Publications by authors named "Minna Aaltonen"

4 Publications

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Inhaled nitric oxide treatment inhibits neuronal injury after meconium aspiration in piglets.

Early Hum Dev 2007 Feb 21;83(2):77-85. Epub 2006 Jun 21.

Research Centre of Applied and Preventive Cardiovascular Medicine (CAPC), University of Turku, Kiinamyllynkatu 10, 20520 Turku, Finland.

Background: Meconium aspiration-induced hypertensive lung injury is frequently associated with neuronal damage. Inhaled nitric oxide (iNO) is widely used in the treatment of pulmonary hypertension, but its effects on the brain are poorly known.

Aims: The aim of this study was to determine the effects of iNO treatment on the neuronal tissue after meconium aspiration.

Study Design: 71 anesthetized, catheterized and ventilated newborn piglets were studied for 6 h. Thirty-five piglets were instilled with a bolus of human meconium intratracheally and 36 piglets with saline instillation served as controls. Nineteen meconium piglets and 17 control piglets were continuously treated with 20 ppm of iNO, started at 30 min after the insult. The extent of neuronal injury was analysed histologically, and the levels of brain tissue lipid peroxidation products, reduced glutathione (GSH), myeloperoxidase activity and oxidized DNA were analysed as indicators of oxidative stress.

Results: iNO treatment diminished the pulmonary hypertensive response caused by meconium aspiration, but did not change systemic or carotid hemodynamics. NO administration was associated with reduced neuronal injury and diminished amount of oxidized DNA in the hippocampus of the meconium piglets. Further, iNO treatment was associated with decreased level of GSH in the cortex, but no change in lipid peroxidation production or myeloperoxidase activity was detected in any of the studied brain areas.

Conclusions: Our results suggest that iNO treatment may inhibit DNA oxidation and neuronal injury in the hippocampus, associated with newborn meconium aspiration.
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http://dx.doi.org/10.1016/j.earlhumdev.2006.05.003DOI Listing
February 2007

Meconium aspiration induces neuronal injury in piglets.

Acta Paediatr 2005 Oct;94(10):1468-75

Research Centre of Applied and Preventive Cardiovascular Medicine (CAPC), University Hospital of Turku, Turku, Finland.

Aim: Meconium aspiration-induced hypertensive lung injury, especially when connected with perinatal asphyxia, has been associated with brain damage. We aimed to determine the neuronal injury induced by pulmonary meconium contamination alone and with concurrent asphyxia.

Methods: 36 anaesthetized and ventilated newborn piglets were haemodynamically monitored for 6 h. Seven piglets without concurrent asphyxia and seven piglets with asphyxia were instilled with a bolus of human meconium intratracheally. Seven piglets had only asphyxia and 15 piglets served as controls. The brains were studied histologically.

Results: Meconium aspiration did not change systemic haemodynamics acutely, while its combination with asphyxia diminished the abrupt postasphyxic systemic hypertensive peak and resulted in a transient increase in carotid artery flow, not seen after isolated asphyxia. Systemic pressure declined after 4 h in all insulted groups, but only isolated asphyxia was associated with a sustained decrease in carotid artery flow. Arterial oxygenation remained normal, except during the acute insults. Brain examination after meconium instillation indicated neuronal injury, especially in the CA3 region of the hippocampus. Asphyxia resulted in neuronal injury in the cortical, cerebellar and hippocampal hilus regions.

Conclusion: Severe meconium aspiration itself may result in hippocampal neuronal injury.
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http://dx.doi.org/10.1111/j.1651-2227.2005.tb01822.xDOI Listing
October 2005

Meconium aspiration induces oxidative injury in the hippocampus of newborn piglets.

Early Hum Dev 2005 May;81(5):439-47

Research Centre of Applied and Preventive Cardiovascular Medicine (CAPC), University of Turku, Kiinamyllynkatu 10, 20520 Turku, Finland.

Background: Meconium aspiration-induced hypertensive lung injury has been associated with neuronal damage in the newborn, but the mechanisms of the injury are poorly known.

Aims: The aim of the study was to determine the contribution of oxidative stress to the brain damage after pulmonary meconium contamination.

Study Design: Sixteen anesthetized and ventilated newborn piglets were studied for 6 h. Eight piglets were instilled with a bolus of human meconium intratracheally and eight piglets with saline instillation served as controls. Brain tissue lipid peroxidation products (TBARS), reduced glutathione (GSH), myeloperoxidase activity and oxidized DNA were analyzed as indicators of oxidative stress.

Results: Meconium aspiration did not change the systemic or carotid hemodynamics, but caused a well-established pulmonary hypertensive response. Sustained increase in additional oxygen demand was also observed after meconium insult, but no actual hypoxemia or hypercarbia was evident during the whole study period. Myeloperoxidase activity was elevated in the cerebellum after pulmonary meconium instillation, whereas concentrations of peroxidation products and glutathione were similar in the cortical, cerebellar and hippocampal regions of the two groups. Still, the amount of oxidized DNA was increased in the hippocampus of the meconium-aspirated piglets when compared to controls.

Conclusions: Our data thus suggest that oxidative injury associated with pulmonary, but not systemic, hemodynamic disturbances may contribute to hippocampal damage after meconium aspiration in newborns.
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http://dx.doi.org/10.1016/j.earlhumdev.2005.03.011DOI Listing
May 2005

Asphyxia aggravates systemic hypotension but not pulmonary hypertension in piglets with meconium aspiration.

Pediatr Res 2003 Mar;53(3):473-8

Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland.

Meconium aspiration and birth asphyxia are both separately connected to significant pulmonary and systemic hemodynamic changes in newborns, but, although these insults frequently coexist, their combined effects on the neonatal circulation are still controversial. To determine the pulmonary and systemic circulatory changes induced by pulmonary meconium contamination with concurrent asphyxia, 41 anesthetized and ventilated newborn piglets (10-12 d) were studied for 6 h. Eleven piglets were instilled with a bolus of human meconium intratracheally, and 10 piglets had meconium instillation with immediate induction of an asphyxic insult. Eight piglets had only asphyxia and 12 ventilated piglets served as controls. Meconium instillation (with and without asphyxia) resulted in a sustained decrease in the oxygenation, which remained, however, on the control level in the asphyxic group. Although meconium insufflation (with and without asphyxia) increased pulmonary artery pressure and vascular resistance progressively during the study period, the meconium-induced hypertensive effect was actually diminished by additional asphyxia. Asphyxia alone did not have any effect on these pulmonary hemodynamic parameters. On the other hand, whereas systemic arterial pressure and vascular resistance remained on the control level after meconium instillation alone, asphyxia (with and without pulmonary meconium insult) resulted in a sustained fall in systemic pressure already by 4 h. Our data thus indicate that although the coexisting asphyxia seems to moderate the meconium aspiration-induced pulmonary hypertensive response, this additional asphyxic insult does not affect the associated hypoxemia, but rather significantly exacerbates systemic hypotension.
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http://dx.doi.org/10.1203/01.PDR.0000049514.02607.03DOI Listing
March 2003
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