| 51. |
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| 52. |
- Jungner, Mårten, et al.
(författare)
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Intracranial pressure following resuscitation with albumin or saline in a cat model of meningitis.
- 2011
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Ingår i: Critical Care Medicine. - 1530-0293. ; Dec, s. 135-140
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE:: To compare the intracranial pressure after resuscitation to normovolemia by using 20% albumin or normal saline in a cat model of meningitis. DESIGN:: Prospective, randomized animal study. SETTING:: University hospital laboratory. SUBJECTS:: Twenty adult, male cats. INTERVENTIONS:: Meningitis was induced by intrathecal injection of Escherichia coli-derived lipopolysaccharide (0.8 × 10 units/kg). Four hours after the lipopolysaccharide injection, the animals were randomized to intravenous treatment with 0.4 mL/kg/hr of 20% albumin or 7.5 mL/kg/hr of 0.9% sodium chloride for 6 hrs (n = 7 per group). A control group receiving lipopolysaccharide but no fluid was also studied (n = 6). MEASUREMENTS AND MAIN RESULTS:: Effects on intracranial pressure, mean arterial pressure, plasma volume (I-albumin technique), plasma oncotic pressure, and brain metabolism via cerebral interstitial lactate/pyruvate ratio and glycerol and glucose levels (microdialysis technique) were evaluated. Plasma volume decreased by approximately 20% and intracranial pressure increased from 10 to approximately 20 mm Hg at 4 hrs after the lipopolysaccharide injection. Six hours later, plasma volume had returned to baseline in both fluid groups while there was a further reduction in the control group. Intracranial pressure was higher in the saline group than in the albumin and control groups and was 25.8 ± 2.8 mm Hg, 18.3 ± 0.6 mm Hg, and 20.4 ± 1.7 mm Hg, respectively. Plasma oncotic pressure was higher in the albumin group than in the saline and control groups. Mean arterial pressure and microdialysis data were within normal range and did not differ among the groups. CONCLUSIONS:: The results showed that the choice of resuscitation fluid may influence intracranial pressure in meningitis. The lower intracranial pressure in the colloid group may be explained by a higher plasma oncotic pressure and less fluid distribution to the brain interstitium.
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| 53. |
- Jungner, Mårten, et al.
(författare)
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Prostacyclin reduces elevation of intracranial pressure and plasma volume loss in lipopolysaccharide-induced meningitis in the cat.
- 2009
-
Ingår i: The Journal of trauma. - 1529-8809. ; 67:6, s. 1345-1351
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Severe meningitis may compromise cerebral perfusion through increases in intracranial pressure (ICP) and through hypovolemia caused by a general inflammation with systemic plasma leakage. From its antiaggregative/antiadhesive and permeability-reducing properties, prostacyclin (PGI2) is a potential adjuvant treatment in meningitis, but previously published data have been ambiguous. The objective of this study was to evaluate the effects of PGI2 on meningitis on ICP, plasma volume, blood pressure, and cerebral oxidative metabolism. METHODS: Meningitis was induced by intrathecal injection of lipopolysaccharide (LPS, 0.8 x 10 units/kg) in cats. Four hours after the injection, the animals were randomized to intravenous treatment with either low-dose PGI2 (1 ng/kg/min) or the vehicle for 6 hours (n = 7 in each group). No LPS and no PGI2 or vehicle was given to three cats (sham group). Effects of treatment on ICP, mean arterial pressure, plasma volume (I-albumin technique), and brain tissue lactate/pyruvate ratio (microdialysis technique) were evaluated. RESULTS: ICP increased from 10.0 mm Hg +/- 1.3 mm Hg and 10.8 mm Hg +/- 1.7 mm Hg to 19.9 mm Hg +/- 1.7 mm Hg and 19.6 mm Hg +/- 3.3 mm Hg in the PGI2 and the vehicle group, respectively, 4 hours after the LPS injection (not significant). ICP increased further to 21.8 mm Hg +/- 4.5 mm Hg and to 25.8 mm Hg +/- 6.0 mm Hg after treatment for 6 hours with PGI2 or vehicle, respectively (p < 0.05). There was no significant difference in arterial pressure between groups. Plasma volume loss was less in the PGI2 group than in the vehicle group at the end of the experiment and urine production and arterial oxygenation was higher in the PGI2 group. Lactate/pyruvate ratio was within the normal range in all groups. CONCLUSION: Low-dose PGI2 may be a beneficial adjuvant therapy for meningitis by reducing elevation of ICP and plasma volume loss.
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| 54. |
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| 55. |
- Koskinen, Lars-Owe, et al.
(författare)
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Severe traumatic brain injury management and clinical outcome using the Lund concept
- 2014
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Ingår i: Neuroscience. - : Elsevier BV. - 0306-4522 .- 1873-7544. ; 283, s. 245-255
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Forskningsöversikt (refereegranskat)abstract
- This review covers the main principles of the Lund concept for treatment of severe traumatic brain injury. This is followed by a description of results of clinical studies in which this therapy or a modified version of the therapy has been used. Unlike other guidelines, which are based on meta-analytical approaches, important components of the Lund concept are based on physiological mechanisms for regulation of brain volume and brain perfusion and to reduce transcapillary plasma leakage and the need for plasma volume expanders. There have been nine non-randomized and two randomized outcome studies with the Lund concept or modified versions of the concept. The non-randomized studies indicated that the Lund concept is beneficial for outcome. The two randomized studies were small but showed better outcome in the groups of patients treated according to the modified principles of the Lund concept than in the groups given a more conventional treatment. This article is part of a Special Issue entitled: Brain compensation. For good?. (C) 2014 IBRO. Published by Elsevier Ltd. All rights reserved.
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| 56. |
- Lundblad, Cornelia, et al.
(författare)
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A mouse model for evaluation of capillary perfusion, microvascular permeability, cortical blood flow, and cortical edema in the traumatized brain.
- 2004
-
Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert Inc. - 1557-9042 .- 0897-7151. ; 21:6, s. 741-753
-
Tidskriftsartikel (refereegranskat)abstract
- Genetically engineered mice have successfully been used to investigate molecular and cellular mechanisms associated with cell dysfunction following brain trauma. Such animals may also offer a possibility to investigate mechanisms involved in posttraumatic hemodynamic alterations. The objective of the study was to establish a mouse model in which important hemodynamic alterations following trauma could be analyzed. C57/BL6 male mice were subjected to controlled cortical impact injury (CCI) or sham-injury. Distribution of blood flow was estimated by determining number of perfused capillaries using FITC-dextran as an intravascular marker. Cortical blood flow was measured using [(14)C]-iodoantipyrine, brain water content (BWC) was measured using a wet vs. dry weight method, and permeability surface area product (PS) was estimated by the transfer constant for [(51)Cr]-EDTA. Number of perfused capillaries in the contusion area was progressively reduced during the first 24 h following trauma by at most 60% relative to a value of 329 +/- 61/mm(2) in sham-injured animals. Blood flow in the contusion area decreased simultaneously by at most 50% relative to a control value of 1.8 +/- 0.4 mL.min(-1).g(-1), and was reduced further in subregions within the contusion area. BWC in the injured hemisphere increased from 79.3 +/- 0.5% at control to at most 79.9 +/- 0.6% at 24 h post trauma. PS in the injured hemisphere increased by 71% at 3 h post trauma relative to a control value of 0.45 +/- 0.1 microL.min(-1).g(-1), and was close to control at 24 h. The present study demonstrates that brain trauma in addition to a reduction in cortical blood flow, reduces number of perfused capillaries, which most likely affects exchange of nutrients and fluid. The CCI in mouse is likely to be a useful tool to elucidate mechanisms involved in hemodynamic alterations following brain trauma.
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| 57. |
- Lundblad, Cornelia, et al.
(författare)
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Hemodynamic and histological effects of traumatic brain injury in eNOS-deficient mice.
- 2009
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Ingår i: Journal of Neurotrauma. - : Mary Ann Liebert Inc. - 1557-9042 .- 0897-7151. ; 26:11, s. 1953-1962
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Tidskriftsartikel (refereegranskat)abstract
- Microvascular dysfunction in the brain, characterized by vasoconstriction, vascular occlusion, and disruption of the blood brain barrier, may adversely affect outcome following traumatic brain injury (TBI). Because of its vasodilating and antiaggregative properties, nitric oxide (NO) produced by nitric oxide synthase in the endothelium (eNOS) is a key regulator of vascular homeostasis. The objective of the present study was to evaluate the role of eNOS in vascular disturbances and histological outcome in the brain following TBI. Cortical blood flow ([(14)C]-iodoantipyrine technique), number of perfused capillaries (FITC-dextran technique), brain water content (wet vs. dry weight), and the transfer constant (K(i)) for [(51)Cr]-EDTA, reflecting permeability, were analyzed 3 h and 24 h after a controlled cortical impact injury (CCI) in eNOS-deficient (eNOS-KO) and wild-type (WT) mice. Cortical contusion volume and cell count in the hippocampus were evaluated 3 weeks after injury. Blood flow in the injured cortex decreased in both groups following trauma. There were no significant differences between the groups at 3 h, but blood flow was lower in eNOS-KO mice than in WT mice 24 h after trauma. Brain water content was higher in the WT mice than in eNOS-KO mice at 24 h. Number of perfused capillaries, K(i), and histological outcome were similar in both groups. We conclude that eNOS is important for maintenance of cerebral blood flow after trauma and that eNOS promotes edema formation by mechanisms other than increased permeability. The vascular effects of eNOS do not, however, influence histological outcome.
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| 58. |
- Lundblad, Cornelia, et al.
(författare)
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Increased cortical cell loss and prolonged hemodynamic depression after traumatic brain injury in mice lacking the IP receptor for prostacyclin.
- 2008
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Ingår i: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 1559-7016 .- 0271-678X. ; 28:2, s. 367-376
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Tidskriftsartikel (refereegranskat)abstract
- Prostacyclin is the major arachidonic acid metabolite of the vascular endothelium and is produced mainly via the cyclooxygenase-2 pathway. By acting on the prostacyclin (IP) receptor on platelets and vascular smooth muscle cells, prostacyclin exerts vasodilatory and antiaggregative/antiadhesive effects. Previous studies have shown that prostacyclin production increases after brain trauma, but the importance of prostacyclin for posttraumatic hemodynamic alterations and neuron survival has not been investigated. This study evaluated if endogenous prostacyclin plays a role in the pathophysiologic process in the brain after brain trauma. This was performed by comparing prostacyclin (IP) receptor-deficient (IP-/-) mice and mice with functional IP receptor (IP+/+) after a controlled cortical injury regarding contusion volume, cerebral blood flow ([14C]iodoantipyrine autoradiography), number of perfused capillaries (fluorescein isothiocyanate-dextran fluorescence technique), the transfer constant (Ki) for [51Cr]EDTA, and brain water content (wet vs dry weight) in the injured and contralateral cortex. Contusion volume was increased in IP-/- mice compared with IP+/+ mice. Three hours after trauma, cortical blood flow was decreased in the injured cortex of both groups and the reduction in blood flow in the cortex of the IP-/- mice persisted from 3 to 24 h, whereas blood flow approached normal values in the IP+/+ mice after 24 h. No differences could be detected between the two genotypes regarding other hemodynamic parameters. We conclude that the prostacyclin IP receptor is beneficial for neuron survival after brain trauma in mice, an effect that may be mediated by improved cortical perfusion.
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| 59. |
- Lundblad, Cornelia, et al.
(författare)
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Inhibition of Rho kinase decreases hydraulic and protein microvascular permeability in cat skeletal muscle.
- 2003
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Ingår i: Microvascular Research. - 1095-9319. ; 66:2, s. 126-133
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Tidskriftsartikel (refereegranskat)abstract
- Rho-associated kinases are involved in regulation of actin–myosin contractility and the organization of the actin cytoskeleton in both endothelial and smooth muscle cells. By influencing the contraction of the intraendothelial filaments, Rho kinases may affect the size of the interendothelial gaps and thereby influence microvascular permeability. The aim of the study was therefore to investigate whether Rho kinases influence hydraulic and protein microvascular permeability. The study was performed on the autoperfused cat skeletal muscle. A capillary filtration coefficient (CFC) technique was used to evaluate changes in hydraulic permeability, and protein permeability was evaluated by estimation of the change in the reflection coefficient for albumin. In the first part of each experiment, the effects on CFC of three doses of the Rho kinase inhibitor Y-27632 of about 0.35, 0.70, and 1.05 μg/h per ml plasma flow were determined. There was a reduction in CFC at the lowest dose, and a tendency to further reduction at the higher doses used, reaching a decrease in CFC of 20%. The effects on CFC of the high and the middle dose did not differ. The reflection coefficient for albumin was increased by 31% following infusion of the highest dose of Y-27632. We conclude that hydraulic and protein microvascular permeability increase by Rho kinase activation, and that Rho kinase is involved in regulation of microvascular permeability.
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| 60. |
- Lundblad, Cornelia, et al.
(författare)
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The permeability-reducing effects of prostacyclin and inhibition of Rho kinase do not counteract endotoxin-induced increase in permeability in cat skeletal muscle.
- 2004
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Ingår i: Microvascular Research. - : Elsevier BV. - 1095-9319 .- 0026-2862. ; 68:3, s. 286-294
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Tidskriftsartikel (refereegranskat)abstract
- cAMP stimulation and Rho kinase inhibition are shown to decrease microvascular permeability during noninflammatory conditions, most likely by decreasing contractility of actomyosin filaments in the endothelial cell, but their effects on permeability during inflammatory conditions are not clarified. The objective of this in vivo study, performed on the autoperfused and denervated calf muscle of the cat, was therefore to evaluate to what extent cAMP stimulation and inhibition of Rho kinase reduce permeability at endotoxemia. Change in osmotic reflection coefficient for albumin was used as a measure of altered protein permeability and change in capillary filtration coefficient (CFC) as a measure of altered fluid permeability. After inducing a significant increase in protein and fluid permeability by infusion of lipopolysaccharide (LPS), we determined to what extent the increased permeability was decreased by the cAMP stimulator prostacyclin [1.0 ng/kg/min intravenously (iv)] or the Rho kinase inhibitor Y-27632 [1.05 μg/ml plasma/h intraarterially (ia)]. These doses are known to decrease permeability under noninflammatory conditions. The reflection coefficient for albumin and CFC were determined before and during LPS, and during LPS plus prostacyclin (n = 6) or LPS plus Y-27632 (n = 6). The reflection coefficient was reduced by about 30% (P < 0.05) and CFC was increased by about 25% (P < 0.05) by LPS, and these permeability parameters were not affected by prostacyclin or Y-27632. We conclude that cAMP stimulation and Rho kinase inhibition reduce permeability by other pathways and mechanisms than those by which permeability is increased during endotoxemia.
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| 61. |
- Lundblad, Cornelia, et al.
(författare)
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Treatment with the sphingosine-1-phosphate analogue FTY 720 reduces loss of plasma volume during experimental sepsis in the rat.
- 2013
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172. ; 57:6, s. 713-718
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Increased vascular leakage leading to hypovolaemia and tissue oedema is common in severe sepsis. Hypovolaemia together with oedema formation may contribute to hypoxia and result in multiorgan failure and death. To improve treatment during sepsis, a potential therapeutic target may be to reduce the vascular leakage. Substances affecting the endothelial barrier are interesting in this respect, as it is suggested that increase in vascular leakage depends on reorganisation of the endothelial cells and breakdown of the endothelial barrier. The agonist of the bioactive lipid sphingosine-1-phosphate, FTY720, has been shown to modulate the integrity of the endothelium and reduce permeability both in vitro and in vivo. The aim of the present study was to determine if FTY720 could reduce the loss of plasma volume during experimental sepsis in rats. METHODS: Sepsis was induced by ligation and incision of the caecum in the rat. Plasma volume was determined before and 4.5 h after induction of sepsis by a dilution technique using (125) I-labelled albumin. RESULTS: FTY720 in a dose of 0.2 mg/kg reduced the loss of plasma during sepsis by approximately 30% compared with vehicle, without any adverse effects on haemodynamic and physiological parameters. The increase in hematocrit and haemoglobin concentration was also found to be higher in the vehicle group. CONCLUSION: FTY720 in a dose without haemodynamic side effects reduces loss of plasma volume during experimental sepsis most likely because of reduction in permeability and may therefore be beneficial in sepsis.
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| 62. |
- Möller, Alma, et al.
(författare)
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Beneficial effects of low-dose prostacyclin on cat intestinal perfusion during endotoxemia as evaluated with microdialysis and oxygen transport variables
- 2001
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Ingår i: Critical Care Medicine. - 1530-0293. ; 29:2, s. 351-358
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To evaluate the effects of low-dose prostacyclin on intestinal perfusion during endotoxemia. Design: A randomized, blinded experimental study. Setting: A university laboratory. Subjects: Sixteen anesthetized cats. Interventions: The animals received endotoxin by continuous intravenous infusion (0.5 mg/kg plus 0.5 mg kg(-1).hr(-1)) and a continuous volume replacement throughout the experiment. Four hours after the start of endotoxin, the animals were randomized to receive an infusion of either prostacyclin at a dose of 1 ng.kg(-1).min(-1) (prostacyclin group) or vehicle (control group) during the next 4 hrs. Measurements and Main Results: Intestinal vascular resistance was calculated from systemic arterial pressure, central venous pressure, and superior mesenteric artery blood flow, and intestinal oxygen delivery and uptake were calculated from superior mesenteric artery and vein blood samples and blood flow. Interstitial lactate, pyruvate, glucose, and glycerol in the ileal wall were measured by using microdialysis. There were no differences in baseline values between the groups, Systemic blood pressure decreased initially but recovered and remained stable in both groups. In the control group, intestinal vascular resistance increased from 10.9 +/- 1.0 to 24.7 +/- 5.3 mm Hg.mL.min(-1).kg(-1) (p < .05) at 8 hrs, and oxygen delivery decreased from 2.6 +/- 0.2 to 1.3 +/- 0.3 ml min(-1).kg(-1) (p <.05), Simultaneously, microdialysis lactate increased from 1.6 +/- 0.1 to 3.6 +/- 0.5 mmol/L (p <.05) with concomitant pyruvate increase and unchanged lactate/pyruvate ratio. Blood lactate increased and ph decreased. In the prostacyclin group at 8 hrs, intestinal vascular resistance of 6.9 +/- 0.8 mm Hg.mL.min(-1) kg(-1) was lower and intestinal oxygen delivery of 3.2 +/- 0.3 was higher (p <.05) than in the control group at 8 hrs. Intestinal oxygen uptake of 0.54 +/- 0.10 mL.min(-1).kg(-1) was higher than in the control group, in which oxygen uptake was 0.26 +/- 0.04 mL.min(-1) kg(-1). Lactate, pyruvate, and pH were normalized at 8 hrs in the prostacyclin group. Conclusion: Low-dose prostacyclin has beneficial effects on small intestinal perfusion during endotoxemia in this experimental cat model.
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| 63. |
- Naredi, S., et al.
(författare)
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An outcome study of severe traumatic head injury using the "Lund therapy" with low-dose prostacyclin
- 2001
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Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley-Blackwell. - 0001-5172 .- 1399-6576. ; 45:4, s. 402-406
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Tidskriftsartikel (refereegranskat)abstract
- Background: There are two independent head injury outcome studies using the “Lund concept”, and both showed a mortality rate of about 10%, and a favourable outcome (Glasgow outcome scale, GOS 4 and 5) of about 70%. The Lund concept aims at controlling intracranial pressure, and improving microcirculation around contusions. Intracranial pressure is controlled by maintaining a normal colloid osmotic pressure and reducing the hydrostatic capillary pressure. Microcirculation is improved by ensuring strict normovolaemia and reducing sympathetic discharge. The endogenous substance prostacyclin with its antiaggregatory/antiadhesive effects may further improve microcirculation, which finds support from a microdialysis‐based clinical study and an experimental brain trauma study. The present clinical outcome study aims at evaluating whether the previously obtained good outcome with the Lund therapy can be reproduced, and whether the addition of prostacyclin has any adverse side‐effects.Methods: All 31 consecutive patients with severe head injury, Glasgow coma scale (GCS) ≤8, admitted to the University Hospital of Umeå during 1998 were included. The Lund therapy including prostacyclin infusion for the first three days at a dose of 0.5 ng kg−1 min−1. Outcome was evaluated according to the GOS >10 months after the injury.Results: One patient died, another suffered vegetative state and 7 severe disability. Of the 22 patients with favourable outcome, 19 showed good recovery and 3 moderate disability. No adverse side‐effects of prostacyclin were observed.Conclusion: The outcome results from previous studies using the Lund therapy were reproduced, and no adverse side‐effects of low‐dose prostacyclin were observed.
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| 64. |
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| 65. |
- Persson, Johan, et al.
(författare)
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Endogenous Nitric Oxide Reduces Microvascular Permeability and Tissue Oedema during Exercise in Cat Skeletal Muscle.
- 2003
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Ingår i: Journal of Vascular Research. - : S. Karger AG. - 1423-0135 .- 1018-1172. ; 40:6, s. 538-546
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Tidskriftsartikel (refereegranskat)abstract
- Based on a proposed increase in the release of the vasodilators nitric oxide (NO) and prostacyclin during exercise, and the fact that these substances have vascular permeability-reducing properties, this study was designed to evaluate (1) possible effects of exercise on hydraulic permeability, (2) whether permeability and muscle swelling are reduced by an increased release of NO and prostacyclin during exercise and (3) whether NO and prostacyclin are involved in exercise hyperaemia. The study was performed on an autoperfused cat calf muscle preparation with ligated lymph vessels, and exercise was induced by somatomotor nerve stimulation. Change in microvascular hydraulic permeability was estimated by a capillary filtration coefficient (CFC) technique. We found that the marked muscle volume increase after the start of the exercise gradually decreased, reaching an isovolumetric state within 25 min where CFC had decreased by about 25% (p < 0.05). CFC recovered completely after exercise was stopped. The decrease in CFC was abolished during blockade of endogenous NO by the NO synthase inhibitor <i>L</i>-NAME, but was preserved during blockade of endogenous prostacyclin by tranylcypromine. The muscle volume increase during exercise was about 60% greater with <i>L</i>-NAME than during vehicle or tranylcypromine (p < 0.01). Neither <i>L</i>-NAME nor tranylcypromine had any effect on exercise hyperaemia. We conclude that microvascular hydraulic permeability is reduced during exercise, that this effect reduces exercise-induced muscle swelling, and that the effects are mediated via release of NO. NO and prostacyclin are not involved in exercise hyperaemia.
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| 66. |
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| 67. |
- Persson, Johan, et al.
(författare)
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Plasma volume expansion and transcapillary fluid exchange in skeletal muscle of albumin, dextran, gelatin, hydroxyethyl starch, and saline after trauma in the cat
- 2006
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Ingår i: Critical Care Medicine. - 1530-0293. ; 34:9, s. 2456-2462
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To compare 5% albumin, 6% dextran 70, 3.5% gelatin, 6% hydroxyethyl starch 130/0.4, and saline regarding their plasma volume expanding effect after a surgical skeletal muscle trauma and their simultaneous effects on transvascular fluid exchange in skeletal muscle. Design: Controlled, prospective, randomized laboratory study. Setting: University research laboratory. Subjects: Thirty-six adult cats. Interventions: Systemic arterial pressure and tissue volume variations of and blood flow to a surgically isolated and autoperfused calf muscle placed in a plethysmograph were recorded. Arterial and venous pressures to the muscle were kept constant. After preparation, plasma volumes were determined by a 125 1 albumin tracer technique just before and 3 hrs after a bolus infusion of the plasma expander (25 mL/kg). Measurements and Main Results: Plasma volume was 20.9 +/- 2.9 mL/kg (n = 36) just before infusion of the plasma expander (normal plasma volume for the cat is 34-37 mL/kg). The remaining volume expansion of the infusion after 3 hrs was 6.8 mL/kg for albumin, 11.2 mL/kg for dextran, 1.8 mL/kg for gelatin, 2.2 mL/kg for hydroxyethyl starch, and 0.9 mL/kg for saline. Plasma volume decreased by 1.1 mL/kg when no solution was given (n = 6 per group). Colloid osmotic pressure was better preserved with dextran and albumin than with the other solutions. Albumin and dextran reduced muscle volume by absorption after 3 hrs, whereas the initial absorption turned to net filtration in the gelatin and hydroxyethyl starch groups. Saline infusion increased muscle volume by filtration for about 20 mins, followed by an approximately constant volume. Conclusion: The relatively poor plasma expansion for all solutions analyzed can most likely be explained by increased transcapillary leakage due to increased microvascular permeability following trauma. Under such circumstances, for equal volumes, plasma expansion was better preserved with 6% dextran 70 than with 5% albumin, which was better than 3.5% gelatin, 6% hydroxyethyl starch 130/0.4, and saline.
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| 68. |
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| 69. |
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| 70. |
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| 71. |
- Rasmussen, Rune, et al.
(författare)
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The effects of continuous prostacyclin infusion on regional blood flow and cerebral vasospasm following subarachnoid haemorrhage: study protocol for a randomised controlled trial
- 2012
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Ingår i: Trials. - : Springer Science and Business Media LLC. - 1745-6215. ; 13
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Tidskriftsartikel (refereegranskat)abstract
- Background: One of the main causes of mortality and morbidity following subarachnoid haemorrhage (SAH) is the development of cerebral vasospasm, a frequent complication arising in the weeks after the initial bleeding. Despite extensive research, to date no effective treatment of vasospasm exists. Prostacyclin is a potent vasodilator and inhibitor of platelet aggregation. In vitro models have shown a relaxing effect of prostacyclin after induced contraction in cerebral arteries, and a recent pilot trial showed a positive effect on cerebral vasospasm in a clinical setting. No randomised, clinical trials have been conducted, investigating the possible pharmacodynamic effects of prostacyclin on the human brain following SAH. Methods: This trial is a single-centre, randomised, placebo-controlled, parallel group, blinded, clinical, pilot trial. A total of 90 patients with SAH will be randomised to one of three intervention arms: epoprostenol 1 ng/kg/min, epoprostenol 2 ng/kg/min or placebo in addition to standard treatment. Trial medication will start day 5 after SAH and continue to day 10. The primary outcome measure is changes in regional cerebral blood flow from baseline in the arterial territories of the anterior cerebral artery, medial cerebral artery and the posterior cerebral artery, measured by CT perfusion scan. The secondary outcomes will be vasospasm measured by CT angiography, ischaemic parameters measured by brain microdialysis, flow velocities in the medial cerebral artery, clinical parameters and outcome (Glasgow Outcome Scale) at 3 months.
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| 72. |
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| 73. |
- Sandestig, Anna, et al.
(författare)
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Therapeutic Hypothermia in Children and Adults with Severe Traumatic Brain Injury.
- 2014
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Ingår i: Therapeutic hypothermia and temperature management. - : Mary Ann Liebert Inc. - 2153-7933 .- 2153-7658. ; 4:1, s. 10-20
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Forskningsöversikt (refereegranskat)abstract
- Great expectations have been raised about neuroprotection of therapeutic hypothermia in patients with traumatic brain injury (TBI) by analogy with its effects after heart arrest, neonatal asphyxia, and drowning in cold water. The aim of this study is to review our present knowledge of the effect of therapeutic hypothermia on outcome in children and adults with severe TBI. A literature search for relevant articles in English published from year 2000 up to December 2013 found 19 studies. No signs of improvement in outcome from hypothermia were seen in the five pediatric studies. Varied results were reported in 14 studies on adult patients, 2 of which reported a tendency of higher mortality and worse neurological outcome, 4 reported lower mortality, and 9 reported favorable neurological outcome with hypothermia. The quality of several trials was low. The best-performed randomized studies showed no improvement in outcome by hypothermia-some even indicated worse outcome. TBI patients may suffer from hypothermia-induced pulmonary and coagulation side effects, from side effects of vasopressors when re-establishing the hypothermia-induced lowered blood pressure, and from a rebound increase in intracranial pressure (ICP) during and after rewarming. The difference between body temperature and temperature set by the biological thermostat may cause stress-induced worsening of the circulation and oxygenation in injured areas of the brain. These mechanisms may counteract neuroprotective effects of therapeutic hypothermia. We conclude that we still lack scientific support as a first-tier therapy for the use of therapeutic hypothermia in TBI patients for both adults and children, but it may still be an option as a second-tier therapy for refractory intracranial hypertension.
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