Increased neutrophil elastase release in patients with cardiopulmonary arrest: role of elastase inhibitor.
OBJECTIVE
To determine the changes in neutrophil elastase levels in patients with cardiac arrest occurring outside the hospital and to evaluate the effects of urinastatin on these changes and on the clinical outcomes of the patients.


METHODS
Prospective study.


METHODS
The Emergency Department and a general ICU in the tertiary care city hospital.


METHODS
Of the 40 patients who had an out-of-hospital cardiac arrest, 38 of the cases were randomized into 2 groups, with 2 cases being excluded because of contradiction to protocol. The control and urinastatin groups consisted of 20 and 18 patients, respectively.


METHODS
Control patients were treated by standard cardiopulmonary resuscitation (CPR) procedures. Patients in the urinastatin group were administered a 100,000 U dose of urinastatin immediately after arrival at the Emergency Department and three 100,000 U doses at 8 h intervals, within the first 24 h after resuscitation.


RESULTS
At the time of arrival at the emergency room (before administration of urinastatin), and at 30 min, 60 min, and 24 h after, the plasma levels of neutrophil elastase and blood gas levels were determined. Concerning the baseline characteristics of patients, causes of cardiac arrest, time duration of pre-hospital care and treatments given during CPR, there was no difference detected between the control and urinastatin groups. In addition, the pH and PaO2 values showed no differences. Neutrophil elastase values had already increased by the time of arrival and continued to do so until 60 min; at 24 h after admission, markedly higher values were obtained. These values were significantly higher in the non-resuscitated cases than in the resuscitated ones. Administration of urinastatin significantly suppressed this increase at 24 h, but did not improve the clinical outcomes, including resuscitation rate and survival rate.


CONCLUSIONS
Accompanying cardiopulmonary arrest and resuscitation, neutrophils are activated and elastase is released. Elevated elastase level is associated with poorer prognosis. Urinastatin can suppress the release of elastase, when utilized at the dose described in this study, did not improve the clinical outcomes of patients who had suffered an out-of-hospital cardiac arrest.
Gando
S
S
Department of Emergency and Critical Care Medicine, Sapporo City General Hospital, Japan.
Tedo
I
I
D000368:Aged; D001794:Blood Pressure; D016887:Cardiopulmonary Resuscitation; D016009:Chi-Square Distribution; D005260:Female; D006023:Glycoproteins / Q000627:therapeutic use*; D006323:Heart Arrest / Q000201:enzymology* / Q000628:therapy; D006801:Humans; D000860:Hypoxia / Q000201:enzymology; D019272:Leukocyte Elastase; D008297:Male; D017202:Myocardial Ischemia / Q000201:enzymology; D015428:Myocardial Reperfusion Injury / Q000201:enzymology; D010196:Pancreatic Elastase / Q000378:metabolism*; D011446:Prospective Studies; D016896:Treatment Outcome; D014361:Trypsin Inhibitors / Q000627:therapeutic use*
D006023:Glycoproteins; D014361:Trypsin Inhibitors; D010196:Pancreatic Elastase; D019272:Leukocyte Elastase; C028665:urinastatin