
Published: December 2008

The effect of acute and sequential volaemic changes on the gastroduodenal flow of saline was assessed in 23 anaesthetized dogs following two different experimental protocols. Hypervolaemia, by i. v. infusion of saline, induced a gradual decrease on gastroduodenal flow which amounted to 76% below control values (P < 0.001) when volaemic expansion attained 5% of body weight. This effect was volume dependent (17% increase on gastroduodenal flow per volume of infused saline equivalent to 0.5% of body weight, P < 0.001), lasted for at least 90 minutes after infusion was completed and was also obtained by expanding previously bled animals. Hypovolaemia due to bleeding was followed by an increase on gastroduodenal flow of about 88% above control values (P < 0.05) when haemorrhage was equal to 3% of body weight. This effect was also volume dependent (23 % increase on gastroduodenal flow per volume of blood shed equivalent to a 0.5% of body weight, P < 0.01) and was reversed after blood volume was restored. These modifications in the resistance of the gastroduodenal segment to the flow of liquid due to acute volaemic changes suggest that the extracellular fluid volume modulates the contractile activity of the gastroduodenal portion of the gut possibly to set a gastroduodenal handling of liquid adequate to cope with volaemic imbalances.
Acute but not chronic gastric sodium administration regulates vasoactive intestinal peptide metabolism by the liver
Authors: HAWLEY C. M. , DUGGAN K. A. , MacDONALD G. J. , SHELLEY S.
Published: December 2008

We have shown previously that gastric sodium loading releases vasoactive intestinal peptide from the intestine and in rabbits on a low sodium diet it appears to decrease vasoactive intestinal peptide metabolism by the liver. To determine the contributions of the low sodium diet and the acute sodium load to changes in vasoactive intestinal peptide metabolism, metabolic clearance studies of vasoactive intestinal peptide infused intraportally were performed. These studies were performed in male New Zealand white rabbits equilibrated on normal and low sodium diets before and after an acute gastric sodium load of 1.5 mmol kg‐1. No difference was detectable in metabolic clearance rates between normal and low salt diets, however, decreases in metabolic clearance rates were observed in response to the sodium load (normal diet P < 0.005, low salt P < 0.0005). Secretion rates also decreased following the gastric sodium load (normal P < 0.005, low salt P < 0.05).

We conclude that hepatic VIP metabolism is decreased by acute gastric sodium loading but it is not affected by chronic sodium intake.
Effects of the nitric oxide synthase inhibitor NG‐nitro‐L‐arginine on the erectile response to cavernous nerve stimulation in the rabbit
Authors: HOLMQUIST F. , STIEF C. G. , JONAS U. , ANDERSSON K‐E.
Published: December 2008

Using a rabbit model, the involvement of the L‐arginine/nitric oxide pathway in penile erection was investigated. The mean basal intracavernous pressure was 21 cm H2O. Cavernous nerve stimulation (4–8 V, 20–30 Hz) increased the pressure to approximately 130 cm H2O. This response was highly reproducible and usually associated with full penile erection. The pressure increase could be quantified in terms of: (1) the slope of the initial, ascending part of the pressure increase; (2) ΔP, which was defined as the maximal pressure obtained by the stimulation minus the basal pressure before the stimulation; (3) T90, which was defined as the time to reach 90 per cent of ΔP. Intrapenile administration of the L‐arginine/nitric oxide synthesis inhibitor NG‐nitro‐L‐arginine had no effect on systemic arterial blood pressure. However, NG‐nitro‐L‐arginine (0.22 and 2.19 mg), administered via the same route, abolished the erectile response induced by cavernous nerve stimulation; T90 increased and slope and ΔP decreased significantly. NG‐nitro‐D‐arginine (2.19), on the other hand, had no inhibitory effect. L‐arginine (21.07 mg), given either directly or after NG‐nitro‐L‐arginine had no consistent effect on the functional response to cavernous nerve stimulation.

The results suggest that pharmacologically induced effects on intracavernous pressure in the rabbit can be described quantitatively, and that this model may be useful to study the mechanisms controlling penile erection in vivo. The pronounced inhibitory action of NG‐nitro‐L‐arginine demonstrates the important role of the arginine/nitric oxide pathway in mediating relaxation of penile smooth muscles necessary for erection.
Parotid secretion of fluid, amylase and kallikrein during reflex stimulation under normal conditions and after acute administration of autonomic blocking agents in man
Authors: JENSEN J. L. , BRODIN P. , BERG T. , AARS H.
Published: December 2008

The purpose of this work was to study the effect of graded mechanical and gustatory stimulation on the secretion of the acinar products fluid and amylase and the ductal product kallikrein from the human parotid gland (n= 9). The involvement of parasympathetic and sympathetic nerves in the salivary reflexes was subsequently examined using receptor blocking agents (n= 4).

Chewing elevated the secretion of all products as compared to rest (P < 0.013). When increasing the length of the chewing object, secretion of fluid (P < 0.013), but not enzymes, further increased. The shift from mechanical to gustatory stimulation with 0.5% citric acid enhanced significantly the secretion of amylase and kallikrein (P < 0.009), while application of 5.0% citric acid increased the secretion of both acinar products (P < 0.009) more than kallikrein. A differentiated reflex control of salivation both with regard to input and output was thereby indicated.

The muscarinic‐cholinergic antagonist oxyphencyclimin reduced median fluid secretion between 54 and 76% depending on the stimuli. During citric acid stimulation, but not during chewing, fluid secretion was reduced about 40% by the beta1‐adrenergic antagonist metoprolol, and about 20% by the alpha1‐adrenergic antagonist prazosin. Median amylase secretion was reduced 30% during chewing and 75% during gustatory stimulation by metoprolol.

It was concluded that the masticatory‐salivary reflex mainly activated parasympathetic pathways producing saliva of low protein content. The gustatory‐salivary reflex activated sympathetic pathways to a higher extent, resulting in saliva with higher protein content. Using this reflex model, kallikrein secretion seemed not to be mediated by any of the tested receptors.
Somatostatin inhibition of phospholipase G activity in isolated rat pancreatic islets
Authors: MALM D. , GIÆVER A. , VONEN B. , BURHOL P. G. , FLORHOLMEN J.
Published: December 2008

We have assessed the effect of somatostatin on the phospholipase C activity in isolated rat pancreatic islets. The phospholipase C activity was measured as the generation of inositol 1,4,5‐trisphosphate and its metabolite inositol 1,3,4‐trisphosphate from the hydrolysis of polyphosphoinositides. Inositol phosphates were measured using anion‐exchange fast protein liquid chromatography analysis of extracts from islets prelabelled with myo‐[3H]inositol.

Somatostatin (1–1000 nmol l‐1) significantly inhibited the glucose‐induced (12 mmol l‐1) phospholipase C activity in a concentration‐dependent manner. The Ca2+ channel blocker verapamil (25 μmol l‐1) also inhibited the glucose‐induced (12 mmol l‐1) phospholipase C, whereas the combination of somatostatin and verapamil did not induce any additional inhibition. At 3.3 mmol l‐1 glucose, the hypoglycaemic sulphonylurea, tolbutamide (1 mmol l‐1), increased the phospholipase C activity. This effect was reversed by somatostatin (100 nmol l‐1). Tolbutamide did not further increase the glucose‐induced (12 mmol l‐1) phospholipase C activity.

However, the somatostatin inhibition of glucose‐induced (12 mmol l‐1) phospholipase C was reversed by tolbutamide. The activator of adenylyl cyclase, forskolin (20 μmol l‐1), did not exert any effect on the PLC‐inhibition of somatostatin, whereas forskolin alone inhibited the phospholipase C activation at 12 mmol l‐1 glucose.

Our study demonstrates that somatostatin inhibits the hydrolysis of polyphosphoinositides in pancreatic islets, apparently via a mechanism dependent on Ca2+ and not on cAMP.
Effects of detraining following short term resistance training on eccentric and concentric muscle strength
Authors: COLLIANDER E. B. , TESCH P. A.
Published: December 2008

Healthy males were examined before and after 12 weeks of accommodated resistance training (three week‐1) and after 12 weeks of detraining. Training consisted of four to five sets of six coupled maximum voluntary bilateral concentric and eccentric (Grp ECCON; n= 10) or 12 concentric (Grp CON; n= 8) quadriceps muscle actions. Concentric and eccentric peak torque at various constant angular velocities and three repetition maximum half‐squat and vertical jump height were measured.

Grp ECCON showed greater (P < 0.05) overall increase in peak torque after training and detraining than Grp CON. Thus, concentric peak torque (0.52 rad s‐1) increased more (P < 0.05) over the experimental period in Grp ECCON and increases in eccentric peak torque were preserved in Grp ECCON only. Increases in peak torque in response to training were greater (P < 0.05) at 0.52 than at 2.62 rad s‐1. Alterations in the torque‐velocity patterns induced by training remained after detraining in Grp ECCON but not in Grp CON. The retained increases (P < 0.05) in half‐squat were 12 and 18% in Grps CON and ECCON, respectively. Neither group showed increased vertical jump height after detraining.

This study showed greater preservation of concentric and eccentric peak torque after detraining following coupled concentric and eccentric than concentric resistance training. Only the former regime induced a change in the shape of torque‐velocity curves that was manifest after detraining. These results suggest that the performance of eccentric muscle actions is critical to optimize increases in muscular strength in response to heavy resistance training, because it probably induce greater and more long‐lived neural adaptations than the performance of concentric actions.
Acute effect of hypobaria and hypoxia on renal nerve activity in anaesthetized rabbits
Authors: SHIBAMOTO T. , UEMATSU H. , MATSUDA Y. , FUJITA T. , SAWANO F. , SAEKI Y. , HAYASHI T. , KOYAMA S.
Published: December 2008

To determine the acute effect of reduced barometric pressure and hypoxia on renal nerve activity, urethane‐anaesthetized and mechanically ventilated rabbits were randomly exposed to the following four separate conditions in a decompression chamber: hypoxic hypoharia (n=71, hypoxic normobaria (n= 5), normoxic hypoharia (n= 8) and slow normoxic hypobaria (n= 7). A combination of rapid decompression and simultaneous adjustment of inspired PO2 was used to simulate an altitude of 6600 m, and renal nerve activity and haemodynamics, such as systemic blood pressure and heart rate, were measured. During both hypoxic hypobaria and hypoxic normobaria, there were significant and similar increases in renal nerve activity at 6600 m (54 ± 7% and 61 ± 13% from each baseline, respectively). However, there were no changes in renal nerve activity during normoxic hypoharia or slow normoxic hypoharia with decompression rates of 1000 or 400 m min‐l, respectively. From these results, we conclude that a reduction in barometric pressure without hypoxia does not affect renal nerve activity in anaesthetized rabbits.
Na+‐H+ exchange is not important for pancreatic HCO‐3 secretion in the pig
Authors: VEEL T. , VILLANGER O. , HOLTHE M. R. , JR. E. J. CRAGOE , RÆDER M. G.
Published: December 2008

Veel, T., Villanger, O., Holthe, M.R., Cragoe jr., E.J. & Reder, M.G. 1992. Na+‐H exchange is not important for pancreatic HCO‐3 secretion in the pig. Acta Physiol Scand144, 239–246. Received 13 September 1991, accepted 14 November 1991. ISSN 0001–6772. University of Oslo, Institute for Experimental Medical Research and Surgical Department, Ullevaal Hospital, Oslo, Norway.

Pancreatic inter‐ and intralobular duct cells extrude H+‐ions to interstitial fluid when they secrete HCO‐3 to pancreatic juice. This study assesses the potential importance of Na+‐H+‐ion exchange for H+‐ion extrusion and secretion of HCO‐3 using the Na+‐H+ exchange blockers amiloride and hexamethylene‐amiloride. Intracellular pH (pH,) in inter‐ and intralobular pancreatic duct epithelium was measured using BCECF fluorescence. H+‐ion efflux was measured using a NH4Cl prepulse, acid‐loading technique. In HCO‐3‐free media, pH1 recovery following acid loading was blocked by amiloride (10‐4 m) and hexamethylene‐amiloride (10‐6 m), demonstrating amiloride‐and hexamethylene‐amiloride‐sensitive Na+‐H+ exchange. However, 5 × 10‐6 M hexamethylene‐amiloride did not reduce secretin‐dependent pancreatic HCO, secretion in vivo. Maximal H+‐efflux through Na+‐H+ exchange was 1.5 ± 0.2μmol min‐1 ml cell volume‐l, i.e. less than 1 % of estimated net H+‐ion efflux during HCO‐3 secretion. Conclusion: amiloride‐ and hexamethylene amiloride sensitive Na+‐H+ exchange is not important for secretin‐dependent pancreatic HCO‐3 secretion in the pig. Other mechanisms for H+ extrusion dominate.
Myogenic vasoconstriction in the rat kidney elicited by reducing perirenal pressure
Authors: CLAUSEN G. , ØIEN A. H. , AUKLAND K.
Published: December 2008

Clausen, G., Øien, A. H. & Aukland, K. 1992. Myogenic vasoconstriction in the rat kidney elicited by reducing perirenal pressure. Acta Physiol Scand 144 277–290. Received 17 April 1991, accepted 2 September 1991. ISSN 0001–6772. Departments of Physiology and Mathematics, University of Bergen, Norway.

Autoregulation of renal blood flow is generally believed to result from tubuloglomerular feedback and/or a vascular myogenic mechanism, but there is no consensus on the relative importance of these mechanisms. We designed an experiment in which tubuloglomerular feedback would tend to oppose a myogenic response: the denervated kidney in sits was enclosed in an airtight chamber and exposed to a 35 mmHg subatmospheric pressure for 1 to 10 minutes. Renal blood flow recorded by an electromagnetic flowmeter fell by 33 % in the course of a few seconds. Renal venous concentration of inulin showed no consistent change, indicating similar reduction in glomerular filtration rate. Since urine flow also fell, it is likely that the tubular flow rate was reduced. The kidney volume expanded by 10–20%, and subcapsular interstitial fluid pressure was reduced from 6.8 to — 8.6 mmHg. Arterial pressure remained unchanged, while renal venous pressure inside the chamber fell from 9.4 to 5.8 mmHg. Normalization of perirenal pressure gave rapid normalization of all parameters. Elevation of ureteral pressure attenuated or even prevented the renal blood flow reduction. Renal decapsulation or sympathetic blockade by phentolamine, or infusion of furosemide or 0.9% NaCl to inactivate tubuloglomerular feedback, did not prevent the renal blood flow reduction. We interpret the results to indicate that myogenic vasoconstriction greatly overpowered TGF and even surpassed the constriction predicted by a mathematical model based on maintenance of the preglomerular wall tension as estimated from transmural pressure.
Intravenous injection of AlbunexR microspheres causes thromboxane mediated pulmonary hypertension in pigs, but not in monkeys or rabbits
Authors: ØISTENSEN J. , HEDE R. , MYRENG Y. , EGE T. , HOLTZ E.
Published: December 2008

østensen, J., Hede, R., Myreng, Y., Ege, T. & Holtz, E. 1992. Intravenous injection of AlbunexR microspheres causes thromboxane‐mediated pulmonary hypertension in pigs, but not in monkeys or rabbits. Acta Physiol Scand144, 307–315. Received J April 1991, accepted 7 October 1991. ISSN 0001–6772. Nycomed AS Research and Development, Oslo, Norway.

Intravenous injection of the ultrasound contrast agent AlbunexR (manufactured by Nycomed AS, Oslo, Norway; 400 million air‐filled albumin microspheres per ml, mean diameter 4 ± 1 μm) caused a dose‐dependent increase of mean pulmonary arterial pressure in nine pigs. The highest dose (0.014 ± 0.002 ml kg‐1) increased mean pulmonary arterial pressure from 17± mmHg to 42 ± 3 mmHg and decreased mean systemic arterial pressure from 111±9 to 93± 12 mmHg. The pressure responses began 22 ± 1 s after particle injection, and reached maximum after 51 ±3 s. No changes in mean pulmonary arterial pressure or mean systemic arterial pressure were observed after AlbunexR injections during treatment with indomethacin (10 mg kg‐1+ 5 mgkg‐1 h‐1 i.v., n= 6) or the thromboxane A2 receptor antagonist HN‐11500 (10 mg kg‐1+ 5 mg kg‐1 h‐l i.v., n= 3). No Doppler enhancement could be detected in a carotid artery following injection of 0.12 ml kg‐1 AlbunexR during indomethacin treatment. In five rabbits, AlbunexR caused Doppler enhancement in a carotid artery, and 0.48 ml kg‐1 did not affect mean pulmonary arterial pressure or other haemodynamic parameters in five rabbits or in three cynomolgus monkeys. The pressure response in pigs may be explained by release of thromboxane A2 from the pulmonary intravascular macrophages during phagocytosis of the microspheres. This response to AlbunexR was totally absent in rabbits and monkeys.
Functional and morphological comparisons between cochlear outer hair cells and muscle tissues in the guinea‐pig
Authors: BRUNDIN L. , WIKLUND N. P. , GUSTAFSSON L. E. , FLOCK Å.
Published: December 2008

Brundin, L., Wiklund, N. P., Gustafsson, L. E. & Flock, AR. 1992. Functional and morphological comparisons between cochlear outer hair cells and muscle tissues in the guinea‐pig. Acta Physiol Scand144, 379–386. Received 24 April 1991, accepted 2i October 1991. ISSN 0001–6772. Departments of Physiology and Urology, and the National Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden

The effect of polylysine on the motility of outer hair cells and various muscle types was compared. Poly‐L‐lysine and its stereoisomer, poly‐D‐lysine, inhibited acoustically induced length changes of isolated outer hair cells from the guinea‐pig hearing organ. The frequency specific displacements of the hearing organ in response to a tone stimulus are also inhibited to polylysine (Brundin et al. 1991). Poly‐L‐lysine, and its stereoisomer, irreversibly attenuated motile responses to transmural stimulation of guinea‐pig ileum, vas deferens and taenia coli in a dose dependent manner, but were without significant effect on motile responses in skeletal and heart muscle. l‐lysine, D‐lysine, and the negatively charged polyaminoacid poly‐L‐aspartate, were without significant effect on outer hair cell and smooth muscle motility.

The inhibitory effect of polylysine in smooth muscle is a direct effect on the muscle cell since polylysine attenuated acetylcholine‐ and adenosine triphosphate‐induced contractions in the ileum, and ATP‐ or noradrenaline‐induced contractions in the vas deferens.

Pillar structures, believed to be of importance to excitation contraction coupling, were compared. In heart and skeletal muscle the pillars span the gap between sarcoplasmic reticulum and T‐tubuli, deeply recessed into the muscle cell. In smooth muscle and outer hair cell the pillars are in closer relation to the cell exterior. The length of the pillars of the outer hair cells exceeds by two times that of smooth and skeletal muscle.

The susceptibility of outer hair cells and smooth muscle tissue to the positively charged polylysine may indicate similarities in membrane or channel composition.
The effect of immobilization on myotendinous junction: an ultrastructural, histochemical and immunohistochemical study
Authors: KANNUS P. , JOZSA L. , KVIST M. , LEHTO M. , JÄRVINEN M.
Published: December 2008

Kannus, P., Jozsa, L., Kvist, M., Lehto, M. & Järvinen, M. 1992. The effect of immobilization on myotendinous junction: an ultrastructural, histochemical and immunohistochemical study. Acta Physiol Scand144, 387–394. Received 28 April 1991, accepted 13 October 1991. ISSN 0001–6772. Tampere Research Station of Sports Medicine, UKK‐Institute, and Department of Surgery, Tampere University Central Hospital, Tampere, Finland; Department of Morphology, National Institute of Traumatology, Budapest, Hungary; and Sports Medical Research Unit, Paavo Nurmi Center, University of Turku, Turku, Finland.

The effect of immobilization on the myotendinous junction of the calf muscles in the rat was studied histochemically, immunohistochemically and morphometrically with a transmission electron microscope.

After 3 weeks of immobilization, the contact area between the muscle cells and tendineal collagen fibres was reduced by almost 50% in both type I (slow‐twitch) and type II (fast‐twitch) muscle fibres. The terminal finger‐like processes of the muscle cells became shallow and cylindrical or were completely atrophied. Their basal membranes were slightly thickened. Histochemically, the most remarkable alteration in the myotendinous junction was the marked decrease in the sulphate containing glyco‐saminoglycans. In the basal lamina of the muscle fibres, the glycosaminoglycan and proteoglycan content was also reduced. Immunohistochemical analyses revealed that the amount of type III collagen was markedly increased on the myotendinous interface, but the amount and distribution of type I collagen was not affected by immobilization.

These findings suggest that immobilization causes degenerative changes at the myotendinous junction, which, in turn, most likely decrease its tensile strength and may predispose it to rupture during activity.
Influence of stretch‐shortening cycle on mechanical behaviour of triceps surae during hopping
Authors: BELLI A. , BOSCO C.
Published: December 2008

Belli, A. & Bosco, A. 1992. Influence of stretch‐shortening cycle on mechanical behaviour of triceps surae during hopping. Acta Physiol Scand144, 401408. Received 20 March 1991, accepted 3 December 1991. ISSN 0001–6772. Laboratories of Physiology, Universities of St Etienne and Lyon, France and Departments of Biology and Physical Activity, University of Jyväskylä, Finland.

Six subjects performed a first series of vertical plantar flexions and a second series of vertical rebounds, both involving muscle triceps surae exclusively. Vertical displacements, vertical forces and ankle angles were recorded during the entire work period of 60 seconds per series. In addition, expired gases were collected during the test and recovery for determination of the energy expenditure. Triceps surae was mechanically modelled with a contractile component and with an elastic component. Mechanical behaviour and work of the different muscle components were determined in both series. The net muscular efficiency calculated from the work performed by the centre of gravity was 17.5±3.0% (mean ± SD) in plantar flexions and 29.9 ± 4.8% in vertical rebounds. The net muscle efficiency calculated from the work performed by the contractile component was 17.4 %% 2.9% in plantar flexions and 16.1 ± 1.47; in vertical rebounds. These results suggest that the muscular efficiency differences do not reflect muscle contractile component efficiency but essentially the storage and recoil of elastic energy. This is supported by the relationship (P < 0.01) found in vertical rebounds between the extra work and the elastic component work. A detailed observation of the mechanical behaviour of muscle mechanical components showed that the strategy to maximize the elastic work depends also on the force‐velocity characteristics of the movement and that the eccentric‐concentric work of the contractile component does not always correspond respectively to the ankle extension‐flexion.
The first breaths of air stimulate noradrenaline turnover in the brain of the newborn rat
Authors: LAGERCRANTZ H. , PEQUIGNOT J. , PEQUIGNOT J.‐M. , PEYRIN L.
Published: December 2008

Lagercrantz, H., Pequignot, J., Pequignot, J.‐M. & Peyrin, L. 1992. The first breaths of air stimulate noradrenaline turnover in the brain of the newborn rat. Acta Physiol Scand144, 433–438. Received 19 July 1991, accepted 3 December 1991. ISSN 0001–6772. Department of Paediatrics (KS), Karolinska Institute, Stockholm, Sweden and UA CNRS 1196, Physiologie, Faculté de Médecine, Université Claude Bernard, Grange Blanche, Lyon, France.

The aim of this study was to analyse the noradrenaline (NA)‐turnover in the brain around birth and its significance for neonatal adaptation. NA and its metabolite 3–methoxy‐4–hydroxyphenylethylene glycol (MHPG) have been measured by high‐pressure liquid chromatography (HPLC) in the pons‐medulla and cortex in rat foetuses and pups. The MHPG/NA ratio was used as an index of NA‐turnover. Catecholamines were also determined in the adrenals for comparison. The MHPG/NA ratios were found to increase 2.7–fold in the pons‐medulla and 2–fold in the cortex during the first day after birth. The surge of NA‐turnover occurred after the pups had been breathing air for two hours. The increase of NA‐turnover was significantly lower in the cortex of rat pups breathing a hypoxic gas mixture or when they were kept in a cooler environment. The differences were less marked in the pons‐medulla. We conclude that breathing air stimulates NA‐turnover in the brain of the newborn rat and this stimulatory effect is modulated by environmental factors.
Water flux and early signs of entrance into phase 111 of fasting in grey seal pups
Authors: NORDØY E. S. , STIJFHOORN D. E. , RÅHEIM A. , BLIX A. S.
Published: December 2008

Norøy, E.S., Stijfhoorn, D.E., Råheim, A. & blix, A.S. 1992. Water flux and early signs of entrance into phase III of fasting in grey seal pups. Acta Physiol Scand144, 477482. Received 11 November 1990, accepted 13 November 1991 ISSN 0001–677. Department of Arctic Biology and Institute of Medical Biology, University of Tromsø, Tromsø, and Institutt for Energiteknikk, Kjeller, Norway.

Body water loss and turnover rate were measured in fasting newly weaned grey seal (Halichaerus grypus) pups without access to water for 52 days, by use of bolus injections of deuterated water. Total body water (N) was 41.8 ±2.3 (SD)% of total body weight at day 3 and 44.5 ± 5.9 (SD)% at day 51 of fasting (P > 0.05), while the water content of body core decreased from 73 to 61 yo over the same period. The average water efflux rate in the same period was 362 ± 17 (SD) ml d‐1, the reduction in N over the same period contributing 35 yo to this end. The biological half‐time of deuterated water was 38.2 ± 3.3 (SD) d. Plasma osmolality increased from a stable level of 329±11(SD)mosmol kg‐1 to 445± 11 (SD) mosmol kg‐1 after day 38 of fasting. Plasma urea was the major contributor to this increase, in spite of a steadily decreasing urine urea concentration (Nordey et al. 1990) throughout the entire experimental period. It is concluded that grey seal pups endure 52 d of fasting without intake of water with a minor dehydration of body core, while they become hyperosmotic due to increased catabolism of protein after 38 d when sparing of the insulating blubber layer in preparation for life in cold water seems to occur.
Prostaglandin D2 increases Cl secretion across canine tracheal epithelium through cyclooxygenase stimulation and cAMP production
Authors: TAMAOKI J. , KANEMURA T. , SAKAI N. , ISONO K. , CHIYOTANI A. , YAMAUCHI F. , TAKIZAWA T. , KONNO K.
Published: December 2008

Prostaglandin (PG) D2 is one cyclo‐oxygenase product of arachidonic acid metabolites that may play a role in the pathogenesis of asthma. To determine the effect of PGD2 on ion transport by airway epithelium and its mechanism of action, we measured bioelectric properties of canine cultured tracheal epithelium under short‐circuit conditions in vitro. PGD2 (10‐7 M) increased short‐circuit current (Isc) from 5.5 ± 1.2 to 14.1 ± 2.9 μA cm‐2 (means ± SE, P < 0.01) when added to the mucosal solution, and to 22.2 ± 3.8 μA cm‐2 (P < 0.001) when added to the submucosal solution, an effect that was accompanied by the corresponding increases in transepithelial potential difference and conductance. These effects were dose‐dependent. The PGD2 induced increase in Isc was not altered by preincubation of cells with autonomic antagonists (phentolamine, propranolol, atropine), the lipoxygenase inhibitor AA‐861, the protein kinase C inhibitor H‐7, or the Na channel blocker amiloride, but it was inhibited by each of indomethacin, piroxicam, the Cl channel blocker diphenylamine‐2‐carboxylate, the Cl transport inhibitor furosemide, and Cl‐free medium. Intracellular adenosine 3′,5′‐cyclic monophosphate (cAMP) levels were dose‐dependently increased by PGD2. These results suggest that PGD2 may selectively stimulate airway epithelial CI secretion via cyclo‐oxygenase‐ and cAMP‐dependent pathway.
Local infusion of IGF‐I into the kidney of pituitary intact rats induces renal growth
Authors: MATEJKA G. L. , JENNISCHE E.
Published: December 2008

To determine whether insulin‐like growth factor I (IGF‐I) exerts growth‐promoting actions on the kidneys of pituitary‐intact animals IGF‐I was infused into the kidney via two different routes using osmotic pumps. In a first set of experiments IGF‐I was infused directly into the tissue by the use of an implanted catheter traversing the kidney. It was found that a dosage of 50 μg IGF‐I wk‐1 but not 20 μg wk‐1 caused a gain in weight of the kidney. The growth was accompanied with morphological alterations among the cortical distal tubules. As a marker for hyperplasia, a monoclonal antibody directed against the Ml subunit of ribonucleotide reductase (RR) was used. The altered cells stained with RR, as also did the tubule cells of the medullary thick ascending limb (mTAL). No RR staining was found in the bulk of renal mass, i.e. the proximal tubules, indicating that possible growth in these cells did not involve cell division. In a second set of experiments IGF‐I at 50, 100 and 300 μg wk‐1 was infused into the renal circulation via a side branch of the renal artery, the suprarenal artery. In these experiments, no growth response or morphological alterations of the tissue were found. These findings demonstrate that IGF‐I, when administered directly into the parenchyme, causes growth of the kidney in normal animals. The data are compatible with a causative role for IGF‐I in the course of renal growth.
High salt alone does not influence the kinetics of the Na+‐H+antiporter
Authors: HOLTBÄCK U. , APERIA A. , CELSI G.
Published: December 2008

During a high‐salt diet, tubular sodium reabsorption is decreased. This study concerns the effect of a high‐salt diet on the proximal tubular (PT) Na+influx pathways. Brush‐border membrane vesicles (BBMV) were prepared from rats on normal‐salt (NS) and rats on high‐salt (HS) diets. The initial uptake rates of Na+were the same in NS and HS rats, both in the absence and the presence of 1 mm amiloride. Vmax and Km for the amiloride‐sensitive Na+/H+antiporter were also the same in the NS (Vmax 3.69 ± 0.31 nmol mg prot‐110 s‐1, Km 6.13 ± 0.58 mm) and HS groups (Vmax 3.54 ± 0.28 nmol mg prot‐110 s‐1, Km 6.18 ± 0.64 mm). There was no difference in the initial uptake rates of the Na+‐glucose and the Na+‐alanine symporters in NS and HS. Vmax and Km for the l‐dopa‐Na+symporter were also the same in NS (Vmax 72 ± 2.5 pmol mg prot‐120 s‐1, Km 98 ± 14 μm) and HS groups (Vmax 78 ± 6.0 pmol mg prot‐120 s‐1, Km 106 ± 4 μm). In summary, HS diet does not change the kinetics of the Na+transporters in the brush‐border membrane of PT cells.
Glycogen breakdown and lactate accumulation during high‐intensity cycling
Authors: MEDBØ J. I.
Published: December 2008

High‐intensity exercise results in a large breakdown of glycogen. The glycogen lost may reappear as hexose phosphates, lactate, or it may be fully oxidized. Part of the lactate produced may be transferred from muscle to blood. There is, however, incomplete information on the relative importance of each endpoint of glycogen breakdown during high intensity exercise. Therefore, 16 healthy men cycled for between 30 s and 3 min until exhaustion. Muscle biopsies were taken from m. vastus lateralis before and immediately after exercise and analysed for glycogen, glucose, glucose‐6‐phosphate and lactate. In addition the blood lactate concentration was measured at exhaustion, and the 02 uptake was measured throughout the exercise for calculation of glycogen oxidation. The muscle glycogen concentration fell by 17–24 mmol kg‐1 wet wt muscle, the muscle glucose and G‐6‐P concentrations rose by 1 and 4 mmol kg‐1 respectively, and the muscle lactate concentration rose by 20–30 mmol kg‐1. The blood lactate concentration at exhaustion was 4–9 mmol l‐1 above pre‐exercise value. Consequently, 60% of the glycogen lost reappeared as lactate within the working muscle, another 20–25% was found as other glycolytic intermediates, 4–13% of the glycogen loss could be accounted for by oxidation. Lactate released to blood could account for ± 10% of all lactate produced. Therefore, when large muscles are heavily engaged, as during high intensity cycling, most of the glycogen broken down appears as lactate within the working muscle.
Hydrogen peroxide stimulates endocytosis in cultured bovine aortic endothelial cells
Authors: SUNDQVIST T. , LIU S. M.
Published: December 2008

Fluid‐phase uptake of macromolecules by cultured bovine aortic endothelial cells was measured using FITC‐dextran (70000 Da). Low doses of hydrogen peroxide added extracellularly stimulated the uptake of macromolecules by the endothelial cells. There was no general increase in the passive permeation or the transport across the cell layer. Moreover, when endothelial cells were stimulated with phorbol myristate acetate (PMA), macromolecules uptake was also enhanced. The PMA effect was blocked with superoxide dismutase (SOD) and catalase, suggesting a pivotal role of oxygen metabolites in fluid phase uptake of macromolecules by endothelial cells.
Potassium currents in isolated human atrial and ventricular cardiocytes
Authors: VARRÓ A. , NÁNÁSI P. P. , LATHROP D. A.
Published: December 2008

The whole‐cell configuration of the patch‐clamp technique was applied to study and compare ion currents in single ventricular and atrial cardiocytes isolated from human myocardium. In ventricular cardiocytes the K+ inward rectifier current (IK1) was three times larger than in atrial cardiocytes, while its inactivation kinetics were twice as slow when measured at ‐140 mV. The magnitude of these variables depended on the test potential but was independent of changes in holding potential. A transient outward current (Ito) was observed in both ventricular and atrial cardiocytes. The amplitude of the inactivating component of Ito was not significantly different in atrial and ventricular cells, but the time course of inactivation was significantly longer in atrial than in ventricular cardiocytes. Steady‐state inactivation of Ito in atrial cells was well described by a two‐state Boltzmann function having a midpoint potential of ‐ 41.4mV and a slope factor of 6.9 mV‐1. No discernible K+ delayed rectifier current (IK) was observed in either cell type. In four of the 12 atrial cells studied, a time dependent inward current was observed at negative test potentials having a 240 ± 21 ms time constant for activation and an amplitude of 101±28pA. This current, which resembled the pacemaker current (It), was not observed in any of the ventricular cells examined.
Substrate preference of isolated perfused rat hearts during hypothermia and rewarming
Authors: STEIGEN T. K. , TVEITA T. , KORVALD C. , SOLBERG T. , BJORDAL E. , YTREHUS K. , LARSEN T. S.
Published: December 2008

Fatty acid and glucose oxidation rates were measured in isolated rat hearts undergoing hypothermia and rewarming. The hearts were perfused in the Langendorff mode with Krebs‐Henseleit bicarbonate buffer containing 11.1 mM glucose plus 0.6 mM albumin‐bound oleic acid as energy substrates. The hearts were stabilized at 37 oC and thereafter cooled progressively to 15 opC over a period of 60 min. The hearts were kept at this temperature for 10 min and then rewarmed to 37 oC during the next 30 min. Control hearts were perfused at 37 oC throughout the whole perfusion period. Trace amounts of [14C]glucose or [14C]oleic acid were included in the perfusate, and the rate of substrate oxidation was determined on the basis of the radioactive CO2 production. In normothermic hearts steady state oxidation rates of glucose and oleate were found to be 0.17 ± 0.01 and 0.51 ± 0.07μmol min‐1 g‐1 dry wt, respectively (mean ± SEM). In response to hypothermia (15 oC) glucose oxidation was reduced by 76% (from 0.17 ± 0.01 to 0.04 ± 0.01 μmol min‐1 g‐1 dry wt) and oleate oxidation by 47% (from 0.51 ± 0.07 to 0.27 ± 0.02 μmol min‐1 g‐1 dry wt). Upon rewarming glucose and fatty acid oxidation rates returned to essentially the same values (0.12 ± 0.02 and 0.45 ± 0.04 μmol min‐1 g‐1 dry wt) as those observed under steady state normothermic conditions. The molar ratio between glucose and fatty acid oxidation was, however, significantly (P < 0.05) lower in hypothermic than in normothermic hearts. This finding indicates a shift in the metabolism of hypothermic hearts towards an even higher preference for fatty acids than that observed in normothermic hearts.
Effect of serotonin receptor blockade on endocrine and cardiovascular responses to head‐up tilt in humans
Authors: MATZEN S. , SECHER N. H. , KNIGGE U. , PAWELCZYK J. , PERKO G. , IVERSEN H. , BACH F. W. , WARBERG J.
Published: December 2008

of blockade of serotonin (5HT) receptors on the integrated cardiovascular and endocrine adaptations during head‐up tilt were investigated in normal men. Incontrolexperiments 50ohead‐up tilt increased heart rate (HR), total peripheral resistance (TPR), plasma renin activity (PRA) and sympathetic activity (plasma noradrenaline; NA). A moderate increase in pituitary‐adrenal hormones (plasma ACTH, β‐END and Cortisol) was observed. After a mean tilt time of 30 ± 5min (n= 20) presyncopal symptoms associated with decreases in HR, TPR and arterial pressure occurred. At this time pituitary hormones, Cortisol, adrenomedullary (plasma adrenaline; A) as well as vagal activity (plasma pancreatic polypeptide) were markedly increased, whereas sympathetic activity (plasma NA) decreased. The 5‐HT1+2receptor antagonist methysergide did not significantly interfere with cardiovascular variables but attenuated the response of NA, prolactin (PRL), β‐endorphin (β‐END) and PRA (P< 0.02). The 5‐HT2‐receptor antagonist ketanserin reduced the tolerated tilt time (10 ± 4 vs. 32 ± 2 min;P< 0.0003,n= 7) but had no significant effects on hormonal variables. The 5‐HT3‐receptor antagonist ondansetron abolished the adrenomedullary response to hypotension without affecting cardiovascular tolerance or the activity of the pituitary‐adrenal axis. The results suggest that serotonergic mechanisms may be involved in the integrated cardiovascular and endocrine responses to central blood volume depletion in humans.
Inducibility of NADP‐specific isocitrate dehydrogenase with endurance training in skeletal muscle
Authors: LAWLER J. M. , POWERS S. K. , CRISWELL D. S.
Published: December 2008

NADP+‐specific isocitrate dehydrogenase (ICDH‐NADP: EC 1 1 1 42) is primarily a mitochondrial matrix enzyme in both mammalian skeletal muscle and heart and has markedly higher activity levels than the NAD+‐specific isozyme. To date, it is unknown whether ICDH‐NADP activity is inducible with in vivo exercise training in locomotor or respiratory skeletal muscle. Therefore, the purpose of this investigation was to quantify alterations in ICDH‐NADP activity in respiratory muscles (costal and crural diaphragm) and locomotor muscles (medial gastrocnemius, plantaris and soleus) following 8 weeks of treadmill endurance training. Ten of the animals had been assigned randomly to an exercise group (TR) and had completed 8 weeks of progressive (5 days week‐1: 45 min day‐1) treadmill endurance training while the remaining 10 animals comprised a sedentary control (C). Mean ICDH‐NADP activities in Tr were significantly higher (P < 0.05) when compared with C in the medial gastrocnemius (61.3%), plantaris (42.9%) soleus (21.4%). Mean costal diaphragm ICDH‐NADP activity noted in trained animals when compared to the sedentary control group was not significantly higher (10.8% greater for TR; P= 0.14). No mean differences (P= 0.58) were noted in the crural diaphragm. The results indicate that ICDH‐NADP is inducible with endurance training in locomotor skeletal muscle. A coefficient of determination of 0.624 (i.e. 62.4% of the variance could be explained) for ICDH‐NADP was calculated, with the oxidative enzyme marker succinate dehydrogenase (P < 0.05) indicating a positive, moderate relationship. We suggest that the upregulation of ICDH‐NADP found in the present study is related to metabolic stress with exercise.
Relationship of oxypurine release to contractile failure in dinitrophenol‐treated rat skeletal muscle
Authors: MAJUMDAR R. , CWIK V. A. , SOLONYNKO G. , BROOKE M. H.
Published: December 2008

The efflux of hypoxanthine and uric acid from skeletal muscle has been noted to follow exercise and metabolic stress both in vivo and in vitro. Since the action of xanthine oxidase and hypoxanthine generates free radicals with potential damaging effect on the muscle membranes, an in vitro model was used to study the relationship of metabolic stress, oxypurine release and muscle contraction. When rat epitrochlearis muscle was exposed to the mitochondrial uncoupler dinitrophenol at 37 oC, lactate release was pronounced and hypoxanthine and uric acid appeared in the incubating medium. The twitch tension, in response to supramaximal stimulation, was reduced to less than 5 % of the initial value. When the same experiment was repeated at 27 oC, hypoxanthine and uric acid formation was inhibited, although lactate release indicated that metabolic stress was still present. Twitch tension was relatively preserved (57% of the initial value). The lower temperature did not alter the decrease in ATP and phosphocreatine levels in the muscle which is produced by dinitrophenol. There was an inverse relationship between oxypurine release and twitch tension in individual muscles (r = 0.80, P < 0.01 for hypoxanthine and r= 0.95, P < 0.0002 for uric acid). Xanthine dehydrogenase/ xanthine oxidase was detected in muscle and between 16 and 22% of the activity was in the oxidase form.
The responses of left ventricular end‐systolic pressure‐diameter relationship to acute pressure overload induced by aortic constriction
Authors: OIKAWA Y. , SHIRATO K. , SAKUMA M. , KATOH A. , NAKAGAWA M. , ISHIGAKI H. , TAKISHIMA T.
Published: December 2008

The aim was to investigate the responses of the left ventricular (LV) end‐systolic pressure‐diameter relationship (ESPDR) to acute pressure overload. ESPDRs were made by 2‐min ascending and descending aortic constrictions before and after administration of propranolol and atropine sulphate (both 0.2 mg kg‐1 i.v.) in eight open‐chest dogs with the pericardium preserved. LV anterior‐posterior diameter was measured with ultrasonic crystals. In the ascending aortic constriction, end‐diastolic pressure (EDP) and end‐diastolic diameter (EDD) were unchanged and ESPDR shifted to the left. In the descending aortic constriction, EDP and EDD increased from 6.8±0.7 to 8.8±0.9mmHg (P < 0.01) and from 32.7±1.4 to 34.5+1.6 mm (P < 0.05) and ESPDR shifted to the right. After administration of propranolol and atropine sulphate, cases having smaller changes in EDD during 2 min constriction (0.3+0.3 mm in all cases of ascending, 0.3 + 0.2 mm in four cases of descending aorta) showed a leftward shift of ESPDR. The remaining four cases of descending aortic constriction with larger changes in EDD (1.8 + 0.8 mm, P < 0.05) showed a rightward shift of ESPDR. An inverse curvilinear correlation was found between percentage changes in EDD and in the slopes. These results suggest that the responses in ESPDR to acute pressure overload were determined by not only changes in the contractile state but also the interplay between adaptation to acute pressure overload (the Anrep effect) and preload.
Alteration of cardiac energy state during development of hypertension in rats of the Lyon strain: a 31 P‐NMR study on the isolated rat heart
Authors: LORTET S. , HECKMANN M. , AUSSEDAT J. , RAY A. , VINCENT M. , SASSARD J. , ZIMMER H.‐G. , ROSSI A.
Published: December 2008

The effect of different chronic blood pressure levels on cardiac energy metabolism was studied by 31P‐NMR spectroscopy in perfused hearts from the Lyon strains of hypertensive (LH), normotensive (LN) and hypotensive (LL) rats at the ages of 12 and 21 weeks. The in vivo assessment of haemodynamic parameters measured at 21 weeks in anaesthetized rats with an ultraminiature catheter pressure transducer confirmed that left ventricular systolic pressure and mean aortic pressure were significantly greater (+ 25 %) in LH rats than in LN and LL rats. In the LL animals, left ventricular systolic pressure was slightly reduced (–10%) and cardiac contractility (estimated by LV dP/dtmax) showed a 24% decreased compared to normotensive animals. The energy state of the cardiomyocytes was characterized at different work levels of isolated rat hearts, by determining the concentration of the free phosphorylated compounds at each work level. Changes in workload were induced by varying the calcium concentration in the perfusion fluid. Increasing extracellular calcium concentration resulted in a similar increase in left ventricular developed pressure (LVDP) in all groups studied. Intracellular pH was not influenced by either the age of the animals or the level of cardiac work, in the three groups of animals. ATP content of the LN and LL rats remained constant during the whole perfusion period while the 12 week‐old LH rats showed a decreased ATP content with increasing cardiac work. In the older LH rats, ATP content was decreased at the highest work level (corresponding to 2 mM calcium). In response to the increase in work, phosphocreatine (PCr) content diminished and inorganic phosphate (Pi) content increased in both LN, LH and LL animals. PCr degradation and Pi accumulation were higher in the LH rats and less in LL rats compared to the LN. These changes were more important in the younger than in the older hypertensive animals. The relationship between LVDP and [Pi]/[PCr] indicates that oxidative metabolism is maximally activated in the young hypertensive rats and suggests that this maximal activation represents an adaptative phase to the increase in blood pressure. Since the difference between the metabolic pattern of the 21 week‐old LH rats and age‐matched LN rats was less pronounced, it is likely that a compensatory stage has been reached at that age.