Drug overdose patients requiring intensive care admission in the Greater Portland Metropolitan Area: An analysis
✍ Scribed by ME Jones; J Jui; L Horenblas; M Albrich; J Herbst; R Eichner; W Hurley; J Hoppoch; J Lindberg; S Boyer; C Chipman
- Publisher
- Elsevier Science
- Year
- 1985
- Tongue
- English
- Weight
- 149 KB
- Volume
- 14
- Category
- Article
- ISSN
- 1097-6760
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✦ Synopsis
East Lansing; supported by grants from the US Army Medical Research and Development Command and the Michigan Heart Association Tissue injury during reperfusion following ischemia is thought to be in part mediated by lipid peroxidation. In vitro studies of lipid peroxidation have shown that the presence of a transitional metal, such as iron , is required for initiation of these reactions by oxygen radical species. The brain has large stores of chemically inert iron. This study examines the hypothesis that this iron is released from tissue stores as a function of the artificial perfusion technique used in resuscitation. Anesthesia was induced in 25 dogs (weighing 20 -30 kg) with IV ketamine and maintained with halothane after intubation. The bilateral parietal skull was trephined without removing the bone fragment. Cardiac arrest was induced by central venous injection of KC1 (0.75 mEq/kg) and confirmed by the arterial and ECG monitors. Five dogs (grou p 1) served as nonischemic controls; brain specimens were taken from these immediately. Brain samples were taken from 5 dogs after 45 minutes of arrest (Group 2) without any resuscitation. In the remaining 15 dogs, after 15 minutes of cardiac arrest, resuscitation was initiated with 100% O2 and CPR in Group 3, IAC-CPR in Group 4, and internal cardiac massage in Group 5. All resuscitation dogs were given epinephrine, 0.02 mg/kg IV bolus followed by continuous infusion of 2 I~g/kg/min. NaHCO 3 was given IV (3 mEq/kg for CPR and IAC-CPR, and 8 mEq/kg for internal massage) at the beginning of resuscitation. After 30 minutes of artificial perfusion, brain samples were taken. Malondialdehyde (MDA) was determined by the thiobarbituric acid method. The brain homogenate was ultrafiltered (Amicon 30,000 mol. wt. filter), and the filtrate was analyzed for iron by the o-phenanthroline assay. The data were analyzed by the statistical method of multivariance. Ultrafiltered iron (nm/100 mg tissue) was 6.2 + 1.9, and the MDA (nm/100 mg tissue) was 6.8 + :9 in the n0nischemic tissue. There was no significant change in MDA in any of the groups. There was no significant change in the iron during 45 minutes of ischemia, nor with 30 minutes of internal massage or IAC-CPR after 15 minutes arrest. However, ultrafilterable iron was increased to 14.1 -+ 5.6 with CPR. We conclude that while prolonged internal cardiac massage is not associated with delocalization of iron during artificial perfusion, CPR is. This study did not demonstrate evidence of lipid peroxidation by the presence of MDA during the acute resuscitation phase. Other investigators, however, have shown a 30-minute lag in the appearance of MDA after in vivo iron initiated lipid peroxidation.