Methylene blue added to a hypertonic-hyperoncotic solution increases short-term survival in experimental cardiac arrest.
OBJECTIVE
Methylene blue (MB), a free-radical scavenger inhibiting the production and actions of nitric oxide, may counteract excessive vasodilatation induced by nitric oxide during cardiac arrest. Effects of MB in cardiac arrest and cardiopulmonary resuscitation were investigated.


METHODS
Randomized, prospective, laboratory animal study.


METHODS
University animal research laboratory.


METHODS
A total of 63 piglets of both sexes.


METHODS
A pig model of extended cardiac arrest (12 mins of untreated cardiac arrest and 8 mins of cardiopulmonary resuscitation) was employed to assess the addition or no addition of MB to a hypertonic saline-dextran solution. These two groups (MB and hypertonic saline-dextran group [MB group] and hypertonic saline-dextran-only group) of 21 animals were each compared with a group receiving isotonic saline (n = 21).


RESULTS
Although the groups were similar in baseline values, 4-hr survival in the MB group was increased (p = .02) in comparison with the isotonic saline group. Hemodynamic variables were somewhat improved at 15 mins after restoration of spontaneous circulation in the MB group compared with the other two groups. The jugular bulb levels of 8-isoprostane-prostaglandin F2alpha and 15-keto-dihydro-prostaglandin F2alpha (indicators of peroxidation and inflammation) were significantly decreased in the MB group compared with the isotonic saline group. Significant differences were recorded between the three groups in levels of protein S-100beta (indicator of neurologic injury), with lower levels in the MB group compared with the isotonic saline and hypertonic saline-dextran-only groups. Troponin I and myocardial muscle creatine kinase isoenzyme arterial concentrations (indicators of myocardial damage) were also significantly lower in the MB group.


CONCLUSIONS
MB co-administered with a hypertonic-hyperoncotic solution increased 4-hr survival vs. saline in an experimental porcine model of cardiac arrest and reduced oxidative, inflammatory, myocardial, and neurologic injury.
Miclescu
Adriana
A
Department of Surgical Sciences/Anesthesiology and Intensive Care, Uppsala University Hospital, Uppsala, Sweden.
Basu
Samar
S
Wiklund
Lars
L
D000818:Animals; D002560:Cerebrovascular Circulation; D003326:Coronary Circulation; D003911:Dextrans / Q000008:administration & dosage*; D004791:Enzyme Inhibitors / Q000008:administration & dosage*; D005260:Female; D005440:Fluid Therapy / Q000379:methods*; D006323:Heart Arrest / Q000628:therapy*; D008297:Male; D008751:Methylene Blue / Q000008:administration & dosage*; D011446:Prospective Studies; D011897:Random Allocation; D015427:Reperfusion Injury / Q000517:prevention & control; D012965:Sodium Chloride / Q000008:administration & dosage*; D016019:Survival Analysis; D013552:Swine
D003911:Dextrans; D004791:Enzyme Inhibitors; C104375:hypertonic saline-dextran solution; D012965:Sodium Chloride; D008751:Methylene Blue