bluuebunny/crossref_metadata_2025 huggingface dataset:
Adrenergic nerves and the alpha2‐adrenoceptor system regulating melanosome aggregation within fish melanophores
Authors: ANDERSSON R. G. G. , KARLSSON J. O. , GRUNDSTRÖM N.
Published: December 2008

Nervous control of melanosome aggregation of melanophores of Labrus ossifagus was studied by electrical field stimulation of isolated scales. Field stimulation elicited a rapid melanosome aggregation which was reversible upon interruption of the stimuli. The response was blocked by guanethidine indicating that adrenergic nerves were stimulated. The melanophore receptors which mediate the nerve‐controlled pigment aggregation were characterized to be of the alpha2‐adrenoceptor subtype, since they were inhibited by yohimbine but not by prazosin. Stimulation of the alpha2‐adrenoceptors by noradrenaline was associated with a significant reduction of the cyclic AMP content of the melanophores. It is suggested that adrenergic nerves control melanosome aggregation via alpha2‐adrenoceptors and that these receptors are coupled to the adenylate cyclase‐cyclic AMP system of the melanophores.
The effect of lighting conditions on plasma levels of gonadotropins in castrated male rats
Authors: JOHANSSON G. , LAAKSO M.‐L. , PORKKA‐HEISKANEN T. , PEDER M. , LINDROOS F.
Published: December 2008

Plasma levels of LH and FSH were measured in castrated male rats kept in a 12/12 h light/dark cycle (control lighting), continuous light or continuous darkness. In Experiment I, the animals were kept in the three illumination conditions for 5 weeks. They were then decapitated for blood collection. In Experiment II, the blood samples were collected daily via permanently implanted aortic cannulae after 7 days of adaptation to the experimental lighting condition. In both experiments, the plasma levels of LH and FSH were higher in the rats kept in continuous light than in those kept in control conditions. After exposure to darkness for 5 weeks, the gonadotropin levels did not differ from the control values. In Experiment II, the levels of FSH were lower in darkness than in the control lighting, but the levels of LH did not change.
The hemodynamic effect of bilateral carotid artery ligation and the morphometry of the main communicating circuit in normotensive and spontaneously hypertensive rats
Authors: FREDRIKSSON KENT , NORDBORG CLAES , JOHANSSON BARBRO B.
Published: December 2008

After reducing the number of patent conduit arteries to the brain by bilateral ligation of the carotid artery, the percentage decrease in blood pressure from the aorta to the internal carotid artery distal to the ligation was larger in spontaneously hypertensive rats than in normotensive rats. The pressure drop corresponded to the degree of hypertension as well as to morphometrically determined structural arterial alteration in the main communicating circuit, i.e. larger media to internal radius ratio and smaller internal radius in the posterior communicating arteries, the proximal part of the posterior cerebral arteries, the basilar artery and the vertebral arteries. The discrepancy between the sum of the luminal cross sectional areas of the communicating circuit and the luminal areas of the ligated conduit arteries was larger in the hypertensive than in the normotensive rats. It is to be expected that occlusion of conduit arteries to the brain will have a larger impact on the cerebral arterial perfusion pressure head in the presence of such hypertensive structural alterations known to increase flow resistance.
Relationship between PGE2and renin release in dog kidneys Effects of afferent arteriolar dilation and adrenergic stimulation
Authors: VIKSE ARILD , HOLDAAS HALLVARD , SEJERSTED OLE M. , KIIL FREDRIK
Published: December 2008

To study the relationship between PGE2and renin release from the kidney, examinations were performed on anesthetized dogs during afferent arteriolar dilation. This condition is known to increase renin release and enhance the stimulatory effects on renin release of β‐adrenergic agonists, such as isoproterenol. Afferent arteriolar dilation induced by constricting the renal artery or occluding the ureter increased PGE2and renin release before, but not after, indomethacin administration. Isoproterenol infusion during afferent arteriolar dilation increased renin release but not PGE2release both before and after indomethacin administration. Phenylephrine, an α‐adrenergic agonist, which also induces afferent arteriolar dilation, increased PGE2and renin release at control blood pressure but not when the afferent arterioles already were dilated by ureteral occlusion. We conclude that afferent arteriolar dilation caused by renal arterial constriction, ureteral occlusion or infusion of phenylephrine increases prostaglandin synthesis which stimulates renin release. The effect of isoproterenol on renin release is independent of prostaglandin synthesis.
Glomerular filtraton rate and PCO2as determinants of lithium reabsorption
Authors: HARTMANN ANDERS , LANGBERG HARALD , HOLDAAS HALLVARD , KIIL FREDRIK
Published: December 2008

To examine whether lithium reabsorption varies in proportion to the bicarbonate‐dependent reabsorption of water and chloride, reabsorption was altered by varying PCO2and glomerular filtration rate (GFR) in volume‐expanded, anesthetized dogs during ethacrynic acid infusion. At constant GFR and plasma bicarbonate concentration, lithium, bicarbonate, chloride and water reabsorption were inversely related to plasma pH during variations in PCO2. Lithium and bicarbonate reabsorption varied by 9±1% and chloride reabsorption by 7±1% as plasma pH was altered by 0.1 unit from plasma pH 7.5. Calculation of reabsorbate concentrations indicated that lithium was reabsorbed as readily as water (reflection coefficient=0). During mechanical constriction of the suprarenal aorta, GFR was reduced at constant plasma pH. Bicarbonate reabsorption fell more than chloride, water and lithium reabsorption. Lithium reabsorption was not significantly reduced until GFR was reduced by 35%. In stop‐flow studies during ouabain infusion, urinary lithium concentrations were reduced below plasma concentrations. This is compatible with passive diffusion of lithium along a lumen‐positive potential exceeding 10 mV in the diluting segment. Thus, lithium reabsorption behaved as expected for bicarbonate‐dependent paracellular reabsorption during variations in PCO2; when GFR is reduced, an additional component of lithium reabsorption is disclosed.
The importance of nervous and humoral factors in the control of vascular resistance, blood flow distribution and net fluid absorption in the cat small intestine during hemorrhage
Authors: REDFORS STAFFAN , SJÖVALL HENRIK
Published: December 2008

The influence of preganglionic (splanchnic) and postganglionic (periarterial) denervation of the cat small intestine on the changes in blood flow and net fluid absorption elicited by hemorrhage was investigated. The compiled data from a previous report indicate that hemorrhage induces a vasoconstriction and a redistribution of blood flow towards the absorptive part of the mucosa. The vasoconstriction was unaffected by a total postganglionic denervation whereas after a preganglionic denervation both the vasoconstriction and the redistribution of blood flow were abolished. We have also shown earlier that hemorrhage induced an increase in net fluid absorption as long as no ischemic mucosal lesions developed. This increase was reduced by postganglionic denervation, and was reversed into a small decrease after preganglionic denervation. On the basis of these findings it is proposed that the increase in vascular resistance, the redistribution of blood flow towards the absorptive part of the mucosa as well as the increase in net fluid absorption observed after hemorrhage all are effects mainly mediated via the splanchnic nerves. Furthermore, humoral factors are of major importance for the increase in vascular resistance observed after hemorrhage. The increase in net fluid absorption was shown to be induced both by direct nervous and by humoral factors.
Renal blood flow and vasodilatory ability prior to and following release of 24 hours bilateral ureteral obstruction in rats
Authors: HOPE ARVID , CLAUSEN GUNNAR
Published: December 2008

Increased renal vascular resistance (RVR) is evident after 24 hours of uni‐and bilateral ureteral obstruction (UUO and BUO). However, to what extent the RVR increase is due to vascular damage versus functional vasoconstriction, or whether obstructed kidneys possess the ability to reduce RVR in response to vasodilatory stimuli, is not clear. During 24 hours of BUO renal blood flow (RBF), recorded electromagnetically, was reduced to about 70% of control and continued to fall by another 18% during ½‐1 hour after release of BUO. Infusion of imidazole, a thromboxane A2synthetase blocker, did not reduce RVR after release of BUO. Whereas RBF autoregulation in response to reduced perfusion pressure was impaired, maximal proportional renal vasodilation induced by acetylcholine was increased, both prior to and after release of BUO, as compared to control and UUO. These different renal vasodilatory responses indicate that the RVR increase during BUO is largely due to a functional vasoconstriction that impairs autoregulatory vasodilation. In contrast, the RVR increase during UUO is probably mainly due to structural damage which does not prevent autoregulation of the RBF level attained.
Age‐ and pressure‐dependent changes of systemic resistance vessels concerning the relationships between geometric design, wall distensibility, vascular reactivity and smooth muscle sensitivity
Authors: FOLKOW B. , KARLSTRÖM G.
Published: December 2008

The resistance vascular function in normotension, and its alterations in primary hypertension and ordinary aging, was analysed concerning the interactions between (1) geometric vascular design, (2) wall distensibility, (3) transmural pressure and (4) smooth muscle activity. Paired hindquarter perfusions were used, comparing hemodynamic resistance characteristics in young, adult and old normotensive (WKY) and spontaneously hypertensive rats (SHR). From the experimental data pressure‐resistance diagrams were constructed, which quantitatively interrelate the four factors in all SHR‐WKY groups. The diagrams show, over a wide pressure range, how altered smooth muscle activity as well as structural adaptation affect resistance vessel distensibility: likewise how distensibility considerably interferes with “active” resistance adjustments. They also show how markedly the range of active resistance responses during ordinary constant‐pressure perfusion is affected whenever pressure is reset to new levels. Finally, the diagrams illustrate the fundamental hemodynamic difference between hypertensive and normotensive resistance vessels, mainly because of factors 1 and 2, which render the hypertensive vessels stronger, stiffer and hyperreactive. Thereby they are capable of a widened response range despite the higher pressure level, which is further accentuated on acute pressure normalization. In contrast, ordinary aging alters resistance vascular behaviour only little, smooth muscle contractility and sensitivity remaining almost unchanged. However, vascular reactivity is moderately enhanced at lower pressures, presumably a geometric consequence of age‐dependent, intimal‐interstitial endowment.
Pharmacological properties of prejunctional α‐adrenoceptors in isolated feline middle cerebral arteries; comparison with the postjunctional α‐adrenoceptors
Authors: SKÄRBY TOR
Published: December 2008

In cat middle cerebral arteries (CMCA) preincubated with 3H‐noradrenaline (NA), the outflow of tritium evoked by electrical stimulation was reduced to 32% by α‐adrenoceptor (α‐receptor) stimulation with oxymetazoline, and increased to 487% by α‐receptor blockade with HEAT. The relative order of potency for α‐receptor agonists on prejunctional receptors was: clonidine ≥ oxymetazoline > phenylephrine, and the antagonist rauwolscine was more potent than prazosin. This indicates that the prejunctional α‐receptors are mainly of α2‐type. Rauwolscine was more potent than prazosin in inhibiting the contractions induced by NA, indicating a predominance of α2‐receptors postjunctionally. Apart from clonidine having higher intrinsic activity pre‐ than postjunctionally, all drugs examined (oxymetazoline, phenylephrine, rauwolscine, HEAT (BE2254), and prazosin) had similar concentration‐effect curves on the pre‐ and postjunctional receptors. Furthermore, the ratios of EC50‐values pre‐ and postjunctionally of rauwolscine, oxymetazoline, and clonidine were all close to unity. These results indicate that pre‐ and postjunctional α2‐receptors in the CMCA have similar pharmacological characteristics and cannot be influenced separately by the presently used drugs.
Disulfiram is protective against postischemic cell death in the liver
Authors: JENNISCHE EVA , HANSSON HANS‐ARNE
Published: December 2008

The effect of the scavenger compound disulfiram (Antabus®) on postischemic cell injury was investigated. Rats were subjected to 90 min of liver ischemia and 3 h of reperfusion. The extent of cell injury was evaluated morphologically by a dye exclusion test and a histochemical stain for calcium. It was found that pretreatment with disulfiram significantly reduced the number of injured cells compared to untreated controls.
Postjunctional α1‐ and α2‐adrenoceptors mediating contraction in isolated human groin arteries and veins
Authors: STEEN STIG , SJÖBERG TRYGVE , SKÄRBY TOR V. C. , NORGREN LARS , ANDERSSON KARL‐ERIK
Published: December 2008

By means of selective agonists and antagonists for α1‐ and α2‐receptors, the α‐receptor subtypes in human groin arteries and veins were characterized and compared. In the arteries the α1‐receptor blocker prazosin caused a concentration‐dependent parallel displacement of the noradrenaline (NA) concentration‐response (cr) curve without reduction of maximum (pA2=9.86); the selective α2‐receptor antagonist rauwolscine in the concentration 10‐8M caused a right‐ward shift of the NA cr‐curve without reduction of Emax, but 10‐7M and 10‐6M caused little or no further shift. In the veins, the two antagonists had the opposite effects. Rauwolscine caused a concentration‐dependent right‐ward shift of the NA cr‐curve without depression of maximum (pA2=9.03); prazosin 10‐9M significantly displaced the NA cr‐curve, whereas 10‐8M and 10‐7M caused little or no further shift. The responses to the α2‐receptor agonist clonidine in the arteries were too small to allow calculations of pEC50 values; in the veins contractions were elicited in all vessel segments investigated (pEC50=6.24). Phenylephrine, selective for α1‐receptors, was significantly more potent in arteries than in veins. NA was significantly more potent in veins than in arteries. It is concluded that in human groin vessels, there is a functional predominance of arreceptors in the arteries and of a2‐receptors in the veins.
Comments on the atropine resistance of the neurogenic contractile response of the rat detrusor muscle
Authors: HAMMARSTRÖM MARGARETA , SJÖSTRAND NILS O.
Published: December 2008

The resistance to atropine or scopolamine of the neurogenic contractile response to field stimulation of intramural nerves of the rat detrusor was studied during the early phase of Wallerian degeneration in vitro and in vivo. The neurogenic contractile response to low frequency stimulation of control bladders was completely resistant to atropine or scopolamine in vitro. As a matter of fact the response was enchanced by the drugs. In vivo a transient shortening of the response could be seen.26–34 h after bilateral extirpation of the pelvic ganglia there was prominent degeneration activity in the bladders in vitro as well as in vivo. Atropine or scopolamine inhibited this activity in vivo but enhanced it in vitro. The neurogenic contractile response to field stimulation of the bladder nerves was blocked in vivo but not in vitro by the antimuscarinic drugs 26–34 h after neurectomy. The results support the concept that the excitatory neurotransmission in the detrusor is essentially cholinergic. An explanation of the difference between the in vivo and the in vitro results based on differencies in degree of blockade of pre‐ and post‐junctional muscarinic receptors and diffusion of the antimuscarinics in the tissue is proposed.
Cation permeability and mechanical properties of the erythrocyte membrane under the influence of lysophosphatidylcholine (LPC) in isotonic and hypotonic media
Authors: ESKELINEN S. , MELA M.
Published: December 2008

The osmotic behaviour of erythrocytes under the influence of lysophosphatidylcholine (LPC) was investigated at temperatures of +4°C and 20°C by allowing them either to swell rapidly in hypotonic media in the presence of LPC or to swell gradually at first and then interact with LPC.Prelytic potassium release, the degree of hemolysis and the cell volume under various osmotic conditions were measured, together with the ‘returning volumes’, i. e.the volumes in an isotonic solution to which the cells returned from that in the hypotonic solution. LPC had a hemolyzing effect on erythrocytes in an isotonic medium and in slightly hypotonic media under all the osmotic conditions investigated, and the degree of hemolysis increased with increasing concentrations of LPC or decreasing temperatures, being greater during gradual than during rapid swelling. LPC also produced a prelytic leakage of potassium connected with the decrease in cell volume in an isotonic medium and in ‘returning volumes’ in all the media and under all the osmotic conditions investigated. The semipermeability of the membrane was preserved in all these cases, however, for osmotic swelling of the erythrocytes was observed, although to a lesser extent than without LPC.During rapid swelling both the curves for the prelytic potassium leakage and the degree of hemolysis were shifted towards more dilute solutions. Since the critical hemolytic volume was not increased, the shift in potassium leakage and hemolysis caused by LPC may be due to increased rigidity in the cell membrane. The curves for both potassium leakage and hemolysis shifted towards more concentrated solutions during gradual swelling, perhaps due to increased membrane fragmentation.
Central hemodynamic effects of adrenaline with special reference to β2‐adrenergic influence on heart rate and cardiac afterload in anesthetized cats
Authors: GUSTAFSSON DAVID , BJÖRKMAN JAN‐ARNE
Published: December 2008

Central hemodynamic responses evoked by i. v.infusions of adrenaline and noradrenaline were studied in normovolemic anesthetized cats with intact adrenoceptors, after selective β2‐blockade (ICI 118,551), and after nonselective β‐blockade (propranolol).The results demonstrated the presence of an important β2‐adrenergic component in the integrated response to ‘physiological’ doses of adrenaline contributing to increased cardiac output, decreased total peripheral resistance and virtually unchanged mean arterial blood pressure. Corresponding β2‐adrenergic effects of noradrenaline were small. The β2‐adrenergic effects of adrenaline on the heart seemed to be both direct and indirect. A moderate direct chronotropic response mediated by β2‐adrenoceptors apparently was present but there was no evidence of a direct β2‐adrenergic inotropic effect. An indirect, quite marked effect on the heart was accomplished by a β2‐adrenergic vasodilator interaction with the α‐adrenergic vasoconstrictor influence on the systemic resistance vessels. This caused a net decrease in total peripheral resistance, thereby preventing an undue increase in cardiac afterload (arterial pressure) which seemed to be essential for evoking ‘optimal’ increases in cardiac output. It is suggested that such adrenaline evoked indirect, β2‐adrenergic improvement of cardiac performance is of functional importance in reflex sympatho‐adrenal circulatory control.
Relationship between the overflow of endogenous and radiolabelled noradrenaline from canine blood perfused gracilis muscle
Authors: KAHAN THOMAS , HJEMDAHL PAUL , DAHLÖF CARL
Published: December 2008

The effects of sympathetic nerve stimulation (SNS) on the overflow of endogenous noradrenaline (NA) and on vasoconstrictor responses were studied in blood perfused canine gracilis muscle in situ. A conventional tracer technique with3H‐labelled NA (3H‐NA) was used in parallel. At rest there was a net extraction of endogenous NA and adrenaline across the tissue. The SNS evoked overflow of endogenous NA was frequency‐dependent and logarithmically correlated to the vasoconstrictor responses. The neuronal uptake inhibitor desipramine doubled the SNS induced overflow of endogenous NA without enhancing the vasoconstrictor responses. A further fourfold increase in NA overflow was caused by a dose of the α‐blocker phenoxybenzamine which reduced the vasoconstrictor responses by 50–75%.Less than 10% of the spontaneous3H efflux was recovered as unmetabolized3H‐NA, whereas virtually all3H overflow evoked by SNS was3H‐NA.The fractional release of NA or3H‐NA per nerve impulse increased with increasing frequencies of SNS under all conditions studied. Although there was a preferential release of the newly stored radiolabelled transmitter, results concerning endogenous NA and3H‐NA overflow were qualitatively similar, also under conditions with marked changes in transmitter overflow. Endogenous NA gave a more reproducible index of transmitter overflow than did3H‐NA and, in particular, total3H.The overflow of endogenous NA closely reflects SNS evoked neuronal release of NA in blood perfused skeletal muscle and seems more suitable than conventional radiotracer techniques for studies of NA release under in vivo conditions.
Prostaglandin E2 in basal gastric secretion and during stimulation of muscarinic receptors in man
Authors: ALY A. , GRÉEN K. , JOHANSSON C.
Published: December 2008

The physiological importance of prostaglandin E2 (PGE2) biosynthesis in the gastric mucosa is unknown. A role of endogenous prostaglandins in protecting the gastrointestinal epithelia has been suggested, but the evidence is unsufficient and rarely supported by concomitant measurement of PG production. Amounts of PGE2 in luminal gastric contents which can be sampled atraumatically may reflect PGE2 synthesis in the gastric mucosa in vivo. To confirm earlier reported measurements made with radioimmunoassay we have measured by gas chromatography ‐ mass spectrometry (GC‐MS) PGE2 in gastric juice of five healthy men under basal conditions and during stimulation of muscarinic receptors with iv. bethanechol which in dog is reported to enhance PGE2 output. PGE2 was detected in all basal samples. The output was in median 32.1 pmol/15 min (range 17.0–105.4, 1 pmol=0.352 ng), which is similar to results from earlier studies. Bethanechol infusion (60 μg x kg‐1 x h‐1) did not affect PGE2 outputs systematically in spite of a significant increase in outputs of acid and chlorides. Stimulation of muscarinic receptors does not seem to influence PGE2 synthesis in gastric mucosa in vivo. Alternatively changes in PGE2 synthesis may be masked by rapid chemical or enzymatical degradation or reabsorption of PGE2.Studies are under way to explore those phenomena.
Influence of suckling and feeding on insulin, gastrin, somatostatin and VIP levels in peripheral venous blood of lactating sows
Authors: UVNÄS‐MOBERG KERSTIN , ERIKSSON MAUD , BLOMQUIST LARS‐E. , KUNAVONGKRIT ANNOP , EINARSSON STIG
Published: December 2008

Blood samples were collected in peripheral venous blood of seven lactating sows, when their piglets were suckling. In four of the experiments samples were also taken when the sows were fed a meal. Gastrin, insulin, somatostatin and VIP levels were measured by radioimmunoassay. Insulin levels increased by—100% for about 10 min in response to suckling, in some experiments even before the suckling occurred, i.e. when the sows, saw, heard and smelt their piglets. In four of the sows suckling caused a biphasic twofold increase in gastrin levels—one immediate peak which lasted for a few min and a second peak of longer duration (about 30–60 min), whereas gastrin levels remained unchanged in three animals. Somatostatin levels usually reflected gastrin levels in a reciprocal way. Thus, a biphasic decrease of somatostatin levels occurred in the high gastrin responders. In contrast, somatostatin levels increased in the experiments, in which gastrin levels did not change. Immediate and short‐lasting (a few minutes long) increases of VIP levels were also induced by suckling. Large litters and long suckling periods appeared to be related to greater changes of the levels of all the peptides measured. Feeding influenced insulin, gastrin and somatostatin levels in the same way as did suckling from both a qualitative and a quantitative point of view. In contrast, VIP levels were not increased by feeding. The possible functional effects of the suckling‐induced release of gastrointestinal hormones and possible mechanisms of their release are discussed.
The effect of intraarterial infusion of prostacyclin on the tubuloglomerular feedback control in the rat
Authors: BOBERG ULF , HAHNE BENGT , PERSSON A. ERIK G.
Published: December 2008

Effects of intraarterial prostacyclin (PGI2) infusions on interstitial hydrostatic and oncotic pressures and on the tubuloglomerular feedback (TGF) control of glomerular filtration rate (GFR) were studied in rat kidneys. The hilar lymph flow rate was used as a measure of interstitial hydrostatic pressure and the lymph protein concentration was used for interstitial oncotic pressure estimation. In the micropuncture experiments the stop‐flow pressure technique was employed for determining the TGF characteristics, i.e. stop‐flow pressure (PSF), maximal reduction of PSF(ΔPSF) and turning point (TP), defined as the end‐proximal flow rate at which 50% of ΔPSFwas obtained. Non‐hypotensive doses of PGI2(50 to 100 ng‐kg‐1B. W.‐min‐1) infused in 30 min evoked an increase in urine and lymph flow rates and a decrease in lymph protein concentration, but did not affect GFR. ΔPSFwas reduced (9.9±1.0 mmHg versus 4.7±2.2 mmHg) and TP increased (22±2 nl/min versus 34±2 nl/min), but the PSFwas unaffected. These changes were seen during the infusion period and during the immediate post‐infusion control period of 30 min. Our data indicate that non‐hypotensive doses of PGI2in some way can affect the renal interstitial pressure and the TGF control system.
Sympathetic stimulation of amylase secretion during a parasympathetic background activity in the rat parotid gland
Authors: ASKING BENGT
Published: December 2008

The amylase secretion in vivo was examined in the rat parotid gland. A comparison was made between individual stimulation of sympathetic and parasympathetic nerves and simultaneous activation of both nerves. When sympathetic stimulation was superimposed on a parasympathetic background activity, amylase secretion was elicited at a frequency far below the threshold for secretion of fluid, and increased in a frequency‐dependent way. This augmented amylase secretion, seen when the two nerves were activated at the same time, gave an amylase output which far exceeded the sum obtained at individual nerve stimulation.

The sympathetic amylase secretion obtained in a background of parasympathetic activity seemed to be dependent entirely on β1‐adrenoceptors. When high sympathetic stimulation frequency (3–10 Hz) was used a reduction in salivary flow was seen, which was accompanied by a reduced amylase output. This effect was counteracted by α‐adrenoceptor blockade. Isoprenaline, injected intravenously during an ongoing parasympathetic activity, was found to evoke an augmented amylase secretion in a similar way as sympathetic nerve stimulation.
Erythrocyte 2,3‐diphosphoglycerate and erythropoietic activity in rabbits with severe bleeding anaemia superimposed on the early post‐natal fall in haemoglobin
Authors: HOLTER P. H. , REFSUM H. E.
Published: December 2008

Erythrocyte 2,3‐diphosphoglycerate (2,3‐DPG), whole blood haemoglobin (Hb), haematocrit (Hct), mean corpuscular haemoglobin concentration (MCHC) and reticulocyte percentage (Rt) were determined before and after bleeding in two groups of suckling chinchilla rabbits. One group was subjected to severe bleeding on the 12th, 15th, 18th and 21st day after birth and studied for 3 weeks, while the other was studied during the first 24 h after one severe bleeding on the 18th day. In the first group Hb and Hct fell to 2.7 g.dl‐1 and 11.5%, respectively, on the 25th day. The fall was accompanied by a marked rise in Rt and decline in MCHC, reaching maximum and minimum on the 29th day, and a simultaneous, temporary decline in 2,3‐DPG. In the other group the acute bleeding was accompanied by a marked fall in Hb and Hct, but no change in Rt and MCHC. 2,3‐DPG was unchanged 8 h after the bleeding, but showed a rise during the following 16 h, definitely beyond the normal rise at this age. It is concluded that severe bleeding anaemia induces a rise in erythrocyte 2,3‐DPG synthesis. However, the effect of the acute rise in 2,3‐DPG is far from sufficient to maintain the O2 delivery capacity of the blood, and is completely offset by the influence of a subsequent change in the erythrocyte population towards younger cells with low 2,3‐DPG.
Distribution of carbonic anhydrase in cells and membranes isolated from pig gastric mucosa
Authors: VEGA FÉLIX V. , OLAISSON HANS , MÅRDH SVEN
Published: December 2008

Mucosal cells were isolated from pig stomachs and then fractionated on linear density gradients of Percoll. Different types of cells were identified by their typical staining and morphology. In disrupted cell fractions, hydration of CO2 by carbonic anhydrase was measured by means of pH‐stat technique. Localization of carbonic anhydrase to certain cell fractions was also studied by histochemical staining. Both parietal cells and carbonic anhydrase were confined to the low and intermediate density fractions of the gradients. Purified membranes from pig gastric mucosa, which contained the acid pump of the stomach, the H,K‐ATPase, also contained a firmly bound carbonic anhydrase of high activity. The enzyme activity in the membranes was inhibited by acetazolamide, furosemide and KSCN. The molecular mass of the carbonic anhydrase was 33 kDA as estimated by its binding of [14C]furosemide followed by polyacrylamide gel electro‐phoresis. Previous suggestions of a role of carbonic anhydrase as a supplier of H+ in the secretion of acid are supported by its high activity and its localization to the same membrane as the acid pump of the stomach.
Mechanisms underlying changes in the contents of neuropeptide Y in cardiovascular nerves and adrenal gland induced by sympatholytic drugs
Authors: LUNDBERG JAN M. , SARIA ALOIS , FRANCO‐CERECEDA ANDERS , THEODORSSON‐NORHEIM ELVAR
Published: December 2008

Neuropeptide Y (NPY) is a recently isolated vasoactive peptide, which is present, together with catecholamines, in sympathetic nerves and in the adrenal medulla. In the present study, we report that pretreatment with sympatholytic agents influences the tissue levels of NPY‐like immunoreactivity (NPY‐LI) in the guinea‐pig. Thus, 24 h after reserpine not only noradrenaline (NA), but also NPY‐LI, was depleted in the heart, spleen and the adrenal gland. The levels of NPY‐LI in the vas deferens and stellate ganglia, however, were unaffected by reserpine in spite of marked depletions of NA. The reserpine‐induced depletion of NPY‐LI was probably caused by enhanced nerve‐impulse flow and subsequent release from cardiovascular nerves in excess of resupply, since it could be prevented by the ganglionic‐blocking agent chlorisondamine. Long‐term (6 days) treatment with chlorisondamine reduced the levels of NPY‐LI in the stellate ganglion. Short‐term treatment (48 h) with guanethidine partially prevented the reserpine‐induced depletion of NPY‐LI, probably due to inhibition of NPY release. Long‐term guanethidine treatment depleted not only NA, but also NPY‐LI from the spleen. Pretreatment with the alpha‐receptor antagonist phenoxybenzamine did not influence the NA levels but reduced the content of NPY‐LI in the spleen via a mechanism that was dependent on intact ganglionic transmission. Since NPY has several cardiovascular actions, changes in NPY mechanisms may contribute to the pharmacological and therapeutical effects of sympatholytic agents.
Test‐dependent antinociceptive effect of spinal serotonin release induced by intrathecalp‐chloroamphetamine in mice
Authors: BERGE ODD‐GEIR , FASMER OLE BERNT , JØRGENSEN HUGO A. , HOLE KJELL
Published: December 2008

The effect of direct intrathecal injection ofp‐chloroamphetamine (PCA) into the lumbar subarachnoid space was investigated in mice. PCA (0.6–20 μg) induced a dose‐related prolongation of response latencies in the tail‐flick test, but failed to affect the hind‐paw lick response in a hot‐plate test employing slowly rising temperature. PCA (5μg)given intracerebroventricularly did, however, significantly elevate the response temperature in the hot‐plate test. The antinociceptive effect of PCA in the tail‐flick test was prevented by spinalization, by pretreatment with the selective serotonergic re‐uptake blocker zimelidine (20 mgkg‐1i. p.) and by the serotonin synthesis inhibitorp‐chlorophenyl‐alanine (300 + 300+ 150 mgkg‐1i. p. 72, 48 and 24 h before test). It is concluded that PCA given intrathecally releases serotonin from spinal terminals, which may under certain conditions induce antinociception.
Skeletal muscle and hormonal adaptation to physical training in the rat: role of the sympatho‐adrenal system
Authors: HENRIKSSON JAN , SVEDENHAG JAN , RICHTER ERIK A. , CHRISTENSEN NIELS JUEL , GALBO HENRIK
Published: December 2008

The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training‐induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague‐Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham‐operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h‐day‐1, 4 days‐week‐1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochromecoxidase, and 3‐hydroxyacyl‐CoA dehydrogenase. In sham‐operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training‐induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham‐operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training‐induced increase in muscle mitochondrial enzymes. The training‐induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.
Tubuloglomerular feedback in hypertensive rats of the Milan strain
Authors: PERSSON A. ERIK G. , BIANCHI G. , BOBERGJ U.
Published: December 2008

In rats of the Milan hypertensive strain (MHS) the disease can be transplanted with the kidney to rats of the Milan normotensive strain (MNS). It has been found that GFR, salt and volume regulation differ between MHS and MNS rats. Tubuloglomerular feedback control mechanism (TGF) is important for body volume regulation and we therefore wanted to study the TGF control in MHS and MNS rats. Whole kidney and micropuncture experiments were done before and during saline volume expansion (5% of body weight). In an initial series of experiments measurements were made of total kidney GFR, urine excretion rate of sodium and potassium and subcapsular interstitial hydrostatic pressure (psc); interstitial oncotic pressure (ρint) was estimated from hilar lymph protein concentration. In a second series, proximal tubular stop‐flow pressure (Psf) was determined upstream from a wax block while the distal nephron was being perfused with Ringer solution at a flow rate varying from 0 to 40 nl min‐. In this way the maximal drop in stop‐flow pressure (ΔPst) and also the turning point (TP), the tubular flow rate at which 50% of this response was achieved, could be determined after saline volume expansion and after 2 h of complete ureteral occlusion. The results showed that GFR was similar in MHS and MNS rats in the control situation, but that during volume expansion it was significantly lower in the MHS group. Interstitial sc and 7tint and net interstitial pressure (psc–πint) were similar in MHS and MNS rats both under control conditions and during volume expansion. The TGF investigation showed a slightly increased Δpst (8.5 vs. 5.2 mmHg) in the MHS animals while pst and TP were normal in the control state (38 mmHg and 21 nl‐min‐1). During volume expansion, however, the TGF sensitivity was significantly higher in the MHS animals than in the normotensive controls, showing a TP of 25 nl‐min‐1 (MNS 39 nl‐min‐1) and a Δsf of 5.6 mmHg, (MNS 1.3 mmHg). During ureteral occlusion the resetting to a low TGF sensitivity that occurs in control animals did not take place in the hypertensive animals. Thus, the feedback sensitivity was reset to a low level in the MNS animals during volume expansion and ureteral occlusion, while the MHS animals were unable to reset this sensitivity in the normal way. This inability might be expected to lead to overloading of the extracellular fluid volume, which may participate in the development and maintenance of the hypertensive disease.
The kinetics of adrenal catecholamine secretion elicited by splanchnic nerve stimulation or by Ach is consistent with non‐exocytotic, multivesicular release on cation exchange basis
Authors: UVNÄS B. , ÅBORG C‐H. , GOINY M.
Published: December 2008

In eight anaesthetized cats, one dog and one pig the left adrenal was activated during a 5–15‐min period by splanchnic nerve stimulation (10–30 V, 0.2‐2 ms) at supramaximal frequencies (10–50 Hz) or by i.a. infusion of acetylcholine in high concentration (10‐4M). The catecholamine (CA) release, as recorded in the adrenal venous outflow, was characterized by a very steep rise to a peak (within < 10 s), followed by a rapid decline which after 5–10 min continued as a ‘steady state’ secretion, still above prestimulatory level. The initial release curve satisfied the straight line equation logB=K√(σ ml) + logBmax, shown previously by us to be characteristic of the cation‐induced amine release from amine‐charged IRC 50 (a synthetic carboxyl cation exchanger resin) and from chromaffin granulesin vitrowhich occurred on superfusion of these materials with isotonic NaCl solution (Uvnäs & Åborg 1984a). The initial CA‐release, which depending on the intensity of the stimulus amounted to between 0.1 and ˜ 5% of the adrenal CA content is suggested to reflect the rapid depletion of a CA pool for immediate release composed of granules ‘lined up’ for secretion adjacent to the plasma cell membrane. On depolarization of this membrane the granules are assumed to become attached to it and CA release to occur as a cation exchange, between CA+in the granule matrix and Na+in the plasma or possibly K+in the cytoplasm. The transition from depletion to ‘steady state’ phase is assumed to reflect resynthesis or other compensatory refilling of the releasable depot evoked by its depletion. Cation exchange is suggested to be a general principle in the release of biogenic amines, including transmitter amines and other co‐stored charged substances, e.g. polypeptides.
The effect of nephrectomy and ureter ligation on plasma neurotensin‐like immunoreactivity levels in the conscious rat
Authors: T‐HEODORSSON‐NORHEIM E. , AL‐SAFFAR A. , SARIA A. , ROSELL S.
Published: December 2008

The effect of nephrectomy and ureter ligation on the concentration of endogenous plasma neurotensin‐like immunoreactivity (p‐NTLI) was studied in conscious rats by means of antiserum 17–8201 which detects NT(1–13) only, and antiserum 0–7709 which detects NT(1–13) and NT(1–8). The unstimulated p‐NTLI concentration did not change significantly during a 25‐h observation period following nephrectomy in comparison with sham operation. However, stimulation of the release of NTLI by intraduodenal administration of oleic acid (0.2 ml) resulted in significantly higher p‐NTLI levels in the nephrectomized rats than in the sham operated rats. Ureter ligation did not significantly affect basal or stimulated p‐NTLI. The data indicate that the kidneys play an important part in the elimination of p‐NTLI released after fat ingestion.
Non‐nicotinic, non‐adrenergic excitatory motor fibres in the preganglionic sympathetic supply to the feline colon. An axon reflex arrangement associated to thin sensory neurons, involving substance P?
Authors: FÄNDRIKS L. , DELBRO D.
Published: December 2008

Experiments were performed on chloralosed cats with ligated adrenals. The peripheral ends of the preganglionic sympathetic nerves to the colon were stimulated and colonic motility was monitored by a volumetric method. Electric nerve stimulation with various intensities elicited inhibitory motor responses and occasionally contractions. Hexa‐methonium and/or guanethidine blocked all inhibitory actions and revealed pure excitatory responses at high stimulation intensities. These colonic contractions were inhibited by atropine. However, atropine‐resistant contractions were sometimes observed, predominantly in the colorectal region. Thoracic sympathetic nerves affected the motility in the proximal colon only, while lumbar sympathetic nerves acted on both proximal and distal parts. Strength‐duration relationships and sensitivity to local heating suggest that the excitatory responses are due to an antidromic activation of thin, possibly afferent nerve fibres. Small doses of substance P injected close i.a. induced colonic contractions unchanged by hexamethonium and/or guanethidine but sensitive to atropine. The neurally‐induced colonic contractions are suggested to be due to an antidromic activation of thin sensory neurons which in the periphery release substance P, in turn activating cholinergic motor neurons, thus constituting an axon reflex arrangement. The possibility of a similar axon reflex mechanism, associated to thin afferents, activating adrenergic inhibitory neurons at the prevertebral ganglionic level is discussed.
Comparison of the Fick principle and the radioactive microsphere method in measuring cardiac output during haemorrhagic shock
Authors: LUNDBERG C. , SCHOENBERG M. H.
Published: December 2008

The applicability of radioactive microspheres in measuring cardiac output (CO) during haemorrhagic shock in the dog was studied. The COs thus determined were compared with CO values obtained simultaneously by the Fick method. In 13 animals simultaneous CO measurements by the two methods were performed prior to and after initial bleeding (down to a mean arterial pressure of 40 mmHg), at the termination of the hypotension period, and 5 and 60 min following blood reinfusion. An excellent correlation (r = 0.97) between the two methods was found for all determinations combined. Furthermore, during each of the five phases of the shock procedure no difference was observed between the two methods of measuring CO and the correlation varied from moderate to excellent (r= 0.61‐0.94). The results suggest that the microsphere method has a precision and validity comparable to those of conventional methods in measuring CO in situations when it is extremely low, as in haemorrhagic shock, in addition to having high accuracy in normal conditions.
The influence of the sympathetic impulse pattern on contractile responses of rat mesenteric arteries and veins
Authors: NILSSON H. , LJUNG B. , SjÖBLOM N. , Wallin B. G.
Published: December 2008

Contractile responses to electrical field stimulation of excised small mesenteric arteries and veins of the rat were compared when stimuli were delivered in irregular bursts or at regular intervals. Spontaneously occurring skin vasoconstrictor impulses in a few‐unit median nerve recording in man were stored on tape and used to trigger a stimulator. Two irregular stimulation sequences at average frequencies of 1.6 and 1.8 Hz, respectively, were used. In the arteries, average contractile responses were significantly greater at an irregular than at an even stimulation frequency, but in the veins, similar degrees of contraction were obtained with the two modes of stimulation. The frequency‐response relationships to continuous regular stimulation showed the artery to respond less than the vein at low frequencies. This apparently explains the difference in behaviour between the vessels to irregular stimulation. The results show that not only the number of impulses, but also their pattern of occurrence, may influence the degree of vasoconstriction. Thus, the normal irregular sympathetic discharge pattern in itself has a bearing on the physiology of neuro‐effector control mechanisms.
Cerebrovascular responses to haemorrhagic hypotension in anaesthetized cats. Effects of α‐adrenoceptor antagonists
Authors: EDVINSSON L. , MacKENZIE E. T. , ROBERT J‐P. , SKÄRBY T. , YOUNG A. R.
Published: December 2008

Haemorrhagic hypotension induces the phenomenon of cerebrovascular autoregulation and, concomitantly, involves an activation of the sympathetic nervous system. As brain vessels in cats have an atypical adrenoceptor distribution we studied the effects of an a‐adrenoceptor antagonist on the autoregulatory response to haemorrhage. Cortical blood flow was studied by the H2technique in chloralose‐anaesthetized cats subjected to a period of graded haemorrhage over 3 h. Three groups of cats were studied: control, i.e. those receiving saline (n= 10); yohimbine‐treated (200/μg‐kg‐1h‐1,n= 7); and prazosin‐treated (50μg‐kg‐1h‐1,n= 6). In the control group, cortical blood flow remained relatively constant when mean arterial pressure was decreased from 102±1 mmHg (mean ± SE) to approximately 50.1 mmHg; thereafter, blood flow decreased with decreasing perfusion pressure. In the arterial pressure range 64‐55 mmHg, cortical blood flow was significantly higher in the yohimbine group (109±12 ml‐100 g‐1min‐1) compared to the control group (69 ±6 ml‐100 g‐1min‐1) and remained higher in the yohimbine‐treated cats at more extreme levels of hypotension. Blood flow did not fall significantly in the yohimbine‐treated cats until mean arterial pressures of 31 ± 1 mmHg were attained. In the prazosin‐treated cats, flow began to decrease at arterial pressures even greater than those observed in the control group. Thus, there is a sympathetic vasoconstriction of brain arteries that is primarily mediated by α2‐adrenoceptors in the feline cerebrovascular bed.