bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ischaemia‐induced injury in glycogen‐depleted skeletal muscle. Selective vulnerability of FG‐fibres
Authors: JENNISCHE EVA 
Published: December 2008

JENNISCHE, E. 1985. Ischaemia‐induced injury in glycogen‐depleted skeletal muscle. Selective vulnerability of FG‐fibres. Acta Physiol Scand, 125,727–734. Received 16 April 1985, accepted 20 July 1985. ISSN 0001–6772. Department of Histology, University of Göteborg, Sweden.The effect of preischaemic glycogen‐depletion on the development of skeletal muscle injury was investigated in rats subjected to tourniquet hind‐limb ischaemia. Glycogen depletion was performed by direct electrical stimulation of the extensor digitorum longus (EDL) muscle during ischaemic conditions. The metabolite load during the subsequent 2.5 h of ischaemia was modified by allowing, or not allowing, a short reperfusion period after termination of the electrical stimulation. The extent of injury was evaluated morphologically after 5 or 15 h of reperfusion, by the combination of an intravital dye exclusion test and a histochemical staining, demonstrating calcium‐precipitates‐Alizarin red S. Minimal damage was found in animals subjected to ischaemia without preceding glycogen depletion. In both groups of preischaemically glycogen‐depleted animals, significant irreversible injury occurred. The injury was significantly less in animals in which a wash‐out period was allowed after termination of stimulation. Fast‐glycogenolytic fibres (FG) were most sensitive to the ischaemic insult during both experimental conditions, while slow‐oxidative fibres (SO) were spared. Fast‐oxidative‐glycogenolytic fibres (FOG) showed an intermediate response. The injury seemed to be established after 5 h of reperfusion, indicating that cells react with an all‐or‐nothing response in the present model.
Effects of a toxic phospholipase A2 (AgTx) from the venom of the Pit viper (Agkistrodon halys (Pallas)) on the crayfish stretch receptor neuron
Authors: RYDQVIST B. , ZHOU J.‐Y. , OTTOSON D. , JIANG M.‐S. , HEILBRONN E. , HAGGBLAD J. 
Published: December 2008

Rydqvist, B., Zhou, J.‐Y., Ottoson, D., Jiang, MA, Heilbronn, E. & Häggblad, J. 1987. Effects of a toxic phospholipase A2 (AgTx) from the venom of the Pit viper (Agkistrodon halys (Pallas)) on the crayfish stretch receptor neuron. Acta Physzol Scand130, 299–305. Received 15 October 1986, accepted 22 December 1986. ISSN 0001–6772. Department of Physiology II, Karolinska Institute, and Unit of Neurochemistry and Neurotoxicology, University of Stockholm, Stockholm, Sweden.Neurotoxicity of an isolated fraction (V) of the venom from the snake Agkistrodon halys (Pallas) was studied on the crayfish stretch receptor using a two‐electrode voltage‐clamp technique. The toxin was previously shown to have less phospholipase A2 activity but to be more toxic in mice compared with bee venom phospholipase A2. At 5 μg ml‐1 (0.35 μM) the AgTx had very little effects on the electrophysiological properties of the receptor neuron whereas at 50 μg m1‐‐1 (3.5 μ) the leak conductance was increased about three times and the net outward (K) current was reduced to 70% of control. The net inward (Na) current was not affected except for a small (+10 mV) shift in the I‐V relationship. The resting membrane potential and the membrane capacitance were not changed by AgTx. These effects of AgTx were similar to those seen after exposure to bee venom phospholipase A, at concentrations 10–20 times lower. At concentrations of AgTx which presynaptically affect the frog neuromuscular transmission (5–10 μg ml‐1) the effects on ion channels in the stretch receptor neuron are very small and probably reflect the low phospholipase A, activity compared with that of bee venom phospholipase A2.
Acute blockade of β1‐receptors in the asphyxiated sheep fetus
Authors: DAGBJARTSSON A. , KJELLMER I. , ROSÉN K. G. 
Published: December 2008

Acute blockade of β1‐receptors in the asphyxiated sheep fetus. Acta Physiol Scand 130, 381–385. Received 5 November 1986, accepted 9 February 1987. ISSN 0001–6772. Department of Paediatrics, Landspitalinn, University Hospital, Reykjavik, Iceland and Department of Physiology and Department of Paediatrics I, University of Goteborg, Sweden.The effects of acute β1‐blockade on fetal cardiovascular reactions during asphyxia were evaluated in 11 exteriorized sheep fetuses. Gestational age was 110–142 days. Asphyxia was induced either by ventilating the mother with low oxygen gas mixture or by mechanical reduction of placental blood flow. During asphyxia all fetuses reacted to metoprolol injection with a decrease in heart rate, myocardial contractility, cardiac output and arterial blood pressure. Five experiments resulted in irreversible fetal cardiovascular collapse. Isoprenaline was given to the fetuses during hypoxia to test the ability to further increase heart rate and activate myocardial β‐adrenoceptors. In those experiments with fetal cardiovascular demise after metoprolol, the isoprenaline injection did not result in a significant tachycardia. The surviving fetuses could increase their heart rate as a sign of a capacity to further increase the sympatho‐adrenergic drive.
Bleeding‐induced decrease in duodenal HCO‐3 secretion in the rat is mediated via α2‐adrenoceptors
Authors: JÖNSON C. , FÄNDRIKS L. 
Published: December 2008

Bleeding‐induced in duodenal HCO‐3 secretion in the rat is mediated via α2‐adrenoceptors. Acta Physiol Scand 130, 387–391. Received 23 January 1987, accepted 23 February 1987. ISSN 6001–6772. Department of Physiology, University of Göteborg, Sweden.This study was performed on chloralosed rats in order to examine the influence of a minor blood loss on duodenal HCO‐3 secretion. The HCO‐3 output was measured by in situ titration in a duodenal segment. Blood loss of 0.6 ml per 100 g body wt (approximately 10% of total blood volume) reduced duodenal HCO‐3 secretion by about 30%. Pretreatment with guanethidine did not affect basal output of HCO‐3 but markedly reduced the bleeding‐induced response. The α2‐adrenoceptor antagonist yohimbine did not affect the basal secretion but almost abolished the depression of duodenal HCO‐3 secretion due to blood loss. Pretreatment with the a,‐adrenoceptor antagonist prazosine or the β‐adrenoceptor antagonist propranolol did neither change basal duodenal HCO‐3 secretion nor the bleeding‐induced decrease in duodenal HCO‐3 secretion. It is suggested that a small blood loss by means of a reflex activation of the sympathetic nervous system, and via the release of transmitter substances from adrenergic nerve endings, reduces the duodenal HCO‐3 secretion. The inhibitory effect is mainly due to activation of α2‐adrenoceptors.
Nervous control of tracheal blood flow in the cat measured by the laser Doppler technique
Authors: MARTLING C.‐R. , GAZELIUS B. , LUNDBERG J. M. 
Published: December 2008

Nervous control of tracheal blood flow in the cat measured by the laser Doppler technique. Acta Physiol Scand 130, 409–417. Received 2 December 1986, accepted 9 February 1987. ISSN 0001–6772. Department of Anaesthesia. Karolinska Hospital and Departments of Pharmacology and Endodontics, Karolinska Institute, Stockholm, Sweden.The tracheal blood flow as determined by the laser Doppler technique was continuously monitored in anaesthetized cats. Electrical stimulation of the right superior laryngeal nerve caused an atropine‐resistant increase in blood flow of the upper trachea. Unilateral vagal nerve stimulation at the cervical level in the presence of atropine induced a frequency‐dependent increase in blood flow of the lower trachea. Intermittent stimulation with bursts of impulses at a high frequency resulted in a considerably larger blood flow increase than a continuous low frequency stimulation giving the same total number of impulses. The ganglionic blocking agent chlorisondamine abolished most of the vagally induced increase in tracheal blood flow when using low threshold parameters (2 V, 0.2 ms) presumably activating preganglionic nerves. High threshold stimulation (10 V, 5 ms) however, still resulted in an increased blood flow suggesting antidromic activation of sensory C fibres. Local mechanical irritation or chemical irritation by capsaicin also increased tracheal blood flow. Furthermore, local application of calcitonin gene‐related peptide on to the mucosa caused a slowly developing, long‐lasting increase in blood flow. Electrical stimulation of the cervical sympathetic trunk and local application of adrenaline reduced tracheal blood flow. In conclusion, vagal nerve stimulation induces an atropine‐resistant increase in tracheal blood flow probably mainly by activating preganglionic parasympathetic nerves and possibly also by antidromic stimulation of C‐fibre afferents.
Lack of casual relationship between medullary blood congestion and tubular necrosis in postischaemic kidney damage
Authors: ANDERSSON G. , JENNISCHE E. 
Published: December 2008

Lack of casual relationship between medullary blood congestion and tubular necrosis in postischaemic kidney damage. Acta Physiol Scand 130, 429–432. Received 29 December 1986, accepted 23 February 1987. ISSN 0001–4772. Department of Histology, Gothenburg University, Sweden.The effect of haemodilution on medullary blood congestion and tubular necrosis was investigated in the rat kidney. Male Sprague‐Dawley rats were subjected to 60 min of unilateral, kidney ischaemia and 24 h of reperfusion. Haemodilution was performed by replacing blood by homologous serum and was done either before induction of ischaemia or during the ischaemic period. Cellular necrosis was evaluated morphologically by a histochemical staining for calcium and a dyeexclusion test. Trapped erythrocytes were visualized by the DAB reaction. It was found that haemodilution could totally prevent medullary congestion. In spite of this, the extent and distribution of necrotic tubular cells in the outer stripe of the outer medulla were the same whether the animal was subjected to haemodilution or not. Our results strongly suggest that the cellular necrosis and the medullary congestion are two separate phenomena occurring at the same time, but without a causal relationship to each other.
Mean power frequency and integrated electromyogram of repeated isokinetic plantar flexions
Authors: GERDLE B. , HEDBERG R. , JONSSON B. , FUGL‐MEYER A. R. 
Published: December 2008

Mean power frequency and integrated electromyogram of repeated isokinetic plantar flexions. Acta Physiol Scand 130, 501–506. Received 29 October 1986, accepted 23 February 1987. ISSN 001–6772. Work Physiology Division, National Board of Occupational Safety and Health, and Department of Physical Medicine and Rehabilitation, University of Umeå, Umeå, Sweden.Peak torque (PT), contraction work (CW), mean power (CP), and time for contraction (t) were recorded for each of 200 full range‐of‐motion repetitive isokinetic (maximum effort) plantar flexions at the preset angular velocity 60 degrees s‐1 (°.s‐1). The subjects were 12 healthy males (42–46 years). Simultaneous recordings of electro‐myographic activity of the three parts of the triceps surae muscle were made. The electromyograms were truly integrated and the mean power frequency was also calculated for each of the contractions. The mechanical variables decreased steeply during approximately the first 70 contractions (the fatigue phase) followed by a steadystate level (the endurance level) with no further significant decrease. The fatigue phase was composed of two parts. The first was characterized by decreases in CW, MPF and in the ratio CW/iEMG, while iEMG and iEMG/t were unaltered. During the second part decreases in iEMG and iEMG/t occurred while MPF and CW/iEMG had stabilized. During the endurance level all the variables were stable but lowered when compared with the initial contractions of the fatigue phase. The results indicated that the mechanical fatigue went through two parts before the steady‐state level was established.
Role of dopamine2‐receptors in mediating renal vascular response to low dose dopamine infusion in the rat
Authors: SERI I. , EKLÖF A. C. , APERIA A. 
Published: December 2008

Role of dopamine2‐receptors in mediating renal vascular response to low dose dopamine infusion in the rat.Acta Physiol Scand130, 563–569. Received 6 November 1986, accepted 15 March 1987. ISSN 0001–6772. Department of Developmental Physiology, Karolinska Institute, St Göran's Children's Hospital, Stockholm, Sweden.The effects of the interaction of dopamine (DA) and the DA2‐receptors on regional blood flows and cardiac output have been studied in the rat. By means of the microsphere technique the blood flow (BF) and vascular resistance (VR) were determined in the kidney, duodenum, spleen, liver, and lung during infusion of DA in the absence and presence of selective DA2‐receptor blockade with S‐Sulpiride (S‐SP), and during infusion of a selective DA2‐receptor agonist (LY‐171555, LY). In order to evaluate the role of the presynaptic DA2‐receptor, the experiments were performed without α‐ and β‐adrenergic blockade. Dopamine was given in such low doses that stimulation of the adrenergic receptors should be negligible. Dopamine, LY and DA + S‐SP did not significantly influence BF and VR in the spleen, liver and lung. Dopamine significantly increased BF and decreased VR in the kidney and the duodenum; LY significantly increased BF in the the kidney but not in the duodenum and decreased VR in both the kidney and the duodenum. In the presence of selective DA,‐receptor blockade, DA did not significantly influence BF or VR in the kidney but in the duodenum BF increased and VR decreased to the same extent as in the absence of blockade. In conclusion; the kidney and the intestine are more abundantly supplied with vascular DA‐receptors than other organs. In the kidney the interaction between DA and the DA2‐receptors significantly contributes the the DA‐induced vasodilation. The interaction between DA and the DA2‐receptors is of less importance for the DA‐induced vasodilatation in the intestine.
Interaction of changes in the third ventricular CSF tonicity, central and systemic AVP concentrations and water intake
Authors: ERIKSSON S. , SIMON—OPPERMANN CH. , SIMON E. , GRAY D. A. 
Published: December 2008

Interaction of changes in the third ventricular CSF tonicity, central and systemic AVP concentrations and water intake. Acta Physiol Scand 130, 575–583. Received 23 January 1987, accepted 8 March 1987. ISSN 0001–6772. Max‐Planck‐Institut für physiologische und klinische Forschung, W. G. Kerckhoff‐Institut, Bad Nauheim, FRG and Department of Physiology I, Karolinska Institute, Stockholm, Sweden.Arginine vasopressin (AVP) is assumed to be involved as a central transmitter or modulator in the control of autonomic functions including thirst. In conscious dogs AVP concentration in cerebrospinal fluid (CSF) from the anterior part of the third ventricle (A3V) was analysed before and after local elevation of CSF osmolality by intracerebroventricular (i.c.v.) infusion of 0.35 m NaCl and after i.c.v. AVP infusion at 46 and 138 fmol ml‐1 for 10 min. In addition, the effects of these i.c.v. infusions on water intake, plasma AVP concentration and blood pressure were investigated. In euhydrated dogs 0.35 M NaCl i.c.v. did not alter AVP concentration in the CSF during the subsequent 2 h. In contrast, plasma AVP concentration had increased significantly from 3.4±0.3 (control) to 6.4 ± 0.7 and 4.7 ± 0.3 fmol ml‐1, 4 and 16 min, respectively, after the hypertonic stimulus. Drinking was stimulated with an average water intake of 14.5 ± 3.7 ml kg‐1 body wt. However, AVP infusion into the A3V did not elicit water intake despite increases of AVP concentration in the A3V by factors up to 40 above control. The same animals responded with spontaneous drinking to 0.35 m NaCl i.c.v. administered 160 min after the end of AVP infusions. Exogenously administered AVP disappeared from the A3V with a time constant of 13.8 min. The results do not support the view that AVP in the A3V CSF per se stimulates drinking.
Mechanisms underlying the small intestinal fluid secretion caused by arachidonic acid, prostaglandin E1 and prostaglandin E2 in the rat in vivo
Authors: BRUNSSON I. , SJÖQVIST A. , JODAL M. , LUNDGREN O. 
Published: December 2008

Mechanisms underlying the small intestinal fluid secretion caused by arachidonic acid, prostaglandin E1 and prostaglandin E2 in the rat in vivo. Acta Physiol Scand130, 633–442. Received 15 January 1987, accepted 27 February 1987. ISSN 0001–6772. Department of Physiology, University of Göteborg, Sweden.Prostanoids were given intraluminally (PGE2) or infused close intra‐arterially (PGE1 and PGE2) or arachidonic acid was administered intraluminally to denervated jejunal segments of the rat in vivo. These experimental manoeuvres caused a net fluid secretion, although a 1000–fold higher concentration of the prostanoids was needed from the luminal than from the vascular side. I.v. hexamethonium or serosally applied lidocaine diminished the induced fluid secretion suggesting that the prostanoids act mainly by eliciting local secretory reflexes in the enteric nervous system. This nervously mediated secretion is not accompanied by any increase in tissue CAMP. However, at higher i.a. concentrations of PGE2 there seems to be a non‐neurogenic effect on the enterocytes associated with an increase in tissue cAMP.
Biological activities of Lipoxin A include lung strip contraction and dilation of arterioles in wiwo
Authors: DAHLÉN S.‐E. , RAUD J. , SERHAN C. N. , BJÖRK J. , SAMUELSSON B. 
Published: December 2008

Biological activities of Lipoxin A include lung strip contraction and dilation of arterioles in vivo. Acta Physiol Scand130, 643–647. Received 7 December 1986, accepted 27 February 1987. ISSN 0001–6772. Departments of Physiology and Physiological Chemistry, Karolinska Institute, and Department of Experimental Medicine, Pharmacia AB, Sweden.Lipoxin A ([5s,6r,15s]‐5,6,15–trihydroxy‐7,9,13–trans‐II‐cis‐eicosatetraenoic acid), a recently characterized lipoxygenation product of arachidonic acid, in submicromolar concentrations elicited long‐lasting contractions of the guinea‐pig lung strip. The response to lipoxin A was not due to release of acetylcholine, histamine, noradrenaline or cyclo‐oxygenase products. 15–hydroperoxyeicosatetraenoic acid (15–HPETE), one precursor of lipoxin A, also contracted the lung strip, but 15–HPETE was less potent and the response was comparatively short‐lived. Furthermore, lipoxin A was inactive on the guinea‐pig trachea whereas 15–HPETE relaxed this preparation. Lipoxin A was also inactive on the guinea‐pig ileum. Intravital microscopy of the hamster cheek pouch disclosed that lipoxin A, as well as 15–HPETE, induced arteriolar dilation but had no effects on microvascular permeability or leucocyte adherence to venular endothelium. Taken together, the leucocyte product lipoxin A displayed a pattern of activity in spasmogenic assays and on the microvasculature that was distinct from those known for prostaglandins, thromboxanes and leukotrienes. The findings indicate that lipoxin A is an additional arachidonic acid derived autacoid with biological actions on smooth muscle in vatro and in vivo.
Actions of some vasodilators on isolated human hand veins
Authors: ARNER M. , HÖGESTÄTT E. D. 
Published: December 2008

Actions of some vasodilators on isolated human hand veins.Acta Physiol Scand130, 671–677. Received 7 October 1986, accepted 16 March 1987. ISSN 0001–6772. Department of Hand Surgery, Malmö General Hospital, and Department of Clinical Pharmacology, University of Lund, Sweden.Vasospasm is a well recognized complication during micro vascular surgery of the hand. In the search for new spasmolytic drug therapies, the effects of papaverine, nitroprusside, nimodipine and lidocaine on isolated human hand veins contracted by several postulated mediators of vasospasm were examined. Mechanical activity was recorded isometrically in ring segments of the vessels. Potassium ions, noradrenaline (NA), 5‐hydroxytryp‐tamine (5‐HT) and prostaglandin F2α(PGF2α) all produced strong contractions that were highly dependent on the presence of extracellular Caa+. Papaverine acted as a non‐selective vasodilator, as it produced an almost identical inhibition of contractile responses to all examined stimulants. Nitroprusside inhibited contractions induced by agonists more than those evoked by K+, whereas the opposite was found for nimodipine. Nitroprusside also seemed to display a certain degree of selectivity among the agonist‐induced responses (NA > PGFaα> 5‐HT). Lidocaine increased the contractile response to K+and at high concentrations (> 10‐‐5M)produced a contractionper se. The clinical efficacy of lidocaine as a vasodilator after topical application therefore seems to reflect an inhibitory action on vasoconstrictor nerves. Papaverine, nitroprusside, nimodipine and lidocaine differ considerably in their profiles of action and therefore deserve to be further evaluated in the treatment of vasospasm during microvascular surgery.
Functional development of the visual system in normal and protein‐deprived rats. IV. Latencies in the specific visual pathway of adult rats
Authors: SJÖSTRÖM A. , CONRADI N. G. , ANDERSSON S. A. 
Published: December 2008

Functional development of the visual system in normal and protein‐deprived rats. IV. Latencies in the specific visual pathway of adult rats. Acta Physiol Scand130, 695–703.It was recently shown that an increase in latency of the cortical visual evoked response (VER) seen in young malnourished animals persists in adult rats given a low protein diet. In the present paper the VER latencies of the specific visual pathway were measured in order to establish the level at which the latency increase occurs in protein‐deprived rats. The VER in the dorsal lateral geniculate nucleus (dLGN) showed no significant differences to onset or peak latencies between control (C) and the protein‐deprived (PD) rats. The dLGN activity was higher in C rats than in PD rats. Late components differed in median values between the two groups, but the individual variations were large. Generally, the VER of the dLGN in PD rats was more stereotype compared with the C rats. Intracortical VER at a depth of 0.4+.5 mm showed a small negative component of short onset latency in both C and PD rats. This component preceded the onset of the initial positivist recorded from the cortical surface by 1–2 ms in C rats and by 3–6 ms in PD rats. Following electical stimulation of the dLGN, no differences in onset latency of the first cortical activity (monosynaptic response) were recorded between C and PD rats, whereas later activity was significantly delayed in PD compared with C rats. The laminar potential pattern was less distinct in PD compared with C rats, and the late components of the evoked response from deep cortical layers were markedly attenuated or lacking. The cortical responses to optic tract stimulation were similar to those of dLGN stimulation, but of an increased latency corresponding to the increase in transmission distance and to the synaptic delay in the dLGN. No increase in synaptic delay through the dLGN was seen in PD rats. The results show that the increased latencies in the cortical surface VER of the PD rats originate mainly from the cortex itself.