Effects of N6-L-phenylisopropyl Adenosine in Rats after Asphyxial Cardiac Arrest.
- Author:
Je Young PARK
1
;
Mi Jin LEE
;
Dong Rul OH
;
Won Jae LEE
;
Se Kyung KIM
Author Information
1. Department of Emergency Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea. emodr@mdhouse.com
- Publication Type:Original Article
- Keywords:
Asphyxia;
Cardiac arrest;
Adenosine;
Histologic damage score
- MeSH:
Adenosine*;
Anesthesia;
Animals;
Asphyxia;
Brain;
Brain Ischemia;
Heart Arrest*;
Ischemia;
Mortality;
Neurons;
Neuroprotective Agents;
Rats*;
Reperfusion Injury;
Resuscitation
- From:Journal of the Korean Society of Emergency Medicine
2002;13(2):135-140
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Cardiac arrest and resuscitation produce global cerebral ischemia and reperfusion injury to the brain, which lead to high mortality and delayed neuronal death. Adenosine has been suggested as an endogenous neuroprotective molecule, acting through multiple potential mechanisms. We investigated the possible neuroprotective effects of adenosine on cerebral recovery following global ischemia induced by asphyxial cardiac arrest. METHODS: Twenty-four rats were randomized into three groups. Group I, II, and III had anesthesia, procedures, and asphyxia for 7 minutes and then survived to 72 hours. Group I(n=8) was not administered N6- L - phenylisopropyl adenosine(L-PIA). Group II(n=8) was administered LPIA(0.8 mg/kg), and group III(n=8) was administered LPIA(1.5 mg/kg) after spontaneous circulation. The dosedependent neuroprotective effects of L-PIA were compared to the control by using a histopathological method. RESULTS: Histological observations of CA1 showed a more significant reduction of neuronal cell loss in groups II and III than in group I(p<0.05). Histological observations of CA2 and CA3 didn't show a significant reduction of neuronal cell loss in groups II and III compared to group I. CONCLUSION: These results show that post-ischemic administration of adenosine protected against delayed neuronal damage in the hippocampal CA1 area following a 7-min asphyxial cardiac arrest in rats.
