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Featured researches published by Björn Gunnarsson.


Perfusion | 1999

Lipid peroxidation during initiation of extracorporeal membrane oxygenation after hypoxia in endotoxemic rabbits

Gerhard Trittenwein; Alexandre Rotta; Björn Gunnarsson; David M. Steinhorn

Initiation of extracorporeal membrane oxygenation (ECMO) in septic children with severe respiratory failure often improves oxygenation but not pulmonary function. The factors affecting pulmonary function following onset of ECMO are not completely understood, but are thought to involve injury mediated, in part, by reactive oxygen species. We hypothesized that induction of ECMO using 100% oxygen as the sweep gas through the oxygenator would increase lipid peroxidation in endotoxin-primed animals after severe hypoxia. We further speculated that provision of oxygenated blood to the pulmonary circulation via venovenous ECMO would promote a greater degree of oxidative damage to the lung as compared to venoarterial ECMO. Eighteen New Zealand White rabbits were assigned to a control group (control) or two intervention groups subjected to 60 min of venoarterial or venovenous ECMO. ECMO was initiated following an intravenous challenge with 0.5 mg/kg of E. coli endotoxin and a period of global hypoxia leading to an arterial pH of 6.99 ± 0.09, PaCO2 of 103 ± 31 mmHg and PaO2 of 27 ± 5 mmHg. Malondialdehyde (MDA), a marker of lipid peroxidation, was measured in lung tissue homogenates and in arterial plasma. Lung tissue MDA demonstrated a strong trend towards an increase in the venoarterial group (1884 ± 945 nmol/g protein) and in the venovenous group (1905 ± 758 nmol/g protein) in comparison to the control group (644 ± 71 nmol/g protein) (p = 0.1; significance at 95% in Scheffe test). Lung tissue MDA in the venovenous group had a significant correlation with mean PaO2 during ECMO by regression analysis (r 2 = 0.678, p = 0.044). The change in blood MDA concentration between pre-ECMO and post-ECMO values was greater in the venovenous group (pre 1.62 ± 0.61 versus post 5.12 ± 0.2.07 μmol/l, p = 0.043) compared with that seen in the venoarterial group (pre 1.46 ± 0.38 versus post 3.9 ± 0.93 μmol/l). Our data support the hypothesis that initiation of ECMO with a circuit gas oxygen concentration of 100% after global hypoxia enhances oxidative damage to lipids in endotoxin-challenged animals. During venovenous ECMO this finding is dependent on PaO2.


Pediatric Anesthesia | 2001

Anaesthetic technique for transoesophageal echocardiography in children

Christopher Heard; Björn Gunnarsson; A.M.B. Heard; E. Watson; J.D. Orie; James E. Fletcher

Objective: To document the safety and efficacy of an anaesthetic technique in paediatric patients undergoing transoesophageal echocardiography (TOE).


Air Medical Journal | 2001

Use of a physiologic scoring system during interhospital transport of pediatric patients

Björn Gunnarsson; Christopher Heard; Alexandre Rotta; Andrew M.B. Heard; Barbara Kourkounis; James Fletcher

OBJECTIVE To determine the incidence of physiologic deterioration in critically ill and injured pediatric patients during interhospital transport with air and ground ambulance DESIGN Prospective, descriptive study SETTING All children were treated in regional hospitals and then transported to a pediatric tertiary care center. PATIENTS Children (n = 100) with a median age of 1.4 years (range 1 week to 18 years) MAIN RESULTS Three sets of physiologic scores were calculated: at the time of referral, on departure from the referring hospital, and arrival at the tertiary care center. The incidence of significant physiologic deterioration based on the calculated physiologic scores was 5.6% (n = 4) during ground and 3.4% (n = 1) during air ambulance transports. Critical events occurred in 15% of ground and 31% of air ambulance transports. CONCLUSION No difference existed in the incidence of adverse events or physiologic deterioration when air ambulance transports were compared with ground ambulance transports for critically ill children by our team. The physiologic scoring system we chose is simple and easy to use for quality assurance.


Critical Care Medicine | 1999

Perflubron (PFOB) protects cell monolayers against direct in vitro oxidative injury

Alexandre Rotta; Björn Gunnarsson; Lynn J. Hernan; Bradley P. Fuhrman; David M. Steinhorn


Critical Care Medicine | 1999

The effect of lung-recruiting ventilatory strategies in acutely injured atelectasis-prone rabbits

Alexandre Rotta; Michael Chilungu; Björn Gunnarsson; David M. Steinhorn


Critical Care Medicine | 1999

Mechanical ventilation strategies induce pulmonary cytokine response

Alexandre Rotta; Björn Gunnarsson; David M. Steinhorn


Critical Care Medicine | 1999

The role of liquid perflubron (PFOB) in the oxidative process in vitro: Interaction with peroxyl radicals

Alexandre Rotta; Björn Gunnarsson; David M. Steinhorn


Critical Care Medicine | 1999

Perflubron (PFOB) protects against fatty acid oxidation in a non-biological, in vitro model

Alexandre Rotta; Björn Gunnarsson; Lynn J. Hernan; David M. Steinhorn


Critical Care Medicine | 1999

Liquid perflubron (PFOB) does not solubilize malondialdehyde (MDA) in vitro

Alexandre Rotta; Björn Gunnarsson; David M. Steinhorn


Critical Care Medicine | 1999

Hyperbaric oxygen exposure does not result in oxidative damage to rabbit lung tissue

Björn Gunnarsson; Alexandre Rotta; David M. Steinhorn

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Alexandre Rotta

Case Western Reserve University

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David M. Steinhorn

Children's Memorial Hospital

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James E. Fletcher

University of North Carolina at Chapel Hill

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A.M.B. Heard

Manchester Royal Infirmary

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