Reduced Urinary Noradrenaline Excretion during Rest, Exercise and Cold Stress in Trained Rats: a Comparison between Physically‐Trained Rats, Cold‐Acclimated Rats and Warm‐Acclimated RatsÖStman, Ingegerd; Sjöstrand, Nils O.
doi: 10.1111/j.1748-1716.1975.tb10045.xpmid: 1189931
Physically trained rats were compared with cold‐acclimated rats. Trained as well as cold‐acclimated rats showed cardiac and adrenal hypertrophy. Cardiac noradrenaline (NA) content was increased in both groups of rats but only the trained rats had an increased cardiac NA concentration. The adrenal NA content was increased in both groups but only the trained rats had an increased adrenal content of adrenaline (A). The spleen of trained rats had an increased NA content, while that of cold‐acclimated rats had a decreased NA content. The submandibular glands of cold‐acclimated rats were enlarged and had an increased NA content. Trained as well as cold‐acclimated rats had lower urinary NA excretions during rest, after exercise and during cold stress when compared with controls. However, only the trained rats had a reduced net increment in NA excretion after exercise, whereas there was no difference between the increments of cold‐acclimated and control rats. Six months after cessation of training, ex‐trained rats still had an increased heart ratio and a reduced urinary NA excretion after exercise. It is suggested that physical training induces “cross tolerance” to cold stress, while cold‐acclimation does not lead to “cross tolerance” to acute exercise.
Effects of Drugs and Nerve Stimulation on the Spleen and Arteries of Two Species of Dogfish, Scyliorhinus canicula and Squalus acanthiasNilsson, Stefan; Holmgren, Susanne; Grove, David J.
doi: 10.1111/j.1748-1716.1975.tb10046.xpmid: 1189932
The effects of drugs and nerve stimulation on the spleen of 2 species of dogfish have been examined by experiments with perfused spleens and isolated spleen and artery strips. Adrenaline, noradrenaline and phenylephrine, acting via alpha adrenoceptors, constrict the perfused spleen of both species, thereby releasing erythrocytes, and contract the isolated spleen and artery strips. Phentolamine competitively antagonizes the excitatory effects of adrenergic agonists. The responses of the spleen to acetylcholine are very irregular, and a rapid desensitization makes evaluation of the mode of action of this drug difficult. In the artery strips acetylcholine produces a dose‐dependent contraction. Fluorescent histochemistry reveals well developed adrenergic innervation of the arteries, and a few adrenergic terminals in the spleen. Stimulation of splenic nerves produces normally splenoconstriction in Squalus, which can be blocked by phentolamine but not by atropine. The nervous control of the Scyliorhinus spleen seems to be poor or lacking. It is concluded that the dogfish spleen, and maybe also the arteries, are to a large extent controlled by circulating catecholamines and (in Squalus) also by sympathetic adrenergic fibres.
Studies of Some Twitch and Fatigue Properties of Different Motor Unit Types in the Ankle Muscles of the Adult CatHammarberg, C.; Kellerth, J‐O.
doi: 10.1111/j.1748-1716.1975.tb10047.xpmid: 171916
Contractile responses of motor units in the gastrocnemius, soleus and pretibial flexor muscles of adult cats were elicited by intracellular stimulation of motoneurones. The motor units were classified into types FF, FR and S (Burke et al. 1971) and their responses to the same stimulation patterns as those used in a previous investigation of whole muscles (Hammarberg and Kellerth 1975 a) were studied. The duration of motoneurone afterhyperpolarization was short in both the fast twitch FF and FR units; it was longer in the soleus S units than in the S units of the pale muscles. Twitch time‐to‐peak was less than 30 ms in the FF and FR units, but exceeded 40 ms in the S units. Soleus S units were slower than S units of the pale muscles. Potentiation was observed in the gastrocnemius units, but not in the soleus S units. A short rest allowed fatigued extensor units of the FF and FR types to regain some contractile strength. This was less evident in the S units which, on the other hand, were extremely resistant to fatigue. Differences in response patterns between corresponding motor unit types of the flexor and extensor muscles were observed. A few fast twitch units were identified in the slow soleus muscle.
The Postnatal Development of Some Twitch and Fatigue Properties of Single Motor Units in the Ankle Muscles of the KittenHammarberg, C.; Kellerth, J‐O.
doi: 10.1111/j.1748-1716.1975.tb10048.xpmid: 1189933
Contractions of single motor units in the gastrocnemius, soleus and pretibial flexor muscles were elicited by intracellular stimulation of the innervating motoneurones. Kittens being 1, 2, 6 and 10 weeks of age were used. The aim was to establish the pattern of postnatal differentiation of the adult motor unit types (Burke et al. 1973, 1974, Hammarberg and Kellerth 1975 b). In the developing type S units of the soleus muscle the mean value for contraction time showed a transient decrease during the early postnatal period, but the twitch half‐relaxation time (HRT), the duration of motoneurone post‐spike afterhyperpolarization (AHP) and the susceptibility to fatigue remained virtually unchanged during the age period studied. In the units of the developing fast twitch muscles the contraction time, HRT and susceptibility to fatigue were significantly different from those of the soleus units already at 1 week of age. At 6–10 weeks of age the contractile characteristics typical of the adult type FF and FR units were attained. The AHP duration gradually decreased up to 10 weeks of age, and it was then considerably shorter than both at 1 week of age and in the adult stage.
Effect of Bulbar Acidification on Gastric Acid Responses to Urecholine in Pavlov Pouch DogsNilsson, Göran
doi: 10.1111/j.1748-1716.1975.tb10049.xpmid: 1189934
Dogs were provided with mucosal septal pouches of the fundic stomach and of the duodenal bulb. Gastric secretion was stimulated by intravenous infusion of submaximal doses of porcine gastrin or the stable choline ester Urecholine. Acid perfusion of bulbar pouches profoundly inhibited acid responses to gastrin. Bulbar acidification produced little or no reduction in acid secretion induced by Urecholine. Small doses of Urecholine do not release gastrin in the dog but may induce acid secretion, mainly by direct cholinergic stimulation of the HC1 glands. The fact that Urecholine‐induced acid secretion was not inhibited in the present experiments is consistent with the hypothesis that the bulbar mechanism does not interfere with cholinergic stimulation acting on the parietal cells.
Relative Contribution of Superficially Bound and Extracellular Calcium to Activation of Contraction in Isolated Rat Portal VeinSigurdsson, Stefan B.; Uvelius, Bengt; Johansson, Börje
doi: 10.1111/j.1748-1716.1975.tb10050.xpmid: 1189935
The spontaneous electrical and mechanical activity of the isolated rat portal vein is abolished after only 2–3 min in nominally Ca‐free medium, and after 5–6 min there is no contractile response to depolarizing (122 mM K+), Ca‐free solution. In the present study we have examined the electrical and mechanical responses of the portal vein to depolarization with simultaneous readministration of Ca2+ (2.5 mM) after periods of variable length in Ca‐free standard solution. After 30 to 60 min of Ca depletion a slow contracture occurred in response to the high‐K+ solution with 2.5 mM Ca2+. When the period in Ca‐free medium was reduced below 30 min an early, faster phase appeared in the contracture response, and this phase was more rapid the shorter the time of Ca depletion. It is suggested that the slow contracture obtained after 30 min or more uses mainly extracellular Ca for activation and that the faster phase seen after shorter periods of Ca depletion is due to release of superficially bound Ca. This latter pool of tissue bound Ca does not alone produce contraction in response to depolarization, suggesting that extracellular Ca is required to trigger the release perhaps through a regenerative process.
Inhibition of Induced Pinocytosis in Amoeba proteus by Membrane Stabilizing DrugsJosefsson, J.‐O.; Johansson, G.; Hansson, S. Elisabeth
doi: 10.1111/j.1748-1716.1975.tb10051.xpmid: 242188
The effect of membrane stabilizing drugs on cation induced pinocytosis was studied in Amoeba proteus. Initially the presence of local anesthetic drugs during a pinocytosis cycle had a stimulating effect on channel formation, however, the capacity to develop pinocytotic channels was reversibly inhibited after a period of treatment with these drugs. Imipramine, vinblastine and the phenothiazines had effects similar to local anaesthetics. The local anesthetics inhibited pinocytosis in the following order: dibucaine>tetracaine> bupivacaine >lidocaine>procaine, and the phenothiazines: thioridazine>prochlorperazine>chlorpromazine > prometazine. Pinocytosis, when induced by Na+ or tris, was more affected by the drugs and by calcium binding agents than pinocytosis induced by K+. After pretreatment with inhibitory concentration of dibucaine (3 × 10‐4 M) the depolarization of the membrane and the conductance increase during pinocytosis were normal, while the increase of oxygen uptake during the pincoytosis cycle was abolished. Addition of Ca++ before, during or after dibucaine treatment decreased the effect of the drug. Conversely, in dibucaine‐treated cells, cation induced pinocytosis was less inhibited by Ca++ than pinocytosis in normal cells. Addition of EGTA to the inducing solutions potentiated the inhibitory effect of the drug. It is suggested that these drugs release Ca++ from the cell surface and at higher concentration or after prolonged incubation time interfere with a Ca++ mechanism which couples the membrane and contractile systems in the cytoplasm.
Kinetics of the Glomerular Ultrafiltration in the Rat Kidney. An Experimental StudyKällskog, Ö.; Lindbom, L. O.; Ulfendahl, H. R.; Wolgast, M.
doi: 10.1111/j.1748-1716.1975.tb10053.xpmid: 1189937
The quantitative relation between the driving forces over the glomerular membrane and the glomerular plasma flow, on the one hand, and the single glomerular filtration rate (SNGFR), on the other, is still uncertain. Micropuncture measurements on Sprague‐Dawley rats made it possible to calculate the net driving force over the glomerular membrane. The single glomerular plasma flow was determined from SNGFR and the single nephron filtration fraction (SNFF). The effective plasma flow was measured with PAH for total kidney and for superficial nephrons. The mean glomerular capillary pressure was found to be 62.6 mm Hg. The results indicate a net driving force of about 13 mm Hg at the distal end of the glomerular capillary. SNGFR was found to be 14.1 nl/min.100 g. SNFF amounted to about 0.27. The filtration fractions determined with the PAH method were in the same range. The results indicate a filtration disequilibrium, in contrast to those of Brenner et al. from measurements on a mutant Wistar rat strain. The filtration fractions seemed to be the same in all glomerular populations. It is clear that the SNGFR is pressure dependent. Our earlier findings of a nonautoregulation of the blood flow through the outer glomeruli were also confirmed.
Effects of Hypoxia of 10–45 Seconds Duration on Energy Metabolism in the Cerebral Cortex of Unanesthetized and Anesthetized RatsNorberg, Karin; Quistorff, Björn; Siesjö, Bo K.
doi: 10.1111/j.1748-1716.1975.tb10054.xpmid: 127509
Glycolytic and citric acid cycle intermediates, as well as organic phosphates, were measured in the cerebral cortex of unanesthetized rats following arterial hypoxia (administration of 6–8 % 0,) of 10 and 20 s duration. There were decreases in glucose‐6‐phosphate and fructose‐6‐phosphate, and increases in fructose‐1,6‐diphosphate, dihydroxyacetone phosphate and 3‐phosphoglycerate, even before pyruvate accumulated. Since measurements of the lactate concentration showed that there was an increased glycolytic rate, the results demonstrate that phosphofructokinase was activated. The glycolytic changes were accompanied by, and probably due to, minor changes in phosphocreatine, ATP, ADP and AMP. Experiments of anesthetized animals showed that hypoxia for 45 s was accompanied by signs of phosphofructokinase activation, even if tissue Pco2 was kept constant. It is concluded that, irrespective of the tissue CO2 tension, hypoxia is accompanied by activation of phosphofructokinase which, at least initially, is responsible for the increased glycolytic rate.