scholarly journals Endogenous brain‐sparing responses in brain pH and PO 2 in a rodent model of birth asphyxia

2020 ◽  
Vol 229 (3) ◽  
Author(s):  
Alexey S. Pospelov ◽  
Martin Puskarjov ◽  
Kai Kaila ◽  
Juha Voipio
Keyword(s):  
2019 ◽  
Author(s):  
Alexey S. Pospelov ◽  
Martin Puskarjov ◽  
Kai Kaila ◽  
Juha Voipio

ABSTRACTAimTo study brain-sparing physiological responses in a rodent model of birth asphyxia which reproduces the asphyxia-defining systemic hypoxia and hypercapnia.MethodsSteady or intermittent asphyxia was induced for 15-45 min in anesthetized 6 and 11 days old rats and neonatal guinea pigs using gases containing 5% or 9% O2 plus 20% CO2 (in N2). Hypoxia and hypercapnia were induced with low O2 and high CO2, respectively. Oxygen partial pressure (PO2) and pH were measured with microsensors within the brain and subcutaneous (“body”) tissue. Blood lactate was measured after asphyxia.ResultsBrain and body PO2 fell to apparent zero with little recovery during 5% O2 asphyxia and 5% or 9% O2 hypoxia, and increased more than twofold during 20% CO2 hypercapnia. Unlike body PO2, brain PO2 recovered rapidly to control after a transient fall (rat), or was slightly higher than control (guinea pig) during 9% O2 asphyxia. Asphyxia (5% O2) induced a respiratory acidosis paralleled by a progressive metabolic (lact)acidosis that was much smaller within than outside the brain. Hypoxia (5% O2) produced brain-confined alkalosis. Hypercapnia outlasting asphyxia suppressed pH recovery and prolonged the post-asphyxia PO2 overshoot. All pH changes were accompanied by consistent shifts in the blood-brain barrier potential.ConclusionRegardless of brain maturation stage, hypercapnia can restore brain PO2 and protect the brain against metabolic acidosis despite compromised oxygen availability during asphyxia. This effect extends to recovery phase if normocapnia is restored slowly, and it is absent during hypoxia, demonstrating that exposure to hypoxia does not mimic asphyxia.


2020 ◽  
Author(s):  
Tommi Ala-Kurikka ◽  
Alexey Pospelov ◽  
Milla Summanen ◽  
Aleksander Alafuzoff ◽  
Samu Kurki ◽  
...  

ABSTRACTBirth asphyxia (BA) is often associated with seizures which emerge during the recovery and may exacerbate the ensuing hypoxic-ischemic encephalopathy. In rodent models of BA, exposure to hypoxia is used to evoke seizures, which commence already during the insult. Here, we introduce a term-equivalent model of BA, in which seizures are triggered after, not during, brain hypoxia. Postnatal day 11-12 rat pups were exposed either to steady asphyxia (15 min; 5 % O2 + 20 % CO2) or to intermittent asphyxia (30 min; three 5+5 min cycles of 9 % and 5 % O2 at constant 20 % CO2). Cortical activity and seizures were recorded in freely-behaving animals. Simultaneous electrode measurements of cortical local field potentials (LFP) and intracortical pH and Po2 were made under urethane-anesthesia. Both protocols decreased blood pH to <7.0 and base excess by 20 mmol/l, and evoked an increase in plasma copeptin (0.2 to 5 nM). Clonic and tonic convulsions were triggered after intermittent but not steady asphyxia, and they were tightly associated with electrographic seizures. During intermittent asphyxia LFP activity was suppressed as brain pH decreased from 7.3 to 6.7. Brain Po2 fell below detection level in 5 % ambient O2 but returned to the baseline level during steps to 9 % O2. Neuronal hyperexcitability and seizures were suppressed in all types of experiments when the post-asphyxia brain pH recovery was slowed down by 5 % CO2. Our data suggest that the recurring hypoxic episodes during intermittent asphyxia promote neuronal excitability, which becomes established as hyperexcitability and seizures only after the suppressing effect of the hypercapnic acidosis is relieved. The present rodent model of BA is to our knowledge the first one in which, consistent with clinical BA, robust behavioral and electrographic seizures are triggered after and not during the BA-mimicking insult.


2010 ◽  
Author(s):  
Daniel M. Noel ◽  
Tammy J. Sluder ◽  
Julia Lehmann ◽  
Jamie D. Whittemore ◽  
Russell W. Brown

2011 ◽  
Author(s):  
Marla K. Perna ◽  
Meredith L. Smith ◽  
Russell W. Brown
Keyword(s):  

2018 ◽  
Vol 2 (S1) ◽  
pp. e000127
Author(s):  
Kushali Tanna ◽  
K M Mehariya ◽  
Suchita Munsi ◽  
Charul Pujani

Aims and Objectives: To study an incidence of myocardial dysfunction in neonates admitted with perinatal asphyxia, to find out its correlation with severity of birth asphyxia and its outcome. Methods: This prospective study was conducted among 40 term neonates admitted in NICU of Civil Hospital Ahmedabad who had suffered with perinatal asphyxia (defined by WHO ), resuscitated as per NRP guidelines-2015 including both intramural and extramural admissions and who developed to hypoxic ischemic encephalopathy as defined by Levene staging. Neonates with congenital heart diseases, major central nervous system malformations and neonatal sepsis were excluded. Myocardial involvement was assessed by clinical evaluation, ECG, Creatinine Kinase Total (25-200IU/L), CK-MB (0-25IU/L) and Troponin I (0-0.03ug/L) measurements. Results: Among 40 cases, 10(25%) neonates had moderate birth asphyxia while 30(75%) had severe birth asphyxia. Respiratory distress was observed in 34(77.5%), poor spontaneous respiration 4(10%),shock in 14(35%),CCF 19(47.5%) while ECG was abnormal in 30(76.7%). Serum levels of CPK Total, CPK- MB and Troponin I were raised in 34(85%), 32(80%) and 28 (70%) neonates, respectively.  Conclusion: There was a direct correlation between ECG changes and enzymatic levels which showed increasing abnormalities with increasing with severity of HIE.  


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1666-P
Author(s):  
CEREN KARACAY ◽  
PETRA KOTZBECK ◽  
BARBARA PRIETL ◽  
CLEMENS HARER ◽  
THOMAS PIEBER
Keyword(s):  

2019 ◽  
Vol 2 ◽  
pp. 1
Author(s):  
Bhushita Lakhkar ◽  
M. M. Patil ◽  
Bhavana Lakhkar ◽  
Bhushan Lakhkar

Objective The study aimed to utilize the neurosonographic findings in neonates in early diagnosis, prediction of their long-term outcome, parental counseling, and early intervention. Methods The study was carried out in neonatal intensive care unit (NICU) of Shri BM Patil Medical College and Hospital. All preterms and term babies with neurological clinical findings were included in the study. Neurosonogram was done within first 7 days in preterms and when indicated in terms. Philips HD11XE ultrasound and color Doppler unit were used with a small footprint probe. Color Doppler images for vessels were performed for screening of vascular changes. Results A total of 215 babies were included, of which 80 (32%) were term and the rest were preterm. Mean weight of term babies was 2.8 kg and that of preterm was 1.2 kg.Among term babies, 78% showed ultrasound abnormality, and among preterm, 42%showed abnormalities. Among term babies, 60% and, among preterms, 30% had birth asphyxia. Periventricular leukomalacia was the most common and earliest finding followed by thalamic hyperechogenicity and intracranial hemorrhage. Intraventricular hemorrhage was more common in preterm babies. Other common finding in NICU was meningitis which was more common in pretrms. Among congenital anomalies, corpus callosal agenesis was more common. Conclusions Point of care ultrasonography along with Doppler study is very useful and safe to use in NICUs. It helps in diagnosis, patient management as well as prediction of many short- and long-term outcomes.


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