Open AccessH 2 Gas Improves Functional Outcome After Cardiac Arrest to an Extent Comparable to Therapeutic Hypothermia in a Rat Model
Author(s) -
Hayashida Kei,
Sano Motoaki,
Kamimura Naomi,
Yokota Takashi,
Suzuki Masaru,
Maekawa Yuichiro,
Kawamura Akio,
Abe Takayuki,
Ohta Shigeo,
Fukuda Keiichi,
Hori Shingo
Publication year - 2012
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.112.003459
Subject(s) - medicine , return of spontaneous circulation , ventricular fibrillation , hypothermia , inhalation , anesthesia , cardiopulmonary resuscitation , resuscitation , ventilation (architecture) , mechanical engineering , engineering
Background All clinical and biological manifestations related to postcardiac arrest ( CA ) syndrome are attributed to ischemia–reperfusion injury in various organs including brain and heart. Molecular hydrogen (H 2 ) has potential as a novel antioxidant. This study tested the hypothesis that inhalation of H 2 gas starting at the beginning of cardiopulmonary resuscitation ( CPR ) could improve the outcome of CA . Methods and Results Ventricular fibrillation was induced by transcutaneous electrical epicardial stimulation in rats. After 5 minutes of the subsequent CA , rats were randomly assigned to 1 of 4 experimental groups at the beginning of CPR : mechanical ventilation ( MV ) with 2% N 2 and 98% O 2 under normothermia (37°C), the control group; MV with 2% H 2 and 98% O 2 under normothermia; MV with 2% N 2 and 98% O 2 under therapeutic hypothermia ( TH ), 33°C; and MV with 2% H 2 and 98% O 2 under TH . Mixed gas inhalation and TH continued until 2 hours after the return of spontaneous circulation ( ROSC ). H 2 gas inhalation yielded better improvement in survival and neurological deficit score ( NDS ) after ROSC to an extent comparable to TH . H 2 gas inhalation, but not TH , prevented a rise in left ventricular end‐diastolic pressure and increase in serum IL ‐6 level after ROSC . The salutary impact of H 2 gas was at least partially attributed to the radical‐scavenging effects of H 2 gas, because both 8‐ OHdG ‐ and 4‐ HNE ‐positive cardiomyocytes were markedly suppressed by H 2 gas inhalation after ROSC . Conclusions Inhalation of H 2 gas is a favorable strategy to mitigate mortality and functional outcome of post‐ CA syndrome in a rat model, either alone or in combination with TH .