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Early adrenaline administration does not improve circulatory recovery during resuscitation from severe asphyxia in newborn piglets.

Linnér, Rikard LU ; Werner, Olof LU ; Perez de Sá, Valéria LU and Cunha Goncalves, Doris LU (2012) In Resuscitation 83(10). p.1298-1303
Abstract
AIM OF THE STUDY: : To investigate the effects of early intravenous adrenaline administration on circulatory recovery, cerebral reoxygenation, and plasma catecholamine concentrations, after severe asphyxia-induced bradycardia and hypotension.



METHODS: One-day old piglets were left in apnoea until heart rate and mean arterial pressure were less than 50min(-1) and 25mmHg, respectively. They randomly received adrenaline, 10 μg kg(-1) (n=16) or placebo (n=15) and were resuscitated with air ventilation and, when needed, closed-chest cardiac massage (CCCM). Eight not asphyxiated animals served as time controls.



RESULTS: CCCM was required in 13 piglets given adrenaline and in 13 given placebo. Time to... (More)
AIM OF THE STUDY: : To investigate the effects of early intravenous adrenaline administration on circulatory recovery, cerebral reoxygenation, and plasma catecholamine concentrations, after severe asphyxia-induced bradycardia and hypotension.



METHODS: One-day old piglets were left in apnoea until heart rate and mean arterial pressure were less than 50min(-1) and 25mmHg, respectively. They randomly received adrenaline, 10 μg kg(-1) (n=16) or placebo (n=15) and were resuscitated with air ventilation and, when needed, closed-chest cardiac massage (CCCM). Eight not asphyxiated animals served as time controls.



RESULTS: CCCM was required in 13 piglets given adrenaline and in 13 given placebo. Time to return of spontaneous circulation was: 72 (66-85) s vs. 77 (64-178) s [median (quartile range)] (p=0.35). Time until cerebral regional oxygen saturation (CrS(O2)) had increased to 30% was 86 (79-152) s vs. 126 (88-309) s (p=0.30). The two groups did not differ significantly in CrS(O2), heart rate, arterial pressure, right common carotid artery blood flow, or number of survivors: 13 and 11 animals. Plasma concentration of adrenaline, 2.5min after resuming ventilation, was 498 (268-868) nmol l(-1)vs. 114 (80-306) nmol l(-1) (p=0.01). Corresponding noradrenaline concentrations were 1799 (1058-4182) nmol l(-1)vs. 1385 (696-3118) nmol l(-1) (ns). In the time controls, the concentrations were 0.4 (0.2-0.6) nmol l(-1) of adrenaline and 1.8 (1.3-2.4) nmol l(-1) of noradrenaline.



CONCLUSION: The high endogenous catecholamine levels, especially those of noradrenaline, may explain why early administered adrenaline did not significantly improve resuscitation outcome. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Resuscitation
volume
83
issue
10
pages
1298 - 1303
publisher
Elsevier
external identifiers
  • wos:000309050600034
  • pmid:22445867
  • scopus:84865865854
  • pmid:22445867
ISSN
1873-1570
DOI
10.1016/j.resuscitation.2012.02.030
language
English
LU publication?
yes
id
a74ec3f7-4a5b-4fea-bf81-f72255098c0a (old id 2431488)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22445867?dopt=Abstract
date added to LUP
2016-04-01 11:10:48
date last changed
2022-02-10 17:23:05
@article{a74ec3f7-4a5b-4fea-bf81-f72255098c0a,
  abstract     = {{AIM OF THE STUDY: : To investigate the effects of early intravenous adrenaline administration on circulatory recovery, cerebral reoxygenation, and plasma catecholamine concentrations, after severe asphyxia-induced bradycardia and hypotension. <br/><br>
<br/><br>
METHODS: One-day old piglets were left in apnoea until heart rate and mean arterial pressure were less than 50min(-1) and 25mmHg, respectively. They randomly received adrenaline, 10 μg kg(-1) (n=16) or placebo (n=15) and were resuscitated with air ventilation and, when needed, closed-chest cardiac massage (CCCM). Eight not asphyxiated animals served as time controls. <br/><br>
<br/><br>
RESULTS: CCCM was required in 13 piglets given adrenaline and in 13 given placebo. Time to return of spontaneous circulation was: 72 (66-85) s vs. 77 (64-178) s [median (quartile range)] (p=0.35). Time until cerebral regional oxygen saturation (CrS(O2)) had increased to 30% was 86 (79-152) s vs. 126 (88-309) s (p=0.30). The two groups did not differ significantly in CrS(O2), heart rate, arterial pressure, right common carotid artery blood flow, or number of survivors: 13 and 11 animals. Plasma concentration of adrenaline, 2.5min after resuming ventilation, was 498 (268-868) nmol l(-1)vs. 114 (80-306) nmol l(-1) (p=0.01). Corresponding noradrenaline concentrations were 1799 (1058-4182) nmol l(-1)vs. 1385 (696-3118) nmol l(-1) (ns). In the time controls, the concentrations were 0.4 (0.2-0.6) nmol l(-1) of adrenaline and 1.8 (1.3-2.4) nmol l(-1) of noradrenaline. <br/><br>
<br/><br>
CONCLUSION: The high endogenous catecholamine levels, especially those of noradrenaline, may explain why early administered adrenaline did not significantly improve resuscitation outcome.}},
  author       = {{Linnér, Rikard and Werner, Olof and Perez de Sá, Valéria and Cunha Goncalves, Doris}},
  issn         = {{1873-1570}},
  language     = {{eng}},
  number       = {{10}},
  pages        = {{1298--1303}},
  publisher    = {{Elsevier}},
  series       = {{Resuscitation}},
  title        = {{Early adrenaline administration does not improve circulatory recovery during resuscitation from severe asphyxia in newborn piglets.}},
  url          = {{https://lup.lub.lu.se/search/files/2445615/3460018.pdf}},
  doi          = {{10.1016/j.resuscitation.2012.02.030}},
  volume       = {{83}},
  year         = {{2012}},
}