bluuebunny/crossref_metadata_2025_split huggingface dataset:
ECG‐changes in the fetal Iamb during asphyxia in relation to beta‐adrenoceptor stimulation and blockade
Authors: Hökegård K.‐H. , Karlsson K. , Kjellmer I. , Rosen K. G. 
Published: December 2008

AbstractProgressive changes in the S‐T interval of the fetal electrocardiogram (FECG) were studied in 14 lamb fetuses, acutely exteriorized and subjected to graded hypoxia. The aims of the study were to investigate whether beta‐adrenoceptor stimulation and hypoxia exerted additive or potentiating effects on the FECG and several cardiovascular parameters and whether the hypoxic changes of the FECG could be blocked by beta‐adrenoceptor blocking agents. The FECG changes were studied in order to correlate them with cardiovascular function, as measured by heart rate, mean arterial pressure, end diastolic pressure, maximum dP/dt and combined cardiac output, estimated by the thermodilution method, as well as with blood gases, acid base status, blood lactate and glucose. Injections of small doses (0.02 to 0.4 μg kg‐1 min‐1) of isoprenaline induced the same pattern of changes in the FECG as we have previously recorded during hypoxia. By increasing the isoprenaline dose an increase in the duration of the FECG changes and amplitude of the T‐wave changes was obtained. Propranolol was found to completely abolish the FECG changes induced by isoprenaline, as well as by mild hypoxia. During severe hypoxia the FECG changes could not be abolished by propranolol. Our previous findings indicated that the hypoxic changes could be regarded as a sign of myocardial glycolysis. Thus, the present finding that even small doses of isoprenaline given to the fetus, initiates the same pattern of FECG changes corroborate this hypothesis.
Metabolic effects of blood flow restriction in adipose tissue
Authors: Belfrage E. , Hjemdahl P. , Fredholm B. B. 
Published: December 2008

AbstractThe metabolic effects of blood flow restriction were studied in isolated blood‐perfused canine subcutaneous adipose tissue. Blood flow restriction (on the average to 20 per cent of control flow) was caused by either mechanical clamping of the arterial inflow or by i.a. injections of methoxamine or angiotensin. Glucose uptake in the adipose tissue was reduced during blood flow restriction. This was partially compensated for by a period of increased glucose uptake following restoration of flow. Blood flow restriction also caused an increase in the venous lactate/pyruvate ratio. The basal lipolytic rate was decreased during blood flow restriction. Lipolysis induced by brief (5 min) sympathetic nerve stimulation (4 Hz) was not inhibited by blood flow restriction as the total amount of glycerol released from the tissue was unaffected. The outflow rate was reduced during blood flow restriction, but glycerol trapped within the tissue was apparently not reutilized by the fat cells as it was released upon flow restoration. FFA outflow following nerve stimulation was, however, inhibited suggesting increased reutilization of FFA within the tissue. This increased reutiliza‐tion may ultimately be caused by the observed change in red./ox.‐balance and/or by the limited carrier capacity (albumin) available during blood flow restriction. Three main conclusions may be drawn from the present results. Firstly, plasma levels of glycerol and FFA do not necessarily reflect adipose tissue lipolysis at a given moment. Secondly, the decreased adipose tissue blood flow seems to be a major cause of the lowered FFA‐levels during hemorrhage. Thirdly, in contrast to hemorrhage, even severe reduction of adipose tissue blood flow is insufficient to cause irreversible ischemic damage.
Lack of specific prostaglandin antagonistic effects of 7‐oxa‐13‐prostynoic acid on ovarian metabolism in vitro
Authors: Magnusson Claes , Selstam Gunnar , Ahrén Kurt 
Published: December 2008

AbstractProstaglandins (PGs) have been proposed to function as obligatory intermediates in the action of luteinizing hormone (LH) (Kuehl et al. 1970). This was based on experiments on isolated mouse ovaries where the substance 7‐oxa‐13‐prostynoic acid (7‐oxa‐13‐PA) was found to block the effect of both PGE1 and LH on ovarian cyclic AMP formation and progesterone synthesis. We have studied whether 7‐oxa‐13‐PA acts as a PG antagonist also on the isolated rat ovary, where PGs of the E type have many effects. Prepubertal rat ovaries were incubated up to 4 h in modified Krebs bicarbonate buffer containing glucose with PGE1 and 7‐oxa‐13‐PA, alone and in combination. PGEj stimulated the uptake of the non‐utilizable amino acids a‐aminoisobutyric acid (AIB) and cycloleucine in an equally wide dose‐range as has earlier been found for the stimulation of lactic acid and cyclic AMP production as well as protein synthesis. 7‐oxa‐13‐PA alone, in concentrations exceeding 25 μMg/ml, stimulated lactic acid production, but inhibited the incorporation of labelled leucine and the uptake of AIB. The uptake of cycloleucine was slightly stimulated. 7‐oxa‐13‐PA did not antagonize the PGE1 effect on lactic acid production. 7‐oxa‐13‐PA diminished the PGE1 effect on the uptake of amino acids and the incorporation into protein, but only in concentrations where it in itself inhibited the protein synthesis. These results show that 7‐oxa‐13‐PA does not act as a PG‐antagonist in the prepubertal rat ovary, since it cannot block the effects of PGs without having marked inherent effects.
Apparent and true vascular resistances to flow in SHR and NCR kidneys as related to the pre/postglomerular resistance ratio
Authors: GÖTHBERG GUNNAR , LUNDIN STEFAN , RlCKSTEN SVEN‐ERIK , FOLKOW BJÖRN 
Published: December 2008

AbstractIn maximally vasodilated SHR and NCR kidneys, perfused with filtrable and non‐filtrable perfusates, analyses have been performed concerning the extent of average renal tissue pressure (Pt) elevation which occurs upon glomerular filtration and causes passive autoregulation of flow. The results illustrate the great importance of distinguishing between ‘apparent’ (PA — PV/flow) and ‘true’ (PA — Pt/flow) renal resistance to flow. This is particularly so when the compared SHR and NCR renal vascular beds differ not only in true total renal resistance but also concerning the structurally determined ratio between the pre‐ and postglomerular resistances. The combined results show that this ratio is considerably elevated in adult SHR kidneys because of structural vascular changes, which is perhaps the most efficient way of resetting the ‘long term barostat function’ of the kidneys in hypertension. It is also illustrated how the altered pre‐/post‐glomerular ratio in SHR in combination with Pt rises can so markedly distort the results of apparently precise in vitro comparisons of SHR and NCR renal vascular beds as to give entirely misleading results, with underestimations of the structurally based vascular hyperreactivity of the preglomerular section in SHR.
Lipoprotein‐lipase activity of human skeletal‐muscle and adipose tissue after intensive physical exercise
Authors: LITHELL HANS , HELLSING KRISTOFFER , LUNDQVIST GUDMAR , MALMBERG PER 
Published: December 2008

AbstractSeven young, healthy subjects performed bicycle exercise with a working load leading to exhaustion after one hour of work. The tests were done in the afternoon in the fed state. The serum insulin concentrations decreased from 22 to 4 mU/1 and plasma glucagon increased from 241 to 340 pg/1 already after 30 min of work. The level of adipose tissue lipoprotein lipase activity (LPLA) did not fall as had been expected, but increased. The skeletal muscle LPLA was unchanged. The results indicate that during the first hour of heavy exercise the heparin‐releasable LPLA in tissues is not influenced by the work induced changes in serum hormone levels.
Axonal transport of adrenaline, noradrenaline and phenylethanolamine‐N‐methyl transferase (PNMT) in sympathetic neurons of the cod, Gadus morhua
Authors: ABRAHAMSSON TOMMY 
Published: December 2008

AbstractThe axonal transport of adrenaline, noradrenaline and phenylethanolamine‐N‐methyl transferase (PNMT) has been studied in vivo in sympathetic neurons of the splanchnic nerve in the cod,Gadus morhua.Adrenaline and noradrenaline are transported at a mean axonal transport rate of 16 mm/day. After correction for a non‐mobile fraction of adrenaline and noradrenaline, which does not contribute to the amine accumulation proximal to a ligature, a maximal rate of transport was calculated to about 45 mm/day for both amines. The increased level of catecholamines in front of a ligature could be depleted by reserpine treatment, which strongly suggests that both amines are stored in granules. PNMT is transported at a slow rate of 2 mm/day. The subcellular distribution of the cod PNMT was exclusively non‐particular. The cod PNMT was further characterized by studying substrate specificity, temperature and pH optima. It is concluded that adrenaline and noradrenaline, stored in granules, are transported in a proximo‐distal direction at a high rate compared to PNMT.
Release of3H‐noradrenaline from the rat vas deferens under various in vitro conditions
Authors: ROSS SVANTE B. , KELDER DIANA 
Published: December 2008

AbstractThe release of3H‐(‐)‐noradrenaline (NA) from rat vas deferensin vitrowas examined under various experimental conditions. It was found that in normal and reserpinized vas deferens the release of NA evoked by (+)‐amphetamine (5 times 10−6M) or low external Na+(26 mM) was antagonized by imipramine methiodide and desipramine, inhibitors of the NA uptake, but was not dependent on the presence of Ca2+in the medium and was not antagonized by the potent local anaesthetic agent bethoxycaine. The release evoked by veratridine in reserpinized tissue was antagonized by the uptake inhibitors but was in normal tissue only partially inhibited in presence of Ca2+but almost completely in absence of Ca2+. The release by high K+(117 mM) + low Na+(26 mM) in normal tissue was dependent on the presence of Ca2+and was antagonized by the muscarinic agonists carbacholine and metacholine and by high concentrations of desipramine. In the reserpinized vasa the corresponding release was not dependent on Ca2+and was not antagonized by the muscarinic agents but was inhibited by high concentrations of desipramine.
Different effects of furosemide on urinary excretion of prostaglandin E2and F2αin rabbits
Authors: OLIW ERNST , ÄNGGÅRD ERIK 
Published: December 2008

AbstractThe effect of a constant infusion of furosemide (130 μg/min i.v. for 60 min, n = 8) was studied on urinary excretion of water, electrolytes and immunoreactive prostaglandin E2(iPGE2) and iPGF2αin chloralose‐urethane anesthetized rabbits. During the furosemide infusion sodium and water excretion increased tenfold and the excretion of potassium and iPGE2two to three times. The excretion of iPGF2α(0.06 ± 0.03 μg/min/100 g kidney weight) was not significantly changed during the furosemide infusion but increased markedly after the infusion and reached a maximum (1.0 ± 0.6 μg/min/100 g) 30 to 45 min later, while the small increase in iPGE2excretion at this time could be attributed to cross‐reaction with PGF2αThe results indicate that PGE2might possibly be involved directly in the action of furosemide, while PGF2αmight participate in sodium and water conserving mechanisms in the rabbit kidney, activated by the drug induced diuresis.
Delayed hypoperfusion in the cerebral cortex of the rat in the recovery period following severe hypoglycemia
Authors: SIESJÖ BO K. , ABDUL‐RAHMAN ALI 
Published: December 2008

Male Wistar rats were starved for 24 h before being injected with insulin (Novo Actrapid®) in a dose of 40 Iukg‐1 i.p. They were then anesthetized with 2–3% halothane, tracheotomized, immobilized with tubo‐curarine chloride (1.5 mg‐kg‐1, i.v.) and connected to a respirator delivering nitrous oxide‐oxygen (3:1). Femoral arterial catheters were inserted for blood pressure recording and blood sampling, and a femoral vein was cannulated for infusions. Goldplated screws were inserted in the skull bone for frontoparietal recording of EEG. Arterial PCO2was adjusted to 35–40 mmHg and body temperature was maintained close to 37oC.Local cerebral blood flow (1‐CBF) was measured with the autoradiographic 14C‐iodoantipyrine technique of Sakurada et al. (1978) as described in detail in a previous communication (Abdul‐Rahman et al. 1979). Measurements were performed in animals in which the spontaneous EEG activity had ceased for 30 min, as well as in those that had been allowed recovery periods of either 5, 30 or 90 min. Recovery was induced by i.v. injection of 0.5 ml of a 50% (w/v) glucose solution in saline followed by i.v. infusion (1 ml/h).
A metabolic basis for the selective vulnerability of neurons in status epilepticus
Authors: SIESJÖ BO K. , ABDUL‐RAHMAN ALI 
Published: December 2008

Unstarved, male Wistar rats (290–410 g) were anesthetized with 2–3% halothane, tracheotomized, and connected to a respirator delivering 70% N20 and 30% 02. Catheters were placed in the femoral arteries and in one femoral vein. Gold‐plated screws were inserted in the skull bone for recording of (frontoparietal) EEG. When the operative procedures were completed, halothane supply was discontinued. Arterial PCO2 was adjusted to 35–40 mmHg, and body temperature was maintained close to 37oC.The animals were allowed a steady state period of about 30 min before seizures were induced by the i.v. injection of bicuculline (1.2 mg‐kg‐1, see Chapman et al. 1977). Just before the injection the animals were bled to a mean arterial blood pressure of about 120 mmHg to avoid too excessive an increase in pressure at the onset of seizures. Local CMRg1 was determined with the method described by Sokoloff et al. (1977). In summary, after 20 min of seizure activity 1 ml of a 14C‐deoxyglucose solution (New England Nuclear), containing 30 μCi, was injected i. v. Over the next 30 min, repeated arterial blood samples were taken for determination of plasma glucose concentration (hexokinase method) and ,4C activity (liquid scintillation counting). At the end of this period, the animals were decapitated and the brains were prepared for quantitative autoradiography. Local CMRgl was calculated from the integrated plasma activity and from the 14C activity in tissue. The latter was determined from the X‐ray films by microdensitometry, either manually (see Abdul‐Rahman et al. 1979) or, in one case, with the automatic microscanning equipment developed in the Laboratory of Cerebral Metabolism, NIMH, Bethesda (courtesy of Dr Louis Sokoloff).
Priority of blood flow to splanchnic organs in humans during pre‐ and post‐meal exercise
Authors: ERIKSEN M. , WAALER B. A. 
Published: December 2008

Cardiac output and superior mesenteric arterial flow in five healthy young men were followed using Doppler ultrasound techniques at rest and during 4 min bouts of bicycle exercise in both a pre‐ and a post‐meal situation. The meal given was mixed and heavy, with an energy content (related to body size) of about 1400–1600 kcal (5.9‐6.9 MJ). Two levels of exercise, 50–65 W and 150–200 W (about 75% of Votmax), were tested, with the subjects cycling in a reclining position.Superior mesenteric arterial flow increased threefold, to about 1.11 min‐1, after the meal. During exercise in the fasting situation there were only modest changes in splanchnic vascular conductance, and moderate increases in superior mesenteric arterial flow were actually recorded. Exercise in the post‐prandial state caused appreciable reductions in splanchnic vascular conductance, and a 38% reduction was observed during the most heavy exercise. However, not even such a decrease in conductance resulted in any definite reduction in superior mesenteric arterial blood flow, which was maintained at the pre‐exercise level.Cardiac output increased by about 1.3 1 min‐1 after the meal. The exercise‐induced increases in cardiac output were of the same order in the fasting and in the post‐prandial state. Variance analyses showed the high cardiac output levels reached during postprandial exercise to be no different from levels that would be reached by pure summation of the changes caused by eating alone and by exercise alone.It is concluded that blood flow to the splanchnic organs in reclining man retains its high pre‐ and post‐prandial priority during short exercise bouts of up to 75% of VoSmax.
Haemorrhage‐induced splenic vasodilation in the rat is mediated by sympathetic vasomotor nerves
Authors: IVERSEN P. O. , BENESTAD H. B. , NICOLAYSEN G. 
Published: December 2008

A marked decrease in splenic vascular resistance, with an increase in blood flow to the spleen, occurs already 5 min after an acute and severe hypotensive bleeding in awake rats. This response is virtually abolished in rats pretreated with a β‐adrenergic blocking agent. We have now studied the contribution of the sympathetic vasomotor innervation and of adrenal gland‐derived catecholamines to the splenic vasodilation.Splenic blood flow was determined with the microsphere method in heavily bled (1.5% of body weight) awake rats. The sympathetic neurones in one group of rats had been chemically destroyed with 6‐hydroxydopamine. In another group of rats we had removed the adrenal glands.In the control and in sympathectomized rats, splenic vascular resistance fell to 35 and 64%, respectively, of baseline 5 min after bleeding. Splenic blood flow about doubled during this period in the control rats, and then declined gradually to baseline over the next 24 h. In the sympathectomized rats, splenic blood flow decreased gradually over the first 12 h to reach 66% of baseline. The removal of the adrenal glands did not appreciably influence the splenic vascular response to bleeding.We conclude that an increased activity in the splenic sympathetic vasomotor neurones is a prerequisite for the observed vasodilation and concomitant large increase in splenic blood flow after haemorrhage in intact, awake rats. Catecholamines from the adrenal glands did not contribute detectably to the splenic vasodilation.
Oxygen or low concentrations of nitric oxide reverse pulmonary vasoconstriction induced by nitric oxide synthesis inhibition in rabbits
Authors: PERSSON M. G. , KALZÉN H. , GUSTAFSSON L. E. 
Published: December 2008

The objective of this study was to investigate the role of nitric oxide and oxygen in the regulation of pulmonary vascular resistance, especially by means of substitution with nitric oxide after inhibition of endogenous nitric oxide formation. In artificially ventilated open‐chest rabbits pulmonary vascular resistance at normoxic ventilation (F102= 21%) was 56±6cmH2O ml‐1 mim‐1 1000‐1 (mRUL). Nw‐nitro‐L‐arginine methyl ester (l‐NAME, 30 mg kg‐1), an inhibitor of NO synthase, increased pulmonary vascular resistance to 122±17 mRUL at normoxic ventilation. In response to l‐NAME there was also an increase in mean arterial blood pressure. Exogenous nitric oxide (0.014‐9 p.p.m. in the inhaled air) dose‐dependently and reversibly counteracted the effect of l‐NAME on pulmonary vascular resistance at normoxic ventilation, without affecting systemic blood pressure. In addition, the L‐NAME‐induced vasoconstriction was critically dependent on oxygen. Thus, during hypoxic ventilation (F1O2= 10%) the pulmonary vascular resistance was increased approximately four‐fold by the presence of L‐NAME (30 mg kg‐1), and increments in F,02 (21–100%) dose‐dependently and reversibly counteracted the effect of L‐NAME on pulmonary vascular resistance.Taken together these findings demonstrate that inhalation of low doses of NO may act as a replacement when endogenous NO synthesis is inhibited, and that pulmonary vasoconstriction induced by NO synthesis inhibition is likely to be the result of interference with oxygen‐dependent regulatory mechanisms. Endogenous NO cooperates with oxygen to evoke a vasodilator component of the pulmonary hypoxic pressor response, balancing a hitherto unknown constrictor mechanism.
Ionic selectivity of the mechano‐electrical transduction channels in the hair cells of the frog sacculus
Authors: Jørgensen F. , Kroese A. B. A. 
Published: December 2008

In the isolated saccular macula of Ratio, esculenta extracellular hair cell receptor currents evoked by mechanical stimulation of the otolithic membrane were recorded under transepithelial voltage clamp conditions. The ionic selectivity of the mechano‐electrical transduction channels of the hair cells was determined by examining the effects of different concentrations of Ca2+ and K+ in the apical solution on the transepithelial voltage at which the extracellular receptor current was zero (Vrev).Changing the concentration of Ca2+ from 0.26 mM to 0.026 and to 2.6 mM at a constant K+ concentration caused changes in Vrev of – 15 + 7 mV (mean±SD; n= 9) and 20±6mV (n= 13), respectively. The relative ionic permeabilities of the transduction channels were estimated from a modified Goldman, Hodgkin and Katz equation, assuming that 80% of the transepithelial resistance is located in the apical membranes of the hair cells. The permeability of the transduction channels for Ca2+ was found to be two orders of magnitude larger than that for K+. The measured effects on Vrev of changing the concentration of K+ at constant ionic strength and at different constant Ca2+ concentrations were well predicted by the same equation.These results indicate that the transduction channels of the frog saccular hair cells are highly selective to Ca2+.
Regional cerebral oxidative and total glucose consumption during rest and activation studied with positron emission tomography
Authors: BLOMQVIST G. , SEITZ R. J. , SJÖGREN I. , HALLDIN C. , STONE‐ELANDER S. , WIDEN L. , SOLIN O. , HAAPARANTA M. 
Published: December 2008

The relationship between regional oxidative and total rCMR in five healthy volunteers in activated and non‐activated areas of the brain has been investigated with positron emission tomography (PET). The tracers [l‐uC]‐D‐glucose and [2‐18F]2‐fluoro‐2‐deoxy‐D‐glucose were used. A previous study has shown that the former may be used to measure the rate of glucose oxidation while the latter tracer is used to measure the total rate of glucose consumption. Regional activation was performed (voluntary finger movements). Use of a computerized brain atlas enabled comparison between the regional oxidative and total rCMRglc in each volume element of the brain for the group of subjects.The values of total and oxidative rCMRgle, when calculated for each volume element of the brain and displayed in a scatter plot, were found to be symmetrically grouped around a straight line which passes close to the origin. The slope of this line varied between the subjects. This indicates that, on the average, the fraction of non‐oxidative glucose utilization is constant within each subject, regardless of the value of rCMRgle and, further, that the fraction of non‐oxidative glucose utilization varies between subjects.The total and oxidative CMRglc in the activated left hand area were 23.4 + 0.9% (mean + SEM) and 11.7 + 0.3%, respectively, higher than in the contralateral homologous non‐activated area. Our interpretation of the difference is that regional activation increases the fraction of non‐oxidative glucose consumption. This interpretation is supported by a previous PET study using [150]Oa, and by studies using MRS technique.