bluuebunny/crossref_metadata_2025 huggingface dataset:
The initiation of non‐micturating contractions in the feline bladder
Authors: SATCHELL P.
Published: December 2008

The extrinsic nervous system of the bladder may not be involved in the initiation of non‐micturating contractions in the cat, because neither the sympathetic or parasympathetic motor drives appear to change their level of activity before the first contraction. This stability of the motor drives may only reflect the absence of afferent drive from the relatively empty bladder. This assumption was examined by recording from the pelvic nerve during bladder filling at a natural rate in pentobarbitone anaesthetized cats. Afferent multifibre nerve activity was always increasing before the onset of non‐micturating contractions. Six out of nine nerve fibres innervating localized bladder wall mechanoreceptors were discharging before the onset of non‐mictating contractions, whereas all had been silent with the bladder empty. Because mechanoreceptor activity preceded the onset of non‐micturating contractions, reflex changes in autonomic motor activity, which have not yet been observed, may have a role in initiating non‐micturating contractions.
Respective effects of malnutrition and phosphate depletion on endurance swimming and muscle metabolism in rats
Authors: BOLLAERT P. E. , GIMENEZ M. , ROBIN‐LHERBIER B. , ESCANYE J. M. , MALLIE J. P. , ROBERT J. , LARCAN A.
Published: December 2008

To examine the respective roles of malnutrition and phosphate depletion on muscle exercise capacity and bioenergetics, phosphate‐depleted, either underfed or partly refed rats; phosphate‐supplemented, either underfed or partly refed rats; and well‐nourished control animals were studied, using swim time to exhaustion and 31P NMR spectroscopy measurements of muscle phosphocreatine, inorganic phosphate, adenosine triphosphate and intracellular pH. Only partly refed rats displayed hypophosphataemia. Swim time to exhaustion was lower in non‐refed rats than in controls. Among the four groups, both refeeding and phosphate depletion positively affected swim time to exhaustion (both with P < 0.02), and swim time to exhaustion was negatively correlated with phosphataemia (P < 0.05). At rest, the ratio of muscle phosphocreatine/inorganic phosphate was lower in the phosphate‐supplemented rats than in controls, whereas muscle phosphocreatine/adenosine triphosphate and intracellular pH were comparable. After non‐tetanic stimulation, the muscle phosphocreatine recovery was slower in the four groups than in controls and closely correlated with exhaustion (P < 0.01). These findings suggest that malnutrition alters the capacity of muscular work, mainly because of a reduced cell oxidative energy availability. These patterns are improved by partial refeeding and clearly influenced by the level of phosphorus intake, whether depletion is capable of improving metabolic alterations or uncontrolled supplementation is deleterious in malnourished animals.
Lactate transport during differentiation of skeletal muscle cells: evidence for a specific carrier in L6 myotubes
Authors: ABIDA K. EL , DUVALLET A. , THIEULART L. , RIEU M. , BEAUDRY M.
Published: December 2008

El abida, K., Duvallet, A., Thieulart, L., Rieu, M. & Beaudry, M. 1992. Lactate transport during differentiation of skeletal muscle cells: evidence for a specific carrier in L6 myotubes. Acta Physiol Scand144, 469471. Received 12 June 1991, accepted 8 October 1991. ISSN 0001–6772. Laboratoire de physiologie des adaptations, CIIU Cochin, 24 rue du Faubourg Saint Jacques, 75104 Paris, France.

Cellular uptake of lactate involves a carrier in numerous types of mammalian cells. In cultured rat L6 myoblasts, lactate diffuses freely. We show that during myogenesis a carrier appears at the myotube stage.

The degree of cellular differentiation was determined by microscopic observation and by measurement of a marker of biochemical differentiation: the increase in specific activity of creatine kinases.
Renal effects of urodilatin and atrial natriuretic peptide in volume expanded conscious dogs
Authors: BESTLE M. H. , BIE P.
Published: December 2008

The renal effects of urodilatin and atrial natriuretic peptide (ANP) were examined in conscious dogs during acute volume expansion maintained through independent infusions of water and NaCl. Peptide was infused in a step‐up fashion, in 40‐min periods at rates of 2.5, 12.5 and 50.0 ng kg‐1 min‐1 (ANP, urodilatin) or 0.5, 2.5 and 10.0 ng kg‐1 min‐1 (second series of urodilatin). ANP immunoreactivity (ANPir) in plasma was measured with an antibody showing 100% cross‐reactivity with urodilatin.

At 50 ng kg‐1 min‐1, ANP increased plasma ANPir some 10‐fold (64 ± 6 pg ml‐1 to 728 ± 82 pg ml‐1) while urodilatin elicited a 25‐fold increase in ANPir (78± 13 pg ml‐1 to 1645 ± 204 pg ml‐1). ANP doubled sodium excretion (61 ± 12 to 124±30 μmol min‐1, P < 0.05) while urodilatin increased sodium excretion to 269 ± 45 μmol min‐1. Both peptides approximately doubled urine flow. Urodilatin at 10 ng kg‐1 min‐1 increased sodium excretion from 57±17μmol min‐1 to 106 ± 25 μmol min‐1, i.e. similar to the response ANP elicited at 50 ng kg‐1 min‐1. In the time control series a significant fall in sodium excretion was observed, despite the continuous replacement of sodium and water.

The results demonstrate that in identical, relatively high doses, the changes in sodium excretion, diuresis, heart rate (HR) and arterial pressures elicited by urodilatin are more pronounced than those of ANP. However, such amounts seem to produce plasma concentrations of urodilatin higher than those of ANP. A given small increase in sodium excretion required higher plasma levels of ANP compared to urodilatin. Therefore, for a given modest plasma level, urodilatin is a more potent natriuretic agent than ANP.
Control of shivering and heart rate in incubating bantam hens upon sudden exposure to cold eggs
Authors: TØIEN Ø.
Published: December 2008

To distinguish shivering released by cooling of the brood patch from shivering released by low core temperature, incubating bantam hens were exposed to water perfused eggs. Responses to a period of egg cooling were compared to the recovery period after egg temperature had been returned to 40 oC, but cloacal temperature (Tb) still was low. At an ambient temperature (Ta) of 23 oC and exposure of the hens to between two and eight eggs cooled to 10–35 oC (series 1), electromyographic (EMG) activity of musculus iliotibialis increased rapidly with an occasional overshoot, and was higher during egg cooling than during recovery. This hysteresis in EMG activity and Tb was weakly correlated to egg temperature and clutch size. Heart rate (HR) showed an almost parallel increased to shivering except that a maximum HR was reached at high shivering intensities. These responses were also present at a Ta of 37 oC when the hens were slightly hyperthermic before exposure to eight eggs at 20 oC (Series 2). At the highest starting Tbs EMG activity increased linearly after a drop in Tb. Shivering in m. pectoralis showed a lower threshold Tb and lower activity than m. iliotibialis during egg cooling, and immediately ceased at the end of egg cooling. Total body thermosensitivity estimated from the recovery periods at low and high Ta was –9.7 and –6.4 W kg‐1oC‐1, respectively.

It is concluded that shivering in incubating birds warming cold eggs probably is stimulated both by peripheral and central thermoreceptors. The peripheral component shows phasic properties typical for skin receptors.
Mechanisms behind cyclic changes in duodenal fluid transport in the fasting state
Authors: MELLANDER A. , ABRAHAMSSON H. , SJÖUVALL H.
Published: December 2008

The relationship between distal duodenal motility, fluid transport and transmural potential difference (PD) was studied in 33 healthy volunteers. Motor activity was registered with a low‐compliance pneumohydraulic system; one pressure channel also served as an intraluminal flowing electrode for registration of transmural PD. Net fluid and bicarbonate transport were measured with a triple lumen perfusion technique.

The relation between net fluid transport (NFT) and transmural PD depended on the current phase of the migrating motor complex (MMC). In phase I and early phase II (low motor activity), a significant net fluid absorption was seen when the perfusate contained glucose (30 HIM). If glucose was substituted with mannitol, NFT was not significantly different from zero and transmural PD was slightly lumen positive. In the early part of the MMC cycle (low motor activity), there was a significant correlation between a more lumen negative transmural PD and a higher net fluid absorption in individual experiments (r =–0.65; P < 0.01).

In late phase II of the MMC cycle (high motor activity), NFT changed significantly in the secretory direction in both Krebs mannitol and Krebs glucose perfused segments, and the perfusate‐related difference in transport rate was no longer statistically significant. In the Krebs mannitol group, transmural PD became significantly more lumen negative, and there was also a decrease in net bicarbonate absorption as well as a slight acidification of the luminal contents. The relationship between transmural PD and NFT was reversed, i.e. a more lumen negative PD was associated with a higher net fluid secretion in individual experiments (r = 0.82; P < 0.05).

The results show that in the fasting state, the distal duodenum alternates between an absorptive and a secretory mode. Fluid secretion is probably generated by activation of an electrogenic secretory process during late phase II of the MMC cycle.
Pattern of descending excitation of presumed propriospinal neurones at the onset of voluntary movement in humans
Authors: MAZEVET D. , PIERROT‐DESEILLIGNY E.
Published: December 2008

Mazevet, D. & Pierrot‐Deseilligny, E. 1994. Pattern of descending excitation of presumed propriospinal neurones at the onset of voluntary movement in humans. Acta Physiol Scand150, 27–38. Received 2 April 1993, accepted 30 July 1993. ISSN 0001–6772. Neurophysiologie Clinique, Rééducation, Hôpital de la Salpêtrière, 47 boulevard de ľ Hôpital, 75651 Paris cedex 13, France.

The pattern of activation of presumed ‘propriospinal’ neurones was investigated in human subjects during phasic voluntary contractions of one of the following muscles: biceps, triceps, flexor carpi radialis (FCR), flexor carpi ulnaris (FCU) and extensor carpi radialis (ECR). Changes in the amplitude of the H reflex (FCR, ECR), or the tendon jerk (biceps, triceps) were used to assess the excitability of the corresponding motorneurone pools after conditioning stimulation. Conditioning stimuli were applied to the musculo‐cutaneous, triceps and ulnar nerves. In most cases reflex facilitation was not observed at rest and was only disclosed at the onset of contraction. The characteristics of this facilitation (3–4 ms central delay, short duration, low threshold, depression when the afferent input was increased) are consistent with those previously attributed to ‘propriospinal’ excitation. It is argued that the contraction‐associated facilitation was descending in origin. The descending facilitation of the ‘propriospinal’ system had a characteristic pattern in that the pathways selected by higher centres were those receiving the afferent feedback from the contracting muscle. These results provide further insight into the organization of human ‘propriospinal’ pathways: (1) it is confirmed that afferents from each muscle activate a specific subset of neurones; and (2) it is suggested that the projections of each subset are divergent, implying that individual neurones project onto diverse motor nuclei, an organization that would favour the coordination of multi‐joint movements. Such an organization is discussed in relation to the possible role of the propriospinal system in the control of normal human upper limb movements.
Adrenergic, cholinergic and VIP‐ergic influence on gastric phasic motility in the rat
Authors: BOJÖ L. , CASSUTO J. , NELLGÅRD P. , JÖNSSON A.
Published: December 2008

Bojö, L., Cassuto, J., Nellgård, P. & Jönsson, A. 1994. Adrenergic, cholinergic and VIP‐ergic influence on gastric phasic motility in the rat. Acta Physiol Scand 150, 67–73. Received 30 December 1992, accepted 23 July 1993. ISSN 0001–6772. Department of Clinical Physiology, Central Hospital Karlstad, Department of Physiology, University of Goteborg and Department of Anaesthesiology, Central Hospital, Molndal, Sweden.

We investigated the effects of adrenergic, cholinergic and vasoactive intestinal polypeptide (VlP)‐ergic agonists and antagonists on the amplitude of gastric phasic contractions in the anaesthetized rat using a volumetric model. The amplitude of the phasic contractions was reduced significantly by atropine, hexamethonium or bilateral cervical vagotomy indicating that cholinergic neural activity involving both muscarinic and nicotinic receptors and intact vagal nerve function are integral parts of the control of basal gastric phasic motility. In contrast, neither selective α1‐, α2‐ or non‐selective β‐blockers had any significant influence on the amplitude of the gastric contractions suggesting that adrenergic neurones are not tonically active in the maintenance of basal phasic motility in the stomach. The amplitude of the gastric phasic contractions was, however, significantly reduced by the α1‐agonist L‐phenylephrine, the α2‐agonist clonidine and a close intraarterial injection of VIP (3 μkg‐1) but not be the selective β1‐agonist, prenalterol, or the β2‐agonist, salbutamol. These data suggest the presence of superimposed inhibitory control of phasic activity by VIP‐ergic stimulation and by adrenergic neurones via α‐receptor stimulation.
Angiotensin II and renal prostaglandin release in the dog. Interactions in controlling renal blood flow and glomerular filtration rate
Authors: BUGGE J. F. , STOKKE E. S.
Published: December 2008

The relationship between angiotensin II and renal prostaglandins, and their interactions in controlling renal blood flow (RBF) and glomerular filtration rate (GFR) were investigated in 18 anaesthetized dogs with acutely denervated kidneys. Intrarenal angiotensin II infusion increased renal PGE2release (veno‐arterial concentration difference times renal plasma flow) from 1.7 ± 0.9 to 9.1 ±0.4 and 6‐keto‐PGFja release from 0.1 ±0.1 to 5.3 ± 2.1 pmol min‐1. An angiotensin II induced reduction in RBF of 20% did not measurably change GFR whereas a 30% reduction reduced GFR by 18 ± 8%. Blockade of prostaglandin synthesis approximately doubled the vasocon‐strictory action of angiotensin II, and all reductions in RBF were accompanied by parallel reductions in GFR. When prostaglandin release was stimulated by infusion of arachidonic acid (46.8± 13.3 and 15.9± 5.4 pmol min‐1for PGE2, and 6‐keto‐PGFja, respectively), angiotensin II did not change prostaglandin release, but had similar effects on the relationship between RBF and GFR as during control. In an ureteral occlusion model with stopped glomerular filtration measurements of ureteral pressure and intrarenal venous pressure permitted calculations of afferent and efferent vascular resistances. Until RBF was reduced by 25–30% angiotensin II increased both afferent and efferent resistances almost equally, keeping the ureteral pressure constant. At greater reductions in RBF, afferent resistance increased more than the efferent leading to reductions in ureteral pressure. This pattern was not changed by blockade of prostaglandin synthesis indicating no influence of prostaglandins on the distribution of afferent and efferent vascular resistances during angiotensin II infusion. In this ureteral occlusion model glomerular effects of angiotensin II will not be detected, and it might well be that the shift from an effect predominantly on RBF to a combined effect on both RBF and GFR induced by inhibition of prostaglandin synthesis is located to the glomerulus. We therefore postulate that renal prostaglandins attenuate the effectsofangiotensin II on glomerular surface area and the filtration barrier, and not on the afferent arterioles as previously suggested.
Thoracic impedance and pulmonary atrial natriuretic peptide during head‐up tilt induced hypovolaemic shock in humans
Authors: PERKO G. , PAYNE G. , LINKIS P. , J0RGENSNE L. G. , LANDOW L. , WARBERG J. , SECHER N. H.
Published: December 2008

Head up and down tilts were used for manipulating the central blood volume in eight volunteers. During head‐up tilt thoracic electrical impedance (TI) increased from 36.7 (33.9–52.1) ohm (mean and range) to 41.9 (36.9–59.2) ohm, heart rate from 60 (49–72) to 80 (65–90) beats min‐1 (P < 0.05) and decreased again to 57 (48–67) beats min‐1 accompanying a fall in mean arterial pressure from 86 (76–97) to 54 (41–79) mmHg and in cardiac output from 9.2 (5.9–12.1) to 6.9 (3.4–8.8) 1 min‐1 (n= 7, P < 0.07). Central venous pressure did not change significantly. Pulmonary arterial mean, 6 (3–12) mmHg, and wedge pressures, 4 (1–9) mmHg, decreased to 4 (1–11) and 1 (0–7) mmHg, respectively, and mixed, 78 (77–79%), and central venous oxygen saturations, 72 (71–73)%, fell to 62 (46–75) and 54 (44–58)%, respectively (P < 0.05). Atrial natriuretic peptide (ANP) was determined from blood of the superior vena cava and pulmonary and brachial arteries. Pulmonary artery ANP, 18.4 (7.5–30.7) pmol l‐1, was higher than in vena cava, 13.3 (5.2–20.9) pmol 1_1 (P < 0.05). At the time of presyncope, pulmonary artery ANP decreased from 20.8 (37.4–10.1) to 13.7 (19.7‐5.7) pmol l‐1, in vena cava from 13.8 (23.1–7.1) to 10.2 (17.9‐6.7) pmol l‐‘ and in the brachial artery from 16.9 (34.1–5.2) to 11.3 (18.5‐5.1) pmol l“1 (P < 0.05). Head‐down tilt did not affect the recorded variables significantly. Thoracic electrical impedance, pulmonary artery pressure and venous oxygen saturations were sensitive indices of the central blood volume as reflected in the release of atrial natriuretic peptide from the right side of the heart.
Elevated free fatty acid levels inhibit glucose phosphorylation in slow‐twitch rat skeletal muscle
Authors: NOLTE L. A. , GALUSKA D. , MARTIN I. K. , ZIERATH J. R. , WALLBERG‐HENRIKSSON H.
Published: December 2008

The effect of increased free fatty acid concentrations on glucose metabolism in rat skeletal muscle was investigated at several different steps in glucose metabolism including glucose transport, glucose phosphorylation, glucose oxidation and glycogen synthesis. In isolated soleus (slow‐twitch) muscles, insulin‐stimulated (100 μml‐1) glucose phosphorylation, but not glucose transport, was inhibited by 26 and 22% in the presence of 1.0 and 2.0 mM oleate, respectively (P< 0.01). Regardless of oleate concentration (0.3 or 2.0 mM), insulin‐stimulated glucose 6‐phosphate levels were elevated to the same extent over the non‐insulin‐stimulated levels in soleus muscles {P < 0.01). Insulin‐stimulated glucose oxidation was inhibited by 44% in soleus muscles exposed to 2.0 mM oleate (P < 0.05), whereas the rate of glucose incorporation into glycogen was not altered. In insulin‐stimulated epitrochlearis (fast‐twitch) muscles, elevated concentrations of oleate had no effect on the rates of glucose transport or glucose phosphorylation, or on the level of glucose 6‐phosphate. These data suggest that increased free fatty acid availability decreases glucose utilization by selectively inhibiting glucose phosphorylation and oxidation in slow‐twitch, but not fast‐twitch skeletal muscle.
Recombinant human insulin‐like growth factor 1 (rh‐IGF‐1) stimulates erythropoiesis in adult, but not in newborn mice
Authors: BECHENSTEEN A. G. , HALVORSEN S. , SKOTTNER A.
Published: December 2008

The in vivo effect of recombinant human insulin‐like growth factor (rh‐IGF‐1) upon erythropoiesis was studied in inbred BALB/C mice. Unweaned, rapidly growing 20 days old mice and adult female mice received subcutaneous rh‐IGF‐1 or control injections every 6 h for 48 h. The mice were killed either 12 or 48 h after the last injection, i.e. a study time of 60 and 96 h, respectively. Bone marrow erythroid colony forming units (CFU‐E), reticulocytes, haematocrit, serum immunoreactive erythropoietin (siEPO) and body and organ weight were measured. An additional group of young mice were given iron prior to the rh‐IGF‐1 injections to ensure sufficient available iron.

No differences in overall body or organ weights were observed. In the young mice erythropoiesis as measured by bone marrow CFU‐E, reticulocytes and haematocrit did not differ between rh‐IGF‐1 group and controls. When iron alone was given, reticulocytes (P < 0.05) and haematocrit (P < 0.0001) increased significantly, but no further stimulation was seen when rh‐IGF‐1 injections were given in addition to iron. The adult female mice responded with significantly increased erythropoiesis as judged by increased reticulocyte counts following rh‐IGF‐1 injections (P < 0.001). No significant effect upon CFU‐E and haematocrit was detected. The reticulocyte response was more pronounced at 96 than at 60 h after the first rh‐IGF‐1 injection. SiEPO was significantly (P < 0.01) lower in the adult 96 h rh‐IGF‐1 group than in the appropriate control group.

In conclusion parenteral iron significantly increased haematocrit in unweaned mice. Short time rh‐IGF‐1 treatment did not stimulate erythropoiesis in these rapidly growing mice, whether or not iron supplementation had been given. In the adult mice, short time rh‐IGF‐1 treatment stimulated in vivo erythropoiesis as shown by a reticulocyte response. Since the siEPO levels dropped in the adult treatment group the increase in reticulocytes suggests a directly stimulatory action of rh‐IGF‐1 upon erythropoiesis.
The effect of putative insulin‐like substances released by the motor nerve on glucose transport in perfused rat muscle
Authors: HAN X. , GALBO H.
Published: December 2008

Motor nerves have been claimed to contain and release immunoreactive insulin. We studied whether release of insulin or other non‐acetylcholine substances is important for (1) the increase in glucose transport normally seen during motor nerve activated contraction, and (2) the increase in insulin sensitivity induced by contractions. Ad 1: Rat hindquarters were perfused and one sciatic nerve was stimulated during motor nerve end plate blockade (Pancuronium bromide, 33 μg ml‐1). Muscle glucose transport (3‐0‐[14C]‐methylglucose (3‐O‐MG) uptake, 3 him) was identical (P > 0.05) in stimulated compared with nonstimulated white gastrocnemius, red gastrocnemius and soleus muscle. This was also true when, prior to end plate blockade, muscles had been stimulated to contract to increase insulin sensitivity. No immunoreactive insulin was found in venous perfusate. Ad 2: Rats had both sciatic nerves cut. One week later hindquarters were perfused and calf muscles of one leg were directly stimulated to contract. Subsequently, 3‐O‐MG uptake in muscle was determined with and without submaximal insulin (100μU ml‐1). In contrast to previous findings in innervated muscle, responses to insulin were identical (P > 0.05) with and without prior contractions. Conclusions: The increase in muscle glucose transport normally seen in response to motor nerve stimulation is related to the contraction process and not even partly mediated by release of insulin‐like substances from the nerve. In contrast, release of a non‐acetylcholine substance from the motor nerve may be involved in the exercise induced increase in insulin sensitivity.
Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans
Authors: KJÆR M. , PERKO G. , SECHER N. H. , BOUSHEL R. , BEYER N. , POLLACK S. , HORN A. , FERNANDES A. , MOHR T. , LEWIS S. F. , GALBO H.
Published: December 2008

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3‐L4. This caused cutaneous sensory anaesthesia below T8‐T9 and complete paralysis of the legs. Cycling was performed for 22.7 ± 2.7 min (mean, SE) (fatigue) and oxygen uptake (Vo2) increased to 1.90 ± 0.13 1 min‐1. Compared with voluntary exercise at the same Vo2, increases in heart rate (HR) (135 ± 7 vs. 130 ± 9 beats min‐1) and cardiac output (16.9 ± 1.1 vs. 17.3 ± 0.9 1 min‐1) were similar, and ventilation (54 ± 5 vs. 45 ± 4 1 min‐1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 ± 4 (rest) to 119 ± 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 ± 3 (rest) to 95 ± 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.
Photochemically induced spinal cord ischaemia in rats: assessment of blood flow by laser Doppler flowmetry
Authors: HAO J.‐X. , HERREGODTS P. , LIND G. , MEYERSON B. , SEIGER Å. , WIESENFELD‐HALLIN Z.
Published: December 2008

A photochemical technique was used to create central nervous system ischaemia in rats. Changes in blood flow in the spinal cord were assessed by laser Doppler flowmetry. The Th11 spinal cord segment was irradiated by an argon ion laser after intravenous injection of an organic dye, erythrosin B, to rats with or without a laminectomy. In the group of laminectomized rats, laser irradiation for 5 s did not influence cord blood flow, but 10 s irradiation caused a 25% decrease of blood flow, which normalized within 20 min. Decreases of 50 and 80% in spinal cord blood flow were noted after 20 s and after 1 min of laser irradiation, respectively, with no recovery observed after 20 min. In the group of rats without a laminectomy, 1 min of laser irradiation caused approximately a 25% decrease of spinal cord blood flow, which gradually recovered within 12 min, whereas 5 min of laser irradiation caused a more severe reduction of spinal cord blood flow (45 %) with some recovery was observed 30 min later. We could thus confirm that the interaction between a photosensitizing dye and laser irradiation reduced the regional spinal cord blood flow and the extent of this effect could be modified by varying the duration of laser irradiation. The present results therefore provide further support for using this photochemical technique to create animal models of central nervous system ischaemia.
Erythropoietin response to acute hypobaric or anaemic hypoxia in gentamicin‐administered rats
Authors: SHIMIZU S. , ENOKI Y. , SAKATA S. , KOHZUKI H. , OHGA Y. , MATSUMURA K.
Published: December 2008

In an attempt to assess the erythropoietin (Epo) production site(s) in rat kidney, Epo response to hypoxia and renal histopathological changes were studied in rats administered with graded doses of gentamicin. Male Sprague‐Dawley rats of 9 to 11 weeks old were used. Following a 14‐day subcutaneous administration (67.5 or 33.8 mg kg‐1 day‐1) of gentamicin, a nephrotoxic aminoglycoside, selective proximal tubular lesions were produced. These gentamicin‐administered rats were compared with normal rats with respect to Epo response to hypoxia. Two different kinds of hypoxic load, either 0.35 atm hypobaric hypoxia (PIO2= 46 torr) or acute anaemia (Ht: 29.3 ± 0.2% and [Hb]: 9.7 ± 0.3 g dl‐1) by withdrawing of blood corresponding to 1–2% of body weight was used. During the hypoxic period of up to 48 h, the peak renal venous plasma Epo titres of 3.1 ± 0.6 and 4.3 ± 0.6 U ml‐1 was observed at the 6th h in normal hypobaric hypoxic and anaemic rats, compared with the prehypoxic value of 0.7 ± 0.1 U ml‐1. The Epo titres then declined gradually. In the rats which were administered gentamicin, Epo response pattern was the same as that observed in the normal rats, but the peak value decreased significantly to 0.8 ± 0.3 and 1.1 ± 0.4 U ml‐1 in hypoxic and anaemic rats (P < 0.05). Histological examination revealed the selective damage to renal proximal convoluted tubules. The Epo response was reduced by the tissue damages, and restoration of the gentamicin‐induced tissue injury was accompanied with restored Epo response to hypoxia. The results suggest that renal proximal convoluted tubules are involved in Epo production under hypoxia.
Nasal heat and water exchange is not an effector mechanism for water balance regulation in grey seals
Authors: SKOG E. B. , FOLKOW L. P.
Published: December 2008

Phocid seals may effectively restrict respiratory heat and water loss by nasal heat and water exchange (NHE), and respiratory heat loss is, in fact, subject to thermoregulatory control. We have investigated whether phocid seals also control NHE and respiratory water loss to regulate water balance. Three resting juvenile female grey seals (Halichoerus grypus) were subjected to: (i) 5 days of food and water deprivation, (ii) intravenous infusion of 1000 ml of a hyperosmotic (930 mM) solution of the diuretic mannitol, and (iii) oral injection of 1500 ml distilled water. During these experiments in air of 0 oC, expired air temperature (Tex) and respiratory frequency (f) were recorded, and urine and blood samples collected. The results were compared with results from control experiments. Five days of food and water deprivation caused an average 10.5% and 20.8% increase in plasma (PO) and urine (UO) osmolality, respectively. Mannitol infusion induced excessive diuresis and caused an average 2.45% reduction of the estimated body water pool. Water loading caused an average 4.5% and 60% reduction in PO and UO, respectively, while urine production increased by 365%, on average. However, in no case did either Tex or f change significantly from mean control levels of 22.4 (range: 20.7–25.2) oC and 7.3 (range: 6.6–8.4) breaths min“1, respectively. Thus, water balance disturbances that initiate renal compensatory mechanisms fail to affect NHE in grey seals. This suggests that control of NHE is not an effector mechanism for regulation of water balance in grey seals.
Is postsystolic shortening area always a marker of myocardial ischaemia?
Authors: BIRKELAND S. , HEXEBERG E.
Published: December 2008

Postsystolic shortening area has been shown to be a sensitive marker of myocardial ischaemia in a one‐vessel model. We tested whether postsystolic shortening provoked by interaction between ischaemic and nonischaemic regions is reduced in a two‐vessel model, one vessel occluded and one subjected to coronary artery stenosis. Regional function in the left ventricular anterior wall was studied by orthogonal sonomicrometry during left coronary underperfusion in 14 pentobarbital‐anaesthetized cats with an acute circumflex coronary artery occlusion. Left coronary underperfusion in two discrete steps decreased subendocardial blood flow in the left ventricular anterior wall to on average 60% (P < 0.001) and 20% (P < 0.001) of control value, while subepicardial flow did not change. End‐diastolic lengths of longitudinal segments increased markedly even during mild subendocardial underperfusion, whereas end‐diastolic lengths of circumferential segments only increased during severe subendocardial underperfusion with concomitant increase of left ventricular end‐diastolic pressure. Systolic shortening, pressure‐length loop area and shortening velocity of circumferential segments did not change. In contrast, systolic shortening and total pressure‐length loop area of longitudinal segments decreased progressively approaching zero values during severe coronary underperfusion. Shortening velocity of longitudinal segments also decreased progressively during experimental protocol whereas postsystolic shortening area did not change. Conclusions: postsystolic shortening area is not a marker of subendocardial ischaemia in a two‐vessel model which indicates that postsystolic shortening is primarily a phenomenon related to model of ischaemia. End‐diastolic lengthening is predominant in the longitudinal axis of the heart during subendocardial ischaemia.
Cardiac hypertrophy alters myocardial response to ischaemia and reperfusion in vivo
Authors: JI L. L. , FU R. G. , MITCHELL E. W. , GRIFFITHS M. , WALDROP T. G. , SWARTZ H.M.
Published: December 2008

The impact of cardiac hypertrophy on myocardial biochemical and physiological responses to ischaemia‐reperfusion (I‐R) was investigated in vivo. Hypertrophy was produced by aortic constriction (PH) or swimming training (TH). Open‐chest rat hearts in PH, TH and a sedentary control group (SC) were subjected: (1) to ischaemia, by surgical occlusion of the main descending branch of the left coronary artery for 30 min; (2) to I‐R, by releasing the occluded blood vessel for 15 min; or (3) to a sham operation. Ischaemia per se had little effect on heart oxidative and antioxidant status, or lipid peroxidation. However, I‐R significantly decreased glutathione (GSH) content, increased glutathione disulfide (GSSG) content, and reduced GSH/GSSG ratio in the SC hearts. These alterations were associated with decreased activities of GSH peroxidase and GSSG reductase, and an increase in lipid peroxidation. Myocardial ATP, total adenine nucleotide content and energy charge in SC were significantly decreased after ischaemia, whereas levels of purine nucleotide derivatives, particularly adenosine, were elevated. No significant alteration of GSH status or adenine nucleotide metabolism occurred after ischaemia or I‐R in hypertrophied hearts. In bodi PH and TH, glutathione content was significantly higher than in SC, whereas activities of GSH peroxidase and GSSG reductase were lower. TH rats maintained a higher heart rate (HR), peak systolic pressure, and energy charge during I‐R. These data indicate that hypertrophied but well‐functioned hearts may be more resistant to I‐R induced disturbances of myocardial oxidative and antioxidant functions.
Skin sympathetic nerve activity and effector function during sleep in humans
Authors: NOLL G. , ELAM M. , KUNIMOTO M. , KARLSSON T. , WALLIN B. G.
Published: December 2008

Multi‐unit sympathetic skin nerve activity (SSA) in the peroneal nerve was recorded together with electrical skin resistance, skin blood flow and (in some subjects) finger blood pressure during sleep in 22 sleep‐deprived healthy subjects. The average strength of sympathetic activity in different sleep stages was measured during 5‐min periods as the area‐under‐curve of the integrated neurogram. Stage 2 sleep was reached by 15 subjects, stages 3–4 by nine and rapid eye movement (REM) sleep by six subjects. Non‐REM sleep was always associated with an increased skin resistance, which was larger in glabrous than in hairy skin (293±48 vs. 175±4% of awake control level, n= 10, P < 0.05). Skin blood flow also increased during sleep, with a mean maximal increase of 397±79% of the awake control level (n= 11, P < 0.05). In spite of these changes of effector function no significant difference in mean SSA was found between the awake control period and periods of non‐REM sleep, but during REM sleep SSA increased with 34% (P < 0.05) compared with the immediately preceding stage 2 period. In stage 2 sleep, K‐complexes were associated with bursts of SSA followed by transient changes of skin resistance, blood flow and arterial blood pressure. When both skin resistance and blood flow were recorded within the innervation area of the impaled fascicle, single bursts or short periods of increased SSA could be succeeded by increased skin blood flow without concomitant skin resistance change. This indicates the existence of specific sympathetic vasodilator fibres in the skin.

Therefore the unchanged strength of multiunit SSA during non‐REM sleep in the face of increases of skin resistance and blood flow may be a consequence of an increased sympathetic vasodilator nerve activity combined with decreases of vasoconstrictor and sudomotor traffic.
Plasma K+changes during intense exercise in endurance‐trained and sprint‐trained subjects
Authors: MEDBØ J. I. , SEJERSTED O. M.
Published: December 2008

Active muscle releases K+, and the plasma K+concentration is consequently raised during exercise. K+is removed by the NaK pump, and training may influence the number of pumps. The plasma K+concentration was therefore studied in five endurance‐trained (ET) and six sprint‐trained (ST) subjects during and after 1 min of exhausting treadmill running. Non‐exhausting bouts of exercise at either lower speed or of shorter duration were also carried out. Blood samples were taken from a catheter in the femoral vein before and at frequent intervals after exercise. The pre‐exercise venous plasma [K+] was (mean ± SEM) 3.68±0.10mmol l‐1(ET) and 3.88 ± 0.06 mmol l‐1(ST). One minute of exhausting exercise was sustained at 5.27 ±0.08 m s‐1(ET) and 5.59 ± 0.06 m s‐1(ST) and caused the plasma K+concentration to rise by 4.4 ± 0.3 (ET) and 4.7 ± 0.3 mmol l‐1(ST; ns) respectively. Three minutes after exercise the K+concentration was 0.48 + 0.08 mmol l‐1(ST) and 0.50 ± 0.07 mmol l‐1(ST) below the pre‐exercise value. During the following 6 min of recovery, the value was unchanged for the ET subjects, while a 0.32 ± 0.06 mmol l‐1rise was seen for the ST subjects. Exercise at reduced intensity or of reduced duration resulted in smaller changes in the K+concentration both during exercise and in the post‐exercise recovery, and for each subject the lowest post‐exercise K+concentration was therefore inversely related to the peak K+concentration during exercise. For a given peak K+concentration, the ST subjects had higher plasma K+concentrations than the ET subjects in the recovery period, suggesting that the two groups of subjects may regulate the K+concentration differently after exercise.
Masticatory‐salivary reflexes mobilize noradrenergic, non‐cholinergic secretory mechanisms in parotid glands of conscious rats
Authors: ASZTELY A. , TOBIN G. , EKSTRÖM J.
Published: December 2008

All rats were maintained on liquid diet, prepared from their ordinary hard pelleted diet, for a week, then fasted 32–33 h and subsequently either fed liquid or pelleted diet for 60–90 min or serving as non‐fed controls. Both the fed and the non‐fed animals had received atropine and α‐ and β‐adrenoceptor antagonists 15 min before the test. The rats given the liquefied chow consumed about twice as much as those given the hard chow. In the parotid glands of the rats given hard chow the number of acinar granules and the total amylase activity were reduced, by 50 and 70%, respectively, as compared with the glands of control rats. In the parotid glands of the rats given liquefied chow the number of acinar granules and the total activity of amylase remained unchanged. The results suggest that non‐adrenergic, non‐cholinergic secretory mechanisms of the rat parotid gland participate in masticatory‐salivary reflexes.
Isolation of acini from nasal glands of the guinea‐pig
Authors: SUNOSE H. , ZHANG W. , ISHIGAKI M. , KATORI Y. , SUZUKI M. , IKEDA K. , TAKASAKA T. , SAITO Y. , NISHIYAMA A.
Published: December 2008

A procedure for isolating the acinar cells of the serous gland in the mammalian nasal septum has been developed. This technique is characterized by meticulous and selective isolation with minimal contamination by the surface epithelial cells and employs enzymatic treatment with collagenase. The isolated cells were confirmed to be serous gland acini as shown by negative staining with Alcian blue and a high electron density of the granules. The acini were more than 90% viable as judged by trypan blue exclusion. Ultrastructural integrity of the cells was well maintained following the isolation procedure. Application of acetylcholine to the isolated acini induced an inward current in a whole‐cell patch clamp and increased intracellular Ca2+ concentration measured by fura‐2. These acetylcholine responses were completely blocked by atropine. These physiological findings directly demonstrated that nasal gland acini possess muscarinic‐activated receptors as previously suggested. These isolated cells hold promise for the in vitro study of secretory mechanisms in the mammalian nasal gland.
Role of afferent renal nerves in renal adaptation to sodium restriction in uninephrectomized rats
Authors: JANSSEN B. J. A. , BOUDIER H. A. J. STRUIJKER , SMITS J. F. M.
Published: December 2008

In the present study we examined the role of the afferent renal nerves in the control of ipsilateral renal adaptation to sodium restriction. Uninephrectomized rats were subjected to selective renal deafferentation or sham operation, instrumented with catheters and housed in metabolism cages to collect urine in 90 min fractions. Only sodium deficient food (0.03% Na+) was allowed. Water and sodium excretion were stabilized via a continuous 48 h infusion (1.25 ml h‐1) of a Ringer's solution. During this period water, sodium and potassium excretion were similar in renal deafferented and sham operated rats. Then, the infusion was exchanged for a modified Ringer's solution, in which the sodium ion was replaced by the choline ion. Measurements were performed over 24 h. During the choline Cl infusion, urine flow increased similarly in renal deafferented and sham‐operated rats. In both groups of rats, sodium excretion decreased within 24 h by more than 95 %, whereas potassium excretion stayed constant. Sodium loss was higher in renal deafferented rats only in the first 90 min period after the exchange of the infusions. These results indicate that afferent renal nerves are not necessary in ipsilateral renal adaptation during 24 h sodium restriction, but may play a modulatory role in correcting transient changes in ipsilateral renal excretory function.
Lysine transport in lactating rat mammary tissue: evidence for an interaction between cationic and neutral amino acids
Authors: SHENNAN D. B. , McNEILLIE S. A. , JAMIESON E. A. , CALVERT D. T.
Published: December 2008

The transport of lysine by the lactating rat mammary gland has been examined to determine whether there is an interaction between cationic and neutral amino acids. Lysine uptake was time dependent and unaffected by replacing Na+ with choline. In the presence of Na+, lysine influx was inhibited by cationic amino acids (arginine, homoarginine, ornithine and lysine) and by a range of neutral amino acids (methionine, glutamine, leucine, phenylalanine, alanine, asparagine, α‐aminoisobutyric acid (AIB), 2‐aminobicyclo [2,2,1] heptane‐2‐carboxylic acid (BCH), proline and tryptophan). Leucine and glutamine also inhibited lysine influx in the absence of Na+ but phenylalanine and proline did not. Lysine efflux from mammary tissue was trans‐accelerated by various cationic amino acids (lysine, arginine, homoarginine and ornithine). In addition, leucine and glutamine were capable of trans‐stimulating lysine efflux in the presence and absence of Na+. It appears that cationic and neutral amino acids stimulated lysine efflux at a single locus.
Intestinal motility responses to neuropeptide γ in vitro and in vivo in the rat: comparison with neurokinin 1 and neurokinin 2 receptor agonists
Authors: RAHMAN M. , LÖRDAL M. , AL‐SAFFAR A. , HELLSTRÖM P. M.
Published: December 2008

We have studied the effect of a novel tachykinin, neuropeptide γ(NPγ) on small intestinal motility in the rat. Experiments were donein vitroon longitudinal muscle strips of duodenum, andin vivoon the migrating myoelectric complex (MMC) of the small intestine.In vitro, contractile effects of NPγ were compared with those of a selective neurokinin 1 (NK1) receptor agonist, substance P methyl ester (SPME), and a selective neurokinin 2 (NK2) receptor agonist, Nle10‐NKA(4–10)(NleNKA). NPγ, SPME and NleNKA caused concentration‐dependent contractions (P< 0.001). NPγ was eight‐fold more potent than NleNKA, and 118‐fold more potent than SPME. Contractile responses to NPγ were reduced by hexamethonium (P< 0.01) and atropine (P< 0.05). The non‐selective NK receptor antagonist spantide I only slightly reduced the contractile response to NPγ, as did the selective NK1 antagonist GR 82334, and the selective NK2 antagonist L‐659877 and MEN 10376.In vivo, effects of NPγ on the MMC were compared with those of the natural tachykinins substance P (SP) and neurokinin A (NKA). NPy disrupted the MMC and induced irregular spiking in a dose‐dependent manner from 25 to 100 pmol kg‐1min‐1i.v. (P< 0.05). The effect of NPγ was more prominent than that of NKA at equal doses, while SP had no effect. Our findings show that NPγ exerts potent stimulatory effects on small intestinal motility, most likely mediated directly via distinct NK receptors on smooth muscle cells, but also indirectly via a cholinergic link.
Carbachol‐induced phosphatidylcholine hydrolysis and choline efflux in rat submandibular gland involves phospholipase D activation and is modulated by protein kinase C and calcium
Authors: DUNÉR‐ENGSTRÖM M. , FREDHOLM B. B.
Published: December 2008

The role of calcium and protein kinase C activation in carbachol‐induced choline efflux from submandibular glands was investigated. The participation of phospholipase D in this signal transduction pathway was demonstrated by the formation of [14C]phospha‐tidylethanol in [14C]lysophosphatidylcholine‐labelled submandibular gland cells treated with carbachol or noradrenaline in the presence of ethanol. Chelation of the intracellular calcium with BAPTA/AM reduced the carbachol stimulated outflow of [3H]choline.* The calcium ionophore A23187 in a high concentration (10 μm) increased the basal [3H]choline outflow, but decreased the carbachol‐induced outflow. Removal of the extracellular calcium enhanced the carbachol‐stimulated outflow, which returned to control when calcium was re‐added to the medium.

Activation of protein kinase C by phorbol‐12,13‐dibutyrate (100 nM) or l‐oleyI‐2‐acetyl‐sn‐glycerol (20 μM) was without effectper se, but enhanced the carbachol‐mediated outflow of [3H]choline. Phorbol‐12,13‐dibutyrate in combination with 1//M A23187 induced a small efflux of [3H]choline. A 2h treatment with phorbol‐12,13‐dibutyrate (1 μM), causing down‐regulation of protein kinase C, significantly decreased the carbachol‐stimulated [3H]choline outflow.

In conclusion, elevation of intracellular calcium levels and protein kinase C activation are of importance for the carbachol‐stimulated outflow of [3H]choline. Inflow of calcium, if anything, reduces the carbachol‐stimulated outflow of [3H]choline. Since phosphatidylcholine breakdown generates diacylglycerol and this could lead to activation of protein kinase C, activation of this signal transduction pathway may be important for the protein content of the saliva and for the known trophic effects of parasympathetic innervation.
Hexokinase kinetics in human skeletal muscle after hyperinsulinaemia, hyperglycaemia and hyperepinephrinaemia
Authors: KATZ A. , RAZ I.
Published: December 2008

The effects of 120 min of euglycaemic hyperinsulinaemia (UH, ∽ 5 mM; 40 mU m‐2 min‐1), UH plus adrenaline infusion (0.05 μgkg‐1 min‐l), and hyperglycaemic normoinsulinaemia (26 mM) on hexokinase kinetics in human skeletal muscle were examined. Biopsies were obtained from the quadriceps femoris muscle before and after each clamp. Total muscle hexokinase activity (HKt) (measured on a 2500 g supernatant) at a saturating level of the substrate glucose (1 mM) averaged 13 mmol kg dry wt‐: min‐1 in the basal state and did not change significantly under any condition. Soluble hexokinase activity (HKS) (16000 g supernatant) accounted for ∽ 65% of HKt in the basal state, and this percentage was not significantly affected by any condition, suggesting that there was no major transfer of HK between cytosol and mitochondria. The activity of HK, and HKs was inhibited by glucose 1,6‐bisphosphate (G‐l,6‐P2) in a concentration dependent manner in the basal state, and the sensitivity to Gl,6‐P2 inhibition was not altered by any condition. The activity of HK, and HK8 in the presence of a subsaturating level of glucose (0.1 mM) accounted for ∽ 70% of the activity at 1 mM glucose, and this percentage was not altered by any condition. These data suggest that under the present conditions alterations in the rates of whole body glucose disposal cannot be associated with alterations in HK distribution between cellular compartments nor its measured kinetics properties.