bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of Anesthetics upon Labile Phosphates and upon Extra‐ and Intracellular Lactate, Pyruvate and Bicarbonate Concentrations in the Rat Brain
Authors: Nilsson Lorentz , Siesjö Bo K. 
Published: December 2008

AbstractThe effects of volatile anesthetics (nitrous oxide, halothane, diethyl ether and cyclopropane), of Fentanyl, and of barbiturates (thiopentone, phenobarbital and amobarbital) on labile phosphates and on intra‐ and extracellular lactate, pyruvate and bicarbonate concentrations of brain tissue were investigated in rats, which were immobilized and artificially ventilated so as to give arterial CO2 tensions of 35–40 mm Hg. It was found that the type or the depth of anesthesia did not significantly influence the tissue concentrations of phosphocreatine, ATP, ADP or AMP. There were very small differences in the tissue lactate concentration in the nonbarbiturate groups, and thus no indication that the lactate concentration varied with the depth of anesthesia. However, in all barbiturate groups there was a lowering of the lactate concentration and an increase in the intracellular pH'. In contrast to the volatile anesthetics the barbiturates gave significant decreases also in the calculated cytoplasmatic NADH/NAD+ ratio. The experiments thus failed to indicate that anesthetics inhibit electron transport or energy transfer reactions in the brain, at least under the conditions studied. In addition, they suggest that barbiturates, including, amobarbital, shift the balance between energy‐yielding and energy‐requiring reactions in favour of an oxidated state.
Antagonism by Calcium of the Inhibitory Action of Prostaglandin E2on Sympathetic Neuro‐transmission in the Cat Spleen
Authors: Hedqvist P. 
Published: December 2008

AbstractExperiments were carried out with the isolated, perfused cat spleen and bovine splenic nerve trunk to study the target for prostaglandin E2induced inhibition of noradrenaline release from sympathetic nervss. Increasing the calcium concentration in the medium perfusing the spleeen was found to increase the outflow of noradrenaline to nerve stimulation and to antagonize the inhibitory action of prostaglandin E2on this parameter. Prostaglandin E2did not affect the noradrenaline releasing effect of tyramine. Atropine did not alter the inhibitory effect of prostaglandin E2on noradrenaline release. Prostaglandin E2did not change the amplitude of action potentials in bovine splenic nerves. There is thus no support for a blocking action on nerve conduction. It is concluded that prostaglandin E2may prevent calcium from gaining access to those sites in sympathetic nerve terminals where it promotes secretion of noradrenaline.
Ontogenesis of Peripheral Adrenergic Neurons in the Rat: Pre‐ and Postnatal Observations
Authors: Champlain J. de , Malmfors T. , Olson L. , Sachs Ch. 
Published: December 2008

AbstractThe early development of the peripheral adrenergic neurons of the rat was followed with the Falck‐Hillarp fluorescence technique. In the 13 day embryo small fluorescent sympathicoblasts with short processes were found in segmentally arranged groups along the dorsal aspect of the embryo. The larger sympathetic ganglia and the strongly fluorescent adrenal medullary cells were easily identifiable at this stage. In the 18 day embryo, fluorescent axon bundles were found in most larger nerve trunks. The outgrowing fluorescent axons had a stronger fluorescence intensity than non‐terminal axons of adult animals until at least 2 weeks after birth. The postnatal development of the plexuse of adrenergic nerves was followed in the iris, auricles of the heart, salivary glands, vas deferens and small intestine. The adrenergic innervation of the gut seemed to develop earlier than that of the other organs. Thus, the duodenal muscle layer had a well developed adrenergic innervation of the plexus of Auerbach at birth while the other organs investigated demonstrated well developed networks of adrenergic nerves from about the fourth day on. It was concluded from some pharmacological experiments that, under optimal conditions, the fluorescence technique can reveal all or almost all adrenergic nerves also during early development.
The Effect of Glucose on Histamine Release from Isolated Rat Peritoneal Mast Cells Induced by Adenosine‐5‘‐Triphosphate
Authors: Diamant B. , Peterson C. 
Published: December 2008

AbstractHistamine release from isolated rat peritoneal mast cells induced by ATP in an aerobic milieu increased in the presence of glucose. Irrespectively whether the cells were exposed to glucose prior to ATP or the two agents were added together to cells, optimal histamine release was noted with 0.3–0.5 mM of glucose and amounted to 1.5–2 times that observed in the absence of glucose. In contrast, under similar conditions compound 48/80‐induced histamine release was not affected by glucose. The velocity of ATP‐induced histamine release and the final amount of histamine released within 30 min of incubation increased in the presence of glucose. A lag period of about 1 min was noted before histamine release occurred when initiated by ATP (3.9 times 10‐5M). This lag period was not changed by glucose. Iodoacetate inhibited histamine release induced by ATP as well as by compound 48/80. The glucose‐activated part of ATP‐induced histamine release seemed especially sensitive to iodoacetate. The results suggest that glucose through its metabolism in the cells exerts an enhancing effect on ATP‐induced histamine release.
Synthesis of Noradrenaline from 3,4‐Dihydroxyphenylalanine (DOPA) and Dopamine in Adrenergic Nerves of Mouse Atrium — Effect of Reserpine, Monoamine Oxidase and Tyrosine Hydroxylase Inhibition
Authors: Jonsson Gösta , Sachs Charlotte 
Published: December 2008

AbstractThein vitrosynthesis of noradrenaline (NA) from 3,4‐dihydroxyphenylalanine (DOPA) and dopamine (DA) in the mouse atrium has been investigated, using isotope, subcellular distribution and histochemical techniques. Incubation of atrial tissue in 5 times 10‐6M14C‐DOPA resulted in a formation of14C‐NA and14C‐DA at a rate of about 0.13 μg/g/hr, and 0.14 μg/g/hr respectively, whereas the same medium concentration of3H‐DA gave a formation of3H‐NA of about 0.25 μg/g/hr. The synthesis of NA and DA was found to be almost exclusively associated with the presence of adrenergic nerves, since it was considerably reduced after pretreatment with 6‐OH‐DA. Pretreatment with reserpine decreased formation of radioactive NA and DA which could be counteracted by nialamide. The effect of reserpine may be explained by inhibition of DA uptake in the amine storage granules. The antagonistic effect of nialamide is certainly due to inhibition of DA catabolism. Tyrosine hydroxylase inhibition produced by H44/68, which depleted the endogenous NA store to about 40% of normal, increased the formation of radioactive NA both from3H‐DA and14C‐DOPA. This may in part be explained by decreased competition of the endogenous precursor DA for DA‐β‐hydroxylase but also in part by increased storage sites available for newly formed NA.
Cytoplasmic Distribution of Endogenous and Exogenous 5‐Hydroxytryptamine in Rat Peritoneal Mast Cells
Authors: Jansson Sten‐Erik 
Published: December 2008

AbstractThe distribution of endogenous and exogenous 5‐hydroxytryptamine (5‐HT) in rat peritoneal mast cells was investigated by in vitro experiments using chemically 5‐HT measurements in granules and supernatants after degranulation of the cells in a ion‐free medium, and histochemically by the formaldehyde‐induced fluorescence in semi‐thin Epon sections. About 20–30% of the total amounts of 5‐HT was found in the supernatant upon degranulation of a practically pure mast cell suspension. It is probably a solubilization artefact, because the formaldehyde‐induced fluorescence was always observed exclusively in the granules, while the intergranular cytoplasm was non‐fluorescent. Even after incubation in exogenous 5‐HT when the 5‐HT content per cell was about 3 times that of normal cells, no intergranular fluorescence was observed. Imipramine, reserpine and, to a lesser extent, ouabain at a concentration of 10‐5 M inhibited the uptake but did not alter the normal granular distribution. This observation implies a reserpine‐resistant uptake of 5‐HT by mast cell granules.
Fate of3H‐Noradrenaline in Canine Subcutaneous Adipose Tissue1
Authors: Fredholm Bertil B. , Rosell Sune 
Published: December 2008

AbstractCanine subcutaneous adipose tissue was isolated and perfused with defibrinated blood at a constant rate. Infused3H‐noradrenaline was taken up by the tissue and released spontaneously into blood. Following a washout period of 40 min or more, plasma samples were withdrawn. Radioactive compounds in venous plasma were separated by chromatography on alumina and Dowex. About 30 per cent of the venous radioactivity was identified as unchanged noradrenaline, about 7 per cent as normetanephrine and 14 per cent as deaminated catechols: deaminated O‐methylated metabolites accounted for about 45 per cent. This indicates the presence in adipose tissue of both monoamineoxidase and catechol‐O‐methyl‐transferase. Upon stimulation of sympathetic nerves to adipose tissue peripheral resistance increased, the3H‐presence in adipose tissue of both monoamine oxidase and catechol‐O‐methyl‐transferase. Upon cessation of the stimulation the peripheral resistance decreased and the outflow of noradrenaline metabolites increased above control values. After dihydroergotamine, nerve stimulation induced a decreased peripheral resistance, an increase of3H‐noradrenaline outflow and no change or an increase in the outflow of noradrenaline metabolites. Totally more radioactivity was released upon nerve stimulation after dihydroergotamine. The changes seen are interpreted to be associated with vascular reactions in adipose tissue.
Metabolism of Subcutaneously Injected14C‐Histamine in Myxine Glutinosa
Authors: Holstein Björn 
Published: December 2008

AbstractThe recovery of total radioactivity,14C‐histamine and14C‐methylhistamine in extracts of wholeMyxine glutinosawas determined after s.c. injection of14C‐histamine. 24 hrs after injection the same parameters were determined in single organs. Total radioactivity declined very slowly, 10 days after administration 71% was recovered. At that time14C‐histamine and14C‐methylhistamine amounted to 44% and 1% respectively of the given dose. The liver was the most efficient organ in extracting radioactivity.
Inhibitory Control of the Abdominal Stretch Receptors of the Crayfish
Authors: Jansen J. K. S. , Njå A. , Walløe L. 
Published: December 2008

AbstractThe efferent activities in the thick and thin “accessory” axons in the dorsal nerve of the crayfish abdomen have been studied during reflex activation from the same and neighbouring segments. The reflex input was either adequate stimulation of the slowly or the rapidly adapting stretch receptor or electrical stimulation of the afferent fibres from the receptors. The results support Eckert's finding (1961a) that the thick accessory nerve is reflexly activated from both the slowly and the rapidly adapting receptors. The thick accessory nerve is most effectively activated ipsilaterally while the thin accessory nerve predominantly participates in crossed reflexes.
Effects of Prostaglandin E1in Canine Subcutaneous Adipose Tissue in Situ1
Authors: Fredholm Bertil B. , Rosell Sune 
Published: December 2008

AbstractThe effect of PGE1on the uptake of glucose and the release of FFA and glycerol before and after sympathetic nerve stimulation (4 cps) was investigated in perfused canine subcutaneous adipose tissuein situ. Glucose uptake was significantly increased by PGE1at all concentrations used (5 times 10‐10to 7 times 10‐7M in blood). The effect of PGE1on the release of FFA and glycerol in unstimulated adipose tissue was inconsistent. Increases as well as decreases were observed. Lipolysis, as measured by glycerol release, induced by nerve stimulation was inhibited dose‐dependently. A 50 per cent inhibition was produced by approximately 1.2 times 10‐7M PGE1. Stimulated FFA release was also inhibited but there was no clear dose‐response relationship. It is concluded that PGE1has similar effects in canine subcutaneous adipose tissue with an intact blood supply as are known to be producedin vitro.
Potentiating Action of Desmethylimipramine on the Cardiovascular Effects of Noradrenaline and Some Other Pressor Agents
Authors: ÅStröm A. 
Published: December 2008

AbstractThe influence of desmethylimipramine (DMI) on the cardiovascular responses to i.v. injected noradrenaline (NA), adrenaline, metaraminol and isoprenaline, as well as to some chemically unrelated pressor agents (angiotensin, vasopressin, and the vasopressin analogue felypressin), was studied in anesthetized dogs and cats. The cardiovascular effects of NA were potentiated very markedly by moderate doses of DMI (0.1–1.0 mg/kg). The responses to adrenaline and metaraminol were only slightly potentiated. In the case of adrenaline, DMI was slightly more effective in enhancing the pressor action of this amine after partial β‐blockade (propranolol). In analogy with the carotid occlusion response, the effect on the peripheral vascular resistance elicited by electrical stimulation of the lumbar sympathetic nerves was not significantly potentiated by DMI.A method of “delayed autoperfusion” was developed to record reflex vasomotor counter‐regulation. DMI was found to reduce the activity of this counter‐regulation suggesting that this may be one way in which this drug potentiates the cardiovascular effects of the non‐catecholamine pressor agents.
Pro‐oxidant effects of normobaric hyperoxia in rat tissues
Authors: AHOTUPA M. , MÄNTYLÄ E. , PELTOLA V. , PUNTALA A. , TOIVONEN H. 
Published: December 2008

Rats were exposed to 100% O2 atmosphere for 12, 36 or 48 h, and their lungs, brain, liver and kidneys were studied for signs of oxidative damage. Oxidative damage at molecular level was estimated by: (1) the appearance of conjugated diene double bonds and (2) the amount of fluorescent chromolipids in lipids extracted from tissues. As important intracellular regulators of oxidative stress, the response of enzymes detoxifying reactive oxygen species was also studied. Macroscopically, the brain and the lungs were most susceptible to oxygen‐induced effects. As an indication of oxidative tissue damage, hyperoxia caused accumulation of fluorescent chromolipids in brain and lung tissues, whereas diene conjugation did not reveal any signs of lipid peroxidation. Accumulation of fluorescent chromolipids was most prominent in the brain, where 99 and 138% increases over the control were detected after 36 and 48 h hyperoxia, respectively. Fluorescent chromolipids appeared in urine already before their concentrations were elevated in tissues. The activity of superoxide dismutase in the brain was initially decreased, followed then by a slight induction of activity at the later time‐points. Pulmonary and hepatic catalase activities were markedly decreased after prolonged (36 and 48 h) hyperoxia.In conclusion, fluorescent chromolipid formation seems to be a sensitive indicator of hyperoxia‐induced oxidative damage in rat tissues. The lipid peroxidation‐derived fluorescent chromolipids are eliminated from the body via urinary excretion. Moreover, impaired detoxication of reactive oxygen may be implicated in tissue damage due to hyperoxia.
Increased resistance to haemorrhage induced by intracerebroventricular infusion of hypertonic NaCl in conscious sheep
Authors: HJELMQVIST H. , ULLMAN J. , GUNNARSSON U. , HAMBERGER B. , RUNDGREN M. 
Published: December 2008

The effect of elevated cerebrospinal fluid Na+ concentration (CSF [Na+]) on the tolerance of blood loss, and concomitant cardiovascular and humoral responses were studied in conscious sheep. A slow (0.7 ml kg‐1 min‐1) venous haemorrhage was continued until the mean systemic arterial pressure suddenly decreased to < 50 mmHg, or in the absence of hypotension, until a total blood loss of 25 ml kg‐1. Significantly more blood had to be removed to induce hypotension in animals receiving an intracerebroventricular (i.c.v.) infusion (0.02 ml min‐1) of 0.5 m NaCl (starting 30 min before haemorrhage and continued throughout the experiment) compared to control haemorrhages without concomitant i.c.v. infusion (22.7 ± 1.2 ml vs 16.9 ± 0.9 ml kg‐1). In one animal, subjected to 0.5 m NaCl infusion, the blood pressure was still maintained at 25 ml kg‐1 of haemorrhage. In spite of a larger blood loss, animals receiving i.c.v. infusion of hypertonic NaCl had an improved recovery of the blood pressure after haemorrhage, due to a better maintained cardiac output rather than to a reinforced increase of the vascular resistance.The improved cardiovascular responses to haemorrhage during elevated CSF [Na+] are not readily explained by the effects on the plasma concentrations of vasopressin, angiotension II or noradrenaline, although the latter was augmented. The plasma protein concentration decreased already during the 30 min of hypertonic NaCl infusion preceding haemorrhage, and the haemodilution caused by the subsequent blood removal was aggravated, which indicates that this treatment also causes transfer of fluid to the plasma compartment.We conclude that elevated CSF [Na+] increases tolerance to haemorrhage and improves cardiovascular function after blood loss in sheep. Since the haemodynamic responses in many respects were similar to those reported in response to the systemic administration of a small volume of hypertonic NaCl solution in haemorrhagic shock, part of the effect of that treatment may be mediated via cerebral effects of increased Na+ concentration.
Evidence for an electrically silent, neurogenic fluid secretion in the rat jejunum in vivo
Authors: HEMLIN M. , MELLANDER A. 
Published: December 2008

The aim of this study was to evaluate the mechanism behind neurogenic fluid secretion in the rat jejunum. In vitro, short‐circuit current (SCC) and potential difference (PD) were measured with the conventional Ussing technique. In vivo, electric parameters and net fluid transport (NFT) were simultaneously recorded with two different techniques. In separate in vivo experiments alkaline secretion (As) was estimated. In vitro, the chloride channel blocking substance 5‐nitro‐2(‐3‐phenylpropyl‐amino)benzoic acid (NPPB) and the loop diuretic substance furosemide (F) inhibited SCC, whereas the carbonic anhydrase inhibitor acetazolamide (Ace) lacked effect. Noradrenaline inhibited SCC and this effect was antagonized by NPPB and F. In vivo, cholera toxin induced a parallel increase in PD/SCC and fluid secretion. Conversely, mesenteric nerve stimulation (MNS) or administration of the nicotinic antagonist hexamethonium (Hx), concomitantly inhibited PD/SCC and fluid secretion. However, there was a poor correlation between the magnitudes of these effects. F inhibited SCC in vivo and also the SCC‐effect of MNS. However, F had no effect on fluid secretion in vivo, nor on the NFT‐effect of MNS. Jejunal As was stimulated by cholera toxin and MNS significantly inhibited As. The present results challenge the current view on the role of electrogenic chloride secretion in intestinal secretion. Alternative mechanisms are tentatively discussed.
Contractions induced by angiotensin I, angiotensin II and bradykinin in isolated smooth muscle from the human detrusor
Authors: ANDERSSON K.‐E. , HEDLUND H. , STAHL M. 
Published: December 2008

In isolated human detrusor preparations angiotensin (At)II 10‐9‐10‐5mcaused concentration‐dependent contractions. The contractile effect was immediate, and had an amplitude which at the highest concentration used, 10‐5m, reached 103 ± 16% of the mean contraction produced by K+124 mm(27.6 ± 1.4 mN). The AtII effect was completely blocked by saralasin 10‐6m, but was not affected by pre‐treatment of the preparations with captopril or enalaprilate. There was a marked tachyphylaxis to the actions of the peptide. AtI (10‐8–10‐5m) also caused contractions which were rapidly developing, and subject to a marked tachyphylaxis. At a concentration of 10‐5m, the mean amplitude was 66 ± 9% of the K+‐induced contraction. The contractions were blocked by saralasin 10‐6m, but not by captopril or enalaprilate 10‐5m. In contrast, contractions produced by AtI in rabbit mesenteric arteries were practically abolished by the angiotensin converting enzyme (ACE) inhibitors. The contractions induced by both Ad and AtII were practically abolished after pre‐treatment in a nominally calcium‐free Krebs solution. However, blockade ofl‐type calcium channels by nifedipine 10‐6mreduced the responses to both AtI 10‐6M (by 38 ± 4%) and AtII 10‐6m(by 39 ± 7%), but never abolished the contractions. Bradykinin (Bk; 3 times 10‐8–10‐5m) had a contractile effect in detrusor preparations which varied widely between strips. At a concentration of 3 times 10‐6m, a maximum was reached amounting to 30 ± 10% of the K+‐induced contraction. Bk‐induced contractions were practically abolished (0–3% of K+‐induced contraction) by a 30 min exposure of the preparations to calcium‐free medium. In the presence of nifedipine 10‐6m, the mean response to Bk 10‐5M did not differ significantly from the control value. Thirty min pretreatment with captopril or enalaprilate 10‐5msignificantly increased the Bk 10‐5minduced contractions. These contractions were significantly reduced by pretreatment for 30 min with indomethacin.The results suggest that Ad, AtII, and Bk all have marked contractile effects on isolated human detrusor smooth muscle. The conversion of AtI to AtII seems to occur through an enzyme which cannot be inhibited by ACE‐inhibitors. ACE‐inhibition can, however, enhance the effects of Bk.
Effects on renal sodium and potassium excretion of vasopressin and oxytocin in conscious dogs
Authors: ANDERSEN S. E. , ENGSTROM T. , BIE P. 
Published: December 2008

Renal effects of arginine vasopressin and oxytocin were studied in conscious dogs, made water‐diuretic by a waterload equivalent to 2% of body weight. Body water and content of sodium were maintained by separate servo‐controlled infusions. Peptides were infused for 60 min at rates of 50 pg kg‐1min‐1(arginine vasopressin) or 1 ng kg‐1min‐1(oxytocin), either separately or combined. Infusions increased plasma arginine vasopressin to 1.9 ± 0.2 (arginine vasopressin alone) and 1.8 ± 0.3 pg kg‐1(arginine vasopressin plus oxytocin and plasma oxytocin to 72 ± 5 (oxytocin alone) and 77 ± 8 pg ml‐1(oxytocin plus arginine vasopressin). Arginine vasopressin or arginine vasopressin plus oxytocin increased urine osmolality similarly by a factor of 13, decreased urine flow to between 5 and 7% of control and decreased free water clearance. Oxytocin reduced urine flow and free water clearance and increased urine osmolality by a factor of 2. Oxytocin and arginine vasopressin separately increased excretion of sodium from 4 ± 2 to 15 ± 6 μmol min‐1and from 7 ± 4 to 25 ± 13 μmol min‐1, respectively. Arginine vasopressin plus oxytocin led to a pronounced natriuresis (13 ± 4 to 101 ± 27 μmol min‐1). Arginine vasopressin and arginine vasopressin plus oxytocin increased the excretion of potassium by a factor of 2.5. Oxytocin and arginine vasopressin plus oxytocin increased urinary Na+/K+ratio by a factor of 3.7.It is concluded, that oxytocin at plasma concentrations of 70–80 pg ml‐1has modest antidiuretic and natriuretic effects and that the combined action of arginine vasopressin oxytocin may elicit supra‐additive natriuretic effects.