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- Alm, Ann-Sophie, et al.
(författare)
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Variation of lipopolysaccharide-induced acute lung injury in eight strains of mice.
- 2010
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier BV. - 1878-1519 .- 1569-9048. ; 171, s. 157-164
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Tidskriftsartikel (refereegranskat)abstract
- Clinical and experimental evidence suggests that genetic variations may play an important role in the development of acute lung injury (ALI). Lipopolysaccharide (LPS)-induced ALI models has been widely applied for pathophysiological and pharmacological research. In order to understand the variation of acute pulmonary reactions between mouse strains and find the optimal strain for target-oriented study, the present study investigated the alterations of acute lung hyperinflation, inflammation and injury in C57BL/6J, Balb/cJ, DBA/1J, CD-1, NMRI, DBA/2J, A/J and C3H/HeN mice after the intra-tracheal challenge with LPS. We found that LPS-induced ALI varied between measured variables, durations and strains. General score of LPS-induced acute lung hyperinflation, inflammation and edema followed the order CD-1, A/J, Balb/c, DBA/2J, C57BL/6J, DBA/1J, NMRI, C3H/HeN mice at 4h, and CD-1, C57BL/6J, Balb/c, C3H/HeN, NMRI, A/J, DBA/2J, DBA/1 mice at 24h. Thus, these data provide useful information to select sensitive or resistant strain mouse for understanding genetic variation of pathogenesis and screening of target-oriented drugs.
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2. |
- Andersson, Johan, et al.
(författare)
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Pulmonary gas exchange is reduced by the cardiovascular diving response in resting humans
- 2008
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier BV. - 1569-9048 .- 1878-1519. ; 160:3, s. 320-324
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Tidskriftsartikel (refereegranskat)abstract
- The diving response reduces the pulmonary O2 uptake in exercising humans, but it has been debated whether this effect is present at rest. Therefore, respiratory and cardiovascular responses were recorded in 16 resting subjects, performing apnea in air and apnea with face immersion in cold water (10 ◦C). Duration of apneas were predetermined to be identical in both conditions (average: 145 s) and based on individual maximal capacity (average: 184 s). Compared to apnea in air, an augmented diving response was elicited by apnea with face immersion. The O2 uptake from the lungs was reduced compared to the resting eupneic control (4.6 ml min−1 kg−1), during apnea in air (3.6 ml min−1 kg−1) and even more so during apnea with face immersion (3.4 ml min−1 kg -1). We conclude that the cardiovascular djustments of the diving response reduces pulmonary gas exchange in resting humans, allowing longer apneas by preserving the lungs’ O2 store for use by vital organs.
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3. |
- Ax, M., et al.
(författare)
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Regional lung ventilation in humans during hypergravity studied with quantitative SPECT
- 2013
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier BV. - 1569-9048 .- 1878-1519. ; 189:3, s. 558-564
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Tidskriftsartikel (refereegranskat)abstract
- Recently we challenged the view that arterial desaturation during hypergravity is caused by redistribution of blood flow to dependent lung regions by demonstrating a paradoxical redistribution of blood flow towards non-dependent regions. We have now quantified regional ventilation in 10 healthy supine volunteers at normal and three times normal gravity (1G and 3G). Regional ventilation was measured with Technegas (Tc-99m) and quantitative single photon emission computed tomography (SPECT). Hypergravity caused arterial desaturation, mean decrease 8%, p<0.05 vs. 1G. The ratio for mean ventilation per voxel for non-dependent and dependent lung regions was 0.81+/-0.12 during 1G and 1.63+/-0.35 during 3G (mean+/-SD), p<0.0001. Thus, regional ventilation was shifted from dependent to non-dependent regions. We suggest that arterial desaturation during hypergravity is caused by quantitatively different redistributions of blood flow and ventilation. To our knowledge, this is the first study presenting high-resolution measurements of regional ventilation in humans breathing normally during hypergravity.
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6. |
- Bergmann, Astrid, et al.
(författare)
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Early and late effects of remote ischemic preconditioning on spirometry and gas exchange in healthy volunteers
- 2020
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier BV. - 1569-9048 .- 1878-1519. ; 271
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: Remote ischemic preconditioning (RIP) may protect remote organs from ischemia-reperfusion-injury (IRI) in surgical and non-surgical patients. There are few data available on RIP and lung function, especially not in healthy volunteers. The null-hypothesis was tested that RIP does not have an effect on pulmonary function when applied on healthy volunteers that were breathing spontaneously and did not experience any intervention. After approval of the Ethics Committee and informed consent of the study subjects, 28 healthy non-smoking volunteers were included and randomized in either the RIP group (n = 13) or the control group (n = 15). In the RIP group, lower limb ischemia was induced by inflation of a blood pressure cuff to a pressure 20 mmHg above the systolic blood pressure. After five minutes the blood pressure cuff was released for five minutes rest. The procedure was repeated three times resulting in 40 min ischemia and reperfusion. Capillary blood samples were taken, and lung function tests were performed at baseline (T1) and 60 min (T2) and 24 h (T3) after RIP. The control group was treated in the same fashion, but the RIP procedure was replaced by a sham protocol.Results: 60 min after RIP capillary pO(2) decreased significantly and returned to baseline level after 24 h in the RIP group. This did not occur in the control group. Capillary pCO(2), variables of lung function tests and pulmonary capillary blood volume remained unchanged throughout the experiment in both groups.Conclusion: Oxygenation is impaired early after RIP which is possibly induced by transient ventilation-perfusion inequality. No late effects of RIP were observed. The null hypothesis has to be rejected that RIP has no effect on respiratory variables in healthy volunteers.
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7. |
- Bergmann, Astrid, et al.
(författare)
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Effect of remote ischemic preconditioning on exhaled nitric oxide concentration in piglets during and after one-lung ventilation
- 2020
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier BV. - 1569-9048 .- 1878-1519. ; 276
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Remote ischemic preconditioning (RIP) may protect target organs from ischemia - reperfusion injury, however, little is known on pulmonary effects of RIP prior to, immediately after and several hours after one-lung ventilation (OLV). The present randomized, controlled, animal experiment was undertaken to analyze these issues.METHODS: After animal ethics committee approval, twelve piglets (26 ± 2 kg) were anesthetized and randomly assigned to a control (n = 6) or to a RIP group (n = 6). For RIP, arterial perfusion of a hind limb was suspended by an inflated blood pressure cuff (200 mmHg for 5 min) and deflated for another 5 min, this was repeated four times. After intubation, mechanical ventilation (MV) was kept constant with tidal volume 10 ml/kg, inspired oxygen fraction (FIO2) 0.40, and positive end-expiratory pressure (PEEP) 5cmH2O. FIO2 was increased to 1 after RIP in the RIP group and after the sham procedure in the control group, respectively, for the time of OLV. OLV was established by left-sided bronchial blockade. After OLV, TLV was re-established until the end of the protocol. Exhaled nitric oxide (NO) was measured by ozon chemiluminiscense and ventilatory and hemodynamic variables were assessed according to the protocol.RESULTS: Hemodynamic and respiratory data were similar in both groups. Arterial pO2 was higher in the RIP group after two hours of OLV. In the control group, exhaled NO decreased during OLV and remained at low levels for the rest of the protocol. In the RIP group, exhaled NO decreased as well during OLV but returned to baseline levels when TLV was re-established.CONCLUSIONS: RIP has no effects on hemodynamic and respiratory variables in juvenile, healthy piglets. RIP improves the oxygenation after OLV and prevents the decline of exhaled NO after OLV.
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8. |
- Bergmann, Astrid, et al.
(författare)
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Pulmonary effects of remote ischemic preconditioning in a porcine model of ventilation-induced lung injury
- 2019
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier. - 1569-9048 .- 1878-1519. ; 259, s. 111-118
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: One-lung ventilation (OLV) may result in lung injury due to increased mechanical stress and tidal recruitment. As a result, a pulmonary inflammatory response is induced. The present randomized, controlled, animal experiment was undertaken to assess the effects of remote ischemic preconditioning (RIP) on diffuse alveolar damage and immune response after OLV.METHODS: Fourteen piglets (26 ± 2 kg) were randomized to control (n = 7) and RIP group (n = 7). For RIP, a blood pressure cuff at hind limb was inflated up to 200 mmHg for 5 min and deflated for another 5 min, this being done four times before OLV. Mechanical ventilation settings were constant throughout the experiment: VT = 10 ml/kg, FIO2 = 0.40, PEEP = 5cmH2O. OLV was performed by left-sided bronchial blockade. Number of cells was counted from BAL fluid; cytokines were assessed by immunoassays in lung tissue and serum samples. Lung tissue samples were obtained for histological analysis and assessment of diffuse alveolar damage (DAD) score.RESULTS: Hemodynamic and respiratory data were similar in both groups. Likewise, no differences in pulmonary tissue TNF-α and protein content were found, but fewer leukocytes were counted in the ventilated lung after RIP. DAD scores were high without any differences between controls and RIP. On the other hand, alveolar edema and microhemorrhage were significantly increased after RIP.CONCLUSIONS: OLV results in alveolar injury, possibly enhanced by RIP. On the other hand, RIP attenuates the immunological response and decreased alveolar leukocyte recruitment in a porcine model of OLV.
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10. |
- Brander, Lukas, et al.
(författare)
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Neural control of ventilation prevents both over-distension and de-recruitment of experimentally injured lungs
- 2017
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier BV. - 1569-9048 .- 1878-1519. ; 237, s. 57-67
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Tidskriftsartikel (refereegranskat)abstract
- Background: Endogenous pulmonary reflexes may protect the lungs during mechanical ventilation. We aimed to assess integration of continuous neurally adjusted ventilatory assist (cNAVA), delivering assist in proportion to diaphragm's electrical activity during inspiration and expiration, and Hering-Breuer inflation and deflation reflexes on lung recruitment, distension, and aeration before and after acute lung injury (ALI).Methods: In 7 anesthetised rabbits with bilateral pneumothoraces, we identified adequate cNAVA level (cNAVA(AL)) at the plateau in peak ventilator pressure during titration procedures before (healthy lungs with endotracheal tube, [HLETT]) and after ALI (endotracheal tube [ALI(ETT)] and during non-invasive ventilation [ALI(NIV)]). Following titration, cNAVA(AL) was maintained for 5 min. In 2 rabbits, procedures were repeated after vagotomy (ALI(ETT+VAG)). In 3 rabbits delivery of assist was temporarily modulated to provide assist on inspiration only. Computed tomography was performed before intubation, before ALI, during cNAVA titration, and after maintenance at cNAVA(AL).Results: During ALI(ETT) and ALI(NIV), normally aerated lung-regions doubled and poorly aerated lung-regions decreased to less than a third (p < 0.05) compared to HLETT; no over-distension was observed. Tidal volumes were <5 ml/kg throughout. Removing assist during expiration resulted in lung de-recruitment during ALI(ETT) but not during ALI(NIV). During ALI(ETT+VAG) the expiratory portion of EAdi disappeared, resulting in cyclic lung collapse and recruitment.Conclusions: When using cNAVA in ALI, vagally mediated reflexes regulated lung recruitment preventing both lung over-distension and atelectasis. During non-invasive cNAVA the upper airway muscles play a role in preventing atelectasis. Future studies should be performed to compare these findings with conventional lung-protective approaches.
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