| 1. |
- Bragadottir, Gudrun, et al.
(författare)
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Low-dose vasopressin increases glomerular filtration rate, but impairs renal oxygenation in post-cardiac surgery patients.
- 2009
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Ingår i: Acta Anaesthesiol Scand. - : Wiley. - 1399-6576. ; 53:8, s. 1052-9
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The beneficial effects of vasopressin on diuresis and creatinine clearance have been demonstrated when used as an additional/alternative therapy in catecholamine-dependent vasodilatory shock. A detailed analysis of the effects of vasopressin on renal perfusion, glomerular filtration, excretory function and oxygenation in man is, however, lacking. The objective of this pharmacodynamic study was to evaluate the effects of low to moderate doses of vasopressin on renal blood flow (RBF), glomerular filtration rate (GFR), renal oxygen consumption (RVO2) and renal oxygen extraction (RO2Ex) in post-cardiac surgery patients. METHODS: Twelve patients were studied during sedation and mechanical ventilation after cardiac surgery. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h. At each infusion rate, systemic haemodynamics were evaluated by a pulmonary artery catheter, and RBF and GFR were measured by the renal vein thermodilution technique and by renal extraction of 51chromium-ethylenediaminetetraacetic acid, respectively. RVO2 and RO2Ex were calculated by arterial and renal vein blood samples. RESULTS: The mean arterial pressure was not affected by vasopressin while cardiac output and heart rate decreased. RBF decreased and GFR, filtration fraction, sodium reabsorption, RVO2, RO2Ex and renal vascular resistance increased dose-dependently with vasopressin. Vasopressin exerted direct antidiuretic and antinatriuretic effects. CONCLUSIONS: Short-term infusion of low to moderate, non-hypertensive doses of vasopressin induced a post-glomerular renal vasoconstriction with a decrease in RBF and an increase in GFR in post-cardiac surgery patients. This was accompanied by an increase in RVO2, as a consequence of the increases in the filtered tubular load of sodium. Finally, vasopressin impaired the renal oxygen demand/supply relationship.
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| 2. |
- Damén, Tor, et al.
(författare)
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Effects of different mean arterial pressure targets on plasma volume, ANP and glycocalyx-A randomized trial.
- 2021
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Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 65:2, s. 220-227
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Tidskriftsartikel (refereegranskat)abstract
- Arterial haematocrit (Hct) has been shown to decrease after anaesthesia induction, most probably because of an increased plasma volume (PV). The primary objective was to quantify change in PV if mean arterial pressure (MAP) was kept at baseline level or allowed to decrease to 60mm Hg. Our secondary objective was to evaluate underlying mechanisms of this response.Twenty-four coronary artery bypass patients were randomized to a higher (90mm Hg, intervention group) or lower (60mm Hg, control group) MAP by titration of norepinephrine. During the experimental procedure, no fluids were administered. Baseline PV was measured by 125 I-albumin and the change in PV was calculated from the change in Hct. Changes in MAP, plasma 125 I-albumin, colloid osmotic pressure, albumin, Mid Regional-pro Atrial Natriuretic Peptide (MR-proANP) and endothelial glycocalyx components were measured from baseline to 50minutes after anaesthesia induction.The MAP during the trial was 93±9mm Hg in the intervention group and 62±5mm Hg in the control group. PV increased with up to 420±180mL in the control group and 45±130mL in the intervention group (P<.001). Albumin and colloid osmotic pressure decreased significantly more in the control group. MR-proANP increased in the control group but no shedding of the glycocalyx layer was detected in either of the groups.Allowing mean arterial pressure to fall to 60mm Hg during anaesthesia induction, increases the plasma volume due to reabsorption of interstitial water, with no ANP-induced degradation of the endothelial glycocalyx.
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| 3. |
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| 4. |
- Kolsrud, Oscar, et al.
(författare)
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Effects of atrial natriuretic peptide on renal function during cardiopulmonary bypass: a randomized pig model.
- 2020
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Ingår i: European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery. - : Oxford University Press (OUP). - 1873-734X. ; 57:4, s. 652-659
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Tidskriftsartikel (refereegranskat)abstract
- Acute kidney injury is a well-known complication after cardiac surgery and cardiopulmonary bypass (CPB). In this experimental animal study, we evaluated the effects of atrial natriuretic peptide (ANP) on renal function, perfusion, oxygenation and tubular injury during CPB.Twenty pigs were blindly randomized to continuous infusion of either ANP (50ng/kg/min) or placebo before, during and after CPB. Renal blood flow as well as cortical and medullary perfusion was measured. Blood was repeatedly sampled from the renal vein. Glomerular filtration rate was measured by infusion clearance of 51Cr-EDTA.Glomerular filtration rate was higher (P<0.001), whereas renal blood flow or renal oxygen delivery was not affected by ANP during CPB. Renal oxygen consumption did not differ between groups during CPB, whereas renal oxygen extraction was higher in the ANP group (P=0.03). Urine flow and sodium excretion were higher in the ANP group during CPB. Blood flow in the renal medulla, but not in the cortex, dropped during CPB, an effect that was not seen in the animals that received ANP.ANP improved renal function during CPB. Despite impaired renal oxygenation, ANP did not cause tubular injury, suggesting a renoprotective effect of ANP during CPB. Also, CPB induced a selectively reduced blood flow in the renal medulla, an effect that was counteracted by ANP.
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| 5. |
- Lackmann, Tim, 1983, et al.
(författare)
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Investigation of turbulence–chemistry interactions in a heavy-duty diesel engine with a representative interactive linear eddy model
- 2020
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Ingår i: International Journal of Engine Research. - : SAGE Publications. - 1468-0874 .- 2041-3149. ; 21:8, s. 1469-1479
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Tidskriftsartikel (refereegranskat)abstract
- Simulations of a heavy-duty diesel engine operated at high-load and low-load conditions were compared to each other, and experimental data in order to evaluate the influence of turbulence–chemistry interactions on heat release, pressure development, flame structure, and temperature development are quantified. A recently developed new combustion model for turbulent diffusion flames called representative interactive linear eddy model which features turbulence–chemistry interaction was compared to a well-stirred reactor model which neglects the influence of turbulent fluctuations on the mean reaction rate. All other aspects regarding the spray combustion simulation like spray break-up, chemical mechanism, and boundary conditions within the combustion chamber were kept the same in both simulations. In this article, representative interactive linear eddy model is extended with a progress variable, which enables the model to account for a flame lift-off and split injection, when it is used for diffusion combustion. In addition, the extended version of representative interactive linear eddy model offers the potential to treat partially premixed and premixed combustion as well. The well-stirred reactor model was tuned to match the experimental results, thus computed pressure and apparent heat release are in close agreement with the experimental data. Representative interactive linear eddy model was not tuned specifically for the case and thus the computed results for pressure and heat release are in reasonable agreement with experimental data. The computational results show that the interaction of the turbulent flow field and the chemistry reduce the peak temperatures and broaden up the turbulent flame structure. Since this is the first study of a real combustion engine (metal engine) with the newly developed model, representative interactive linear eddy model appears as a promising candidate for predictions of spray combustion in engines, especially in combustion regimes where turbulence–chemistry interaction plays an even more important role like, example given, in low-temperature combustion or combustion with local extinction and re-ignition.
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| 6. |
- Millinger, Johan, 1978, et al.
(författare)
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Arterial Blood Flow and Effects on Limb Tissue Perfusion During Endoshunting of the Common Iliac Artery in an Experimental Porcine Model
- 2024
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Ingår i: EJVES VASCULAR FORUM. - 2666-688X. ; 61, s. 54-61
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Temporary arterial shunting is an established method to prevent tissue ischaemia. Although less well established, shunting might also be achieved through endovascular and hybrid techniques, known as endoshunting. Endoshunting offers advantages, for example, enabling minimally invasive access and avoiding complete occlusion of the donor artery. In an ex vivo bench test, volume flow in various interconnected endoshunt systems has been tested previously. This study aimed to investigate the capacity of the best performing endoshunt system in vivo. Methods: Six anaesthetised pigs had their common iliac arteries (CIAs) explored, with the left CIA serving as the experimental and the right CIA as the control. Mean arterial pressure, regional blood flow, endoshunt flow, and regional oxygen extraction and lactate production were recorded. Distal muscle perfusion was monitored using near infrared spectroscopy (NIRS). Each experiment involved baseline registration, cross clamping of the left CIA, a 120 minute endoshunt session, and restoration of native flow. Results: During cross clamping, NIRS values on the experimental side reached the lowest measurable value. Following endoshunt activation, there were no NIRS value differences between the experimental and control extremities whereas the average arterial flow decreased in both the experimental (270-140 mL/min, p = .028) and control extremities (245-190 mL/min, p = .25), with a greater drop on the endoshunted side (48% vs. 22%, respectively). Lactate levels temporarily increased by 42% in the endoshunted limb on endoshunt activation but were normalised within an hour. Oxygen extraction remained constant at 55% on the control side but increased to 70% on the endoshunted side (p = .068). Conclusion: In this animal model, a flow optimised endoshunt system appeared to provide sufficient blood flow and restored stable tissue perfusion. Although arterial flow was slightly lower and oxygen extraction slightly higher on the endoshunted side, the endoshunt seemed to deliver adequate perfusion to prevent significant ischaemia.
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| 7. |
- Millinger, Johan, 1978, et al.
(författare)
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Optimisation of Volume Flow Rates when Using Endovascular Shunting Techniques: An Experimental Study in Different Bench Flow Circuits
- 2023
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Ingår i: EJVES Vascular Forum. - : Elsevier BV. - 2666-688X. ; 58, s. 5-10
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Acute tissue ischaemia may arise due to arterial emergencies or during more complex vascular procedures and may be mitigated by temporary shunting techniques. Endovascular shunting (ES) techniques enable percutaneous access and shunting from the donor artery without the need to completely interrupt the arterial flow in the donor artery. An endoshunt system may also cover longer distances than most conventional shunts. The aim was to investigate and optimise the flow rates in different endovascular shunt systems.Methods: Step 1: The flow capacity of different ES configurations was compared with the flow capacity of a 9 Fr Pruitt-Inahara shunt (PIS). An intravenous bag with 0.9% NaCl, pressurised to 90 mmHg, was connected simultaneously to a PIS and to one of the tested ES configurations. The two shunt systems were then opened at the same time. The delivered fluid volumes from the shunt systems were collected and measured. The volume flow rate was subsequently calculated. Steps 2 and 3: Within a heart lung machine circuit, pressure -flow charts were constructed for the individual ES components and for the fully connected optimised endoshunt systems. The flow rate was increased in steps of 40-50 mL/min while monitoring the driving pressure, enabling the creation and comparison of the pressure -flow charts for the individually tested components. In total, seven individual inflow and outflow potential ES components were investigated with inflow and outflow diameters ranging from 6 to 15 Fr.Results: ES systems based on standard donor introducers led to substantially lower volume flow than the corresponding PIS volume flow, whereas ES systems based on dedicated 6 or 8 Fr dialysis access introducers (Prelude Short Sheet, Merit Medical) matched PIS flow rates. The introduction of 30 cm long 1/400 perfusion tubing within the ES system did not affect volume flow for any of the tested ES configurations.Conclusion: Endoshunting techniques can match PIS volume flow rates over short and long distances. The achieved ES flow rate is highly dependent on the components used within the ES system.
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| 8. |
- Nygren, Andreas, 1967, et al.
(författare)
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Autoregulation of human jejunal mucosal perfusion during cardiopulmonary bypass.
- 2006
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Ingår i: Anesthesia and analgesia. - 1526-7598. ; 102:6, s. 1617-22
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Tidskriftsartikel (refereegranskat)abstract
- Animal studies have suggested that autoregulation of intestinal blood flow is severely impaired during cardiopulmonary bypass (CPB). We investigated the jejunal mucosal capacity to autoregulate perfusion during nonpulsatile CPB (34 degrees C) in 10 patients undergoing elective cardiac surgery. Changes in mean arterial blood pressure (MAP) were induced by altering the CPB flow rate randomly for periods of 3 min from 2.4 L/min/m2 to either 1.8 or 3.0 L/min/m2. Jejunal mucosal perfusion (JMP) was continuously recorded by laser Doppler flowmetry. A typical pattern of flow motion (vasomotion) was recorded in all patients during CPB. Variations in CPB flow rates caused no significant changes in mean JMP, jejunal mucosal hematocrit, or red blood cell velocity within a range of MAP from 50 +/- 15 to 74 +/- 16 mm Hg. The vasomotion frequency and amplitude was positively correlated with CPB flow rate. IV injections of prostacyclin (10 microg, Flolan) blunted vasomotion and increased JMP from 192 +/- 53 to 277 +/- 70 (P < 0.05) perfusion units despite a reduction in MAP from 59 +/- 12 to 45 +/- 10 mm Hg (P < 0.05). Prostacyclin-induced vasodilation resulted in loss of mucosal autoregulation (pressure-dependent perfusion). We conclude that autoregulation of intestinal mucosal perfusion is maintained during CPB in humans.
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| 9. |
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| 10. |
- Nygren, Andreas, 1967, et al.
(författare)
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Norepinephrine and intestinal mucosal perfusion in vasodilatory shock after cardiac surgery
- 2007
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Ingår i: Shock. - : Ovid Technologies (Wolters Kluwer Health). - 1073-2322. ; 28:5, s. 536-543
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Tidskriftsartikel (refereegranskat)abstract
- Patients with norepinephrine-dependent vasodilatory shock after cardiac surgery (n = 10) were compared with uncomplicated postcardiac surgery patients (n = 10) with respect to jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and splanchnic oxygen demand/supply relationship. Furthermore, the effects of norepinephrine-induced variations in MAP on these variables were evaluated in vasodilatory shock. Norepinephrine infusion rate was randomly and sequentially titrated to target MAPs of 60, 75, and 90 mmHg (0.25 +/- 0.24, 0.37 +/- 0.21, and 0.55 +/- 0.39 mug/kg per minute, respectively). Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell (RBC) velocity (laser Doppler flowmetry) as well as gastric-arterial PCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. Splanchnic oxygen extraction was 71 +/- 16% in the vasodilatory shock group and 41 +/- 9% in the control group (P < 0.001), whereas splanchnic lactate extraction did not differ between the two groups. Jejunal mucosal perfusion (61%; P < 0.001), RBC velocity (35%; P < 0.01), and arterial-gastric mucosal PCO2 gradient (150%; P < 0.001) were higher in the vasodilatory shock group compared with those of the control group. Jejunal mucosal perfusion, jejunal mucosal hematocrit, RBC velocity, arterial-gastric mucosal PCO2 gradient, splanchnic oxygen extraction, and splanchnic lactate extraction were not affected by increasing infusion rates of norepinephrine. In patients with norepinephrine-dependent vasodilatory shock after cardiac surgery, intestinal mucosal perfusion was higher, whereas splanchnic and gastric oxygen demand/supply relationships were impaired compared with postoperative controls, suggesting that intestinal mucosal perfusion is prioritized in vasodilatory shock. Increasing MAP from 60 to 90 mmHg with norepinephrine in clinical vasodilatory shock does not affect intestinal mucosal perfusion and gastric or global splanchnic oxygen demand/supply relationships.
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| 11. |
- Nygren, Andreas, 1967, et al.
(författare)
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Norepinephrine causes a pressure-dependent plasma volume decrease in clinical vasodilatory shock.
- 2010
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Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 54:7, s. 814-20
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Recent experimental studies have shown that a norepinephrine-induced increase in blood pressure induces a loss of plasma volume, particularly under increased microvascular permeability. We studied the effects of norepinephrine-induced variations in the mean arterial pressure (MAP) on plasma volume changes and systemic haemodynamics in patients with vasodilatory shock. METHODS: Twenty-one mechanically ventilated patients who required norepinephrine to maintain MAP > or =70 mmHg because of septic/postcardiotomy vasodilatory shock were included. The norepinephrine dose was randomly titrated to target MAPs of 60, 75 and 90 mmHg. At each target MAP, data on systemic haemodynamics, haematocrit, arterial and mixed venous oxygen content and urine flow urine were measured. Changes in the plasma volume were calculated as 100 x (Hct(pre)/Hct(post)-1)/ (1-Hct(pre)), where Hct(pre) and Hct(post) are haematocrits before and after intervention. RESULTS: Norepinephrine doses to obtain target MAPs of 60, 75 and 90 mmHg were 0.20+/-0.18, 0.29+/-0.18 and 0.42+/-0.31 microg/kg/min, respectively. From 60 to 90 mmHg, increases in the cardiac index (15%), systemic oxygen delivery index (25%), central venous pressure (CVP) (20%) and pulmonary artery occlusion pressure (33%) were seen, while the intrapulmonary shunt fraction was unaffected by norepinehrine. Plasma volume decreased by 6.5% and 9.4% (P<0.0001) when blood pressure was increased from 60 to 75 and 90 mmHg, respectively. MAP (P<0.02) independently predicted the decrease in plasma volume with norepinephrine but not CVP (P=0.19), cardiac index (P=0.73), norepinephrine dose (P=0.58) or urine flow (P=0.64). CONCLUSIONS: Norepinephrine causes a pressure-dependent decrease in the plasma volume in patients with vasodilatory shock most likely caused by transcapillary fluid extravasation.
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| 12. |
- Nygren, Andreas, 1967, et al.
(författare)
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Vasopressin decreases intestinal mucosal perfusion: a clinical study on cardiac surgery patients in vasodilatory shock.
- 2009
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Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 1399-6576 .- 0001-5172. ; 53:5, s. 581-8
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery. METHODS: Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) > or = 60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. RESULTS: The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous-hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin. CONCLUSIONS: Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction.
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| 13. |
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| 14. |
- Nygren, Andreas, 1967, et al.
(författare)
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Vasopressors and intestinal mucosal perfusion after cardiac surgery: Norepinephrine vs. phenylephrine.
- 2006
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Ingår i: Critical care medicine. - 0090-3493. ; 34:3, s. 722-9
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To evaluate the potential differential effects of norepinephrine, an alpha1-, beta1-, and beta2-receptor agonist, to the alpha1-agonist phenylephrine on jejunal mucosal perfusion, gastric-arterial PCO2 gradient, and the global splanchnic oxygen demand-supply relationship after cardiac surgery. DESIGN: A randomized, prospective, interventional crossover study. SETTING: A university cardiothoracic intensive care unit. PATIENTS: Ten patients were studied during propofol sedation and mechanical ventilation after uncomplicated coronary artery bypass surgery. INTERVENTIONS: Each patient received randomly and sequentially norepinephrine (0.052+/-0.009 microg/kg/min) and phenylephrine (0.50+/-0.22 microg/kg/min) to increase mean arterial blood pressure by 30%. MEASUREMENTS AND MAIN RESULTS: Data on jejunal mucosal perfusion, jejunal mucosal hematocrit, and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial Pco2 gradient (tonometry) and splanchnic oxygen extraction were obtained before (control) and during a 30-min drug infusion period after the target mean arterial blood pressure was reached. The procedure was sequentially repeated for the second vasopressor. Both drugs induced a 40-46% increase in systemic vascular resistance with no change in cardiac index. Neither jejunal mucosal perfusion, jejunal mucosal hematocrit, red blood cell velocity, nor gastric-arterial Pco2 gradient was affected by any of the vasopressors. Splanchnic oxygen extraction increased from 38.2% to 43.1% (p<.001) with norepinephrine and from 39.3% to 47.5% (p<.001) with phenylephrine. This increase was significantly more pronounced with phenylephrine compared with norepinephrine (p<.05). Mixed venous-hepatic vein oxygen saturation gradient increased with both drugs (p<.01), and the increase was more pronounced with phenylephrine (p<.05). Splanchnic lactate extraction was not significantly affected by any of the vasopressors. CONCLUSIONS: Phenylephrine induced a more pronounced global alpha1-mediated splanchnic vasoconstriction compared with norepinephrine. Neither of the vasoconstrictors impaired perfusion of the gastrointestinal mucosa in postcardiac surgery patients. The lack of norepinephrine-induced, alpha1-mediated impairment of gastrointestinal perfusion is not explained by a beta2-mediated counteractive vasodilation but instead by possible mucosal autoregulatory escape.
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| 15. |
- Nygren, Andreas, 1967
(författare)
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Vasopressors and intestinal mucosal perfusion. Studies in cardiac surgical and critically ill patients
- 2006
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- During trauma, surgery and critically illness, splanchnic ischemia and reperfusion damage maythreaten the barrier function of the intestinal mucosa, leading to bacterial translocation, immuneactivation and subsequent development of systemic inflammatory response syndrome. Detection,prevention and treatment of intestinal mucosal hypoperfusion are therefore important forprevention of complications in critically ill patients. In this thesis, the intestinal mucosalperfusion, measured by laser Doppler flowmetry, has been studied during and after cardiacsurgery and in critically ill patients with vasodilatory shock, with focus on the effects ofvasopressor treatment.The intestinal mucosal perfusion was evaluated postoperatively in eighteen cardiac surgerypatients. Elevation of the systemic perfusion pressure with norepinephrine induced no change inintestinal mucosal perfusion, whereas the combination of norepinephrine and dopamine causedincreased mucosal perfusion. Furthermore, the differential effects of phenylephrine, a pure á1-adrenoceptor agonist, and norepinephrine, which has both á1-constricting and â1- dilatingproperties, were investigated postoperatively in ten patients. Intestinal mucosal perfusion was notaltered by the vasopressors, whereas both drugs increased the global splanchnic oxygen extraction.This increase was more pronounced with phenylephrine, indicating a more pronounced globalsplanchnic vasoconstriction, compared to norepinephrine,In ten critically ill patients with multi organ failure and norepinephrine-dependentvasodilatory shock, the effects of norepinephrine-induced variations in perfusion pressure onglobal splanchnic and intestinal mucosal perfusion were evaluated. The intestinal mucosalperfusion and the global splanchnic oxygenation were not altered despite a change in meanarterial pressure from 60 to 90 mmHg.The autoregulation of intestinal mucosal perfusion during cardiopulmonary bypass wastested in ten cardiac surgery patients. Variations in perfusion pressure induced by alterations incardiopulmonary bypass flow rate revealed an intact autoregulatory capacity of the intestinalmucosa. Vasodilation with prostacyclin increased jejunal mucosal perfusion and abolished theautoregulatory capacity of the mucosa. The amplitude and frequency of the cyclic oscillation ofthe mucosal perfusion (vasomotion) increased with increasing perfusion pressureIn conclusion: Intestinal mucosal perfusion is not affected by clinical relevant doses of thevasopressors norepinephrine and phenylephrine, in postoperative patients and critically illpatients with vasodilatory shock. Phenylephrine causes a more pronounced global splanchnicvasoconstriction compared to norepinephrine. Addition of dopamine increases intestinal mucosalperfusion during norepinephrine infusion. Autoregulation of intestinal mucosal perfusion isintact during cardiopulmonary bypass.
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| 16. |
- Singh, Sukhi, 1990, et al.
(författare)
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Adrenaline Improves Platelet Reactivity in Ticagrelor-Treated Healthy Volunteers
- 2019
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Ingår i: Thrombosis and Haemostasis. - : Georg Thieme Verlag KG. - 0340-6245 .- 2567-689X. ; 119:5, s. 735-743
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Administration of agents that enhance platelet reactivity may reduce the perioperative bleeding risk in patients treated with the adenosine diphosphate (ADP)-receptor antagonist ticagrelor. Adrenaline potentiates ADP-induced aggregation and activation in blood samples from ticagrelor-treated patients, but it has not previously been evaluated in vivo.METHODS: Ten healthy male subjects were included in an interventional study. A loading dose of ticagrelor (180 mg) was administered, followed 2 hours later by a gradually increased intravenous adrenaline infusion (0.01, 0.05, 0.10 and 0.15 µg/kg/min; 15 minutes at each step). Blood pressure, heart rate, platelet aggregation (impedance aggregometry), platelet activation (flow cytometry), clot formation (rotational thromboelastometry) and adrenaline plasma concentration were determined before and after ticagrelor administration and at the end of each adrenaline step.RESULTS: = 0.007).CONCLUSION: Infusion of adrenaline at clinically relevant doses improves in vivo platelet reactivity and clot formation in ticagrelor-treated subjects. Adrenaline could thus potentially be used to prevent perioperative bleeding complications in ticagrelor-treated patients. Studies in patients are necessary to determine the clinical importance of our observations.TRIAL REGISTRY NUMBER: ClinicalTrials.gov NCT03441412.
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| 17. |
- Singh, Sukhi, 1990, et al.
(författare)
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Intraoperative infusion of noradrenaline improves platelet aggregation in patients undergoing coronary artery bypass grafting: a randomized controlled trial
- 2019
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Ingår i: Journal of Thrombosis and Haemostasis. - : Elsevier BV. - 1538-7933 .- 1538-7836. ; 17:4, s. 657-665
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Tidskriftsartikel (refereegranskat)abstract
- Background New approaches to prevent bleeding complications during cardiac surgery are needed. Objective To investigate if noradrenaline (NA) enhances platelet aggregation in patients undergoing coronary artery bypass grafting (CABG). Patients/Methods Twenty-four patients undergoing coronary artery bypass grafting (CABG) were included in a prospective parallel-group randomized study. All patients but one were treated with acetylsalicylic acid (ASA). In the treatment group (n = 12), mean arterial blood pressure (MAP) was maintained at pre-induction levels by NA infusion. In the control group (n = 12), NA was administered only if MAP decreased below 60 mmHg. Platelet aggregation (impedance aggregometry with ADP, arachidonic acid [AA] and thrombin-receptor activating peptide [TRAP] as initiators) and clot formation (clotting time, clot formation time and maximum clot firmness by EXTEM, INTEM and FIBTEM tests with thromboelastometry) were assessed before and 50 min after anesthesia induction (before cardiopulmonary bypass was initiated). Results All patients in the treatment group received NA (median dose after 50 min 0.09 (range 0-0.26) mu g kg(-1) min(-1)). Four patients in the control group also received NA (0.03-0.12 mu g kg(-1) min(-1)). There were differences between the treatment group and the control group in ADP- and AA-induced aggregation changes (ADP, +16 [25th-75th percentiles, 5-26] vs. -7 [-19 to -1] U; AA, +12 [-4 to 16] vs. -9 [-13 to 1] U). INTEM maximum clot firmness increased in the treatment group but not in the control group. Conclusion Infusion of clinically relevant doses of NA enhanced platelet aggregation and clot firmness in ASA-treated CABG patients. NA infusion is hence a potential new method to acutely improve platelet reactivity in patients on antiplatelet therapy undergoing surgery.
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| 18. |
- Thorén, Anders, 1955, et al.
(författare)
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Cardiopulmonary bypass in humans--jejunal mucosal perfusion increases in parallel with well-maintained microvascular hematocrit.
- 2005
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Ingår i: Acta anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 49:4, s. 502-9
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: An imbalance between splanchnic oxygen supply and demand occurs during cardiopulmonary bypass (CPB) in man, which might disrupt the intestinal mucosal barrier function. The aim of the present study was to evaluate the effects of mild hypothermic CPB on intestinal mucosal perfusion in man undergoing cardiac surgery. Additionally we aimed to identify variables, which independently could predict changes of intestinal mucosal microcirculatory variables during CPB. METHODS: Jejunal mucosal perfusion (JMP), jejunal mucosal hematocrit (JMHt), red blood cell (RBC) velocity and arteriolar vasomotion using endoluminal jejunal laser Doppler flow metry were studied in eight cardiac surgical patients before and during CPB at a temperature of 34 degrees C. RESULTS: Cardiopulmonary bypass and the accompanied hemodilution (25-30%) induced a 44% increase in JMP (P < 0.05) and a 42% increase in RBC velocity (P < 0.01), with no change in JMHt. The oscillation amplitude of JMP, at a fundamental frequency of 2.8 cycles min(-1), increased with 175% (P < 0.05) during CPB. Splanchnic oxygen extraction increased by 64% during CPB (P < 0.05). Stepwise multiple regression analysis identified systemic hematocrit, arterial O2 and CO2 tension and splanchnic oxygen extraction as independent predictors of RBC velocity during CPB (R2=0.63, P < 0.001). The oscillation amplitude of JMP was predicted by RBC velocity and splanchnic oxygen extraction (R2= 0.68, P <0.0001). CONCLUSIONS: The increase in RBC velocity and enhanced arteriolar vasomotion, as well as maintained jejunal mucosal hematocrit, are microcirculatory, compensatory mechanisms for the splanchic oxygen supply/demand mismatch seen during cardiopulmonary bypass in humans.
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