Cardiac arrest and resuscitation: brain iron delocalization during reperfusion.

We hypothesize that brain injury from cardiac arrest occurs during reperfusion and is in part mediated by iron-dependent lipid peroxidation. We conducted a study to examine the time course of brain iron delocalization and lipid peroxidation in an animal model of cardiac arrest and resuscitation. Assays for brain tissue iron in low-molecular-weight species (LMWS iron) used the o-phenanthroline test on an ultrafiltered (molecular weight less than 30,000) tissue sample; malondialdehyde (MDA), a product of lipid peroxidation, in brain tissue was assayed by the thiobarbituric acid test (TBA). Samples of the parietal cortex from 11 nonischemic control dogs (Group 1) had LMWS iron levels of 9.6 +/- 4.9 nmol/100 mg tissue and MDA levels of 7.7 +/- 2.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 15 minutes of cardiac arrest (Group 2) had LMWS iron levels of 9.3 +/- 3.1 nmol/100 mg tissue and MDA levels of 6.1 +/- 1.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 45 minutes of cardiac arrest (Group 3) had LMWS iron levels of 6.7 +/- 3.3 nmol/100 mg tissue and MDA levels of 5.6 +/- 0.4 nmol/100 mg tissue. There was no significant difference among the three groups for either LMWS iron or MDA. Five dogs were subjected to 15 minutes of cardiac arrest and definitive resuscitation by internal cardiac massage and defibrillation (Group 4). Following resuscitation the chest was closed and the dogs were given intensive care for two hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Perfusion of the cerebral cortex by use of abdominal counterpulsation during cardiopulmonary resuscitation.

Perfusion of the cerebral cortex (rCCBF) during resuscitation from cardiac arrest was studied using 24 large dogs and three different resuscitation models. Conventional cardiopulmonary resuscitation (CPR) was compared with interposed abdominal compression CPR (IAC-CPR) and with IAC-CPR together with infusion of epinephrine. Conventional CPR produced a mean rCCBF of only 11% (0.057 +/- 0.07 ml/min/g) normal perfusion (0.54 +/- 0.14 ml/min/g). Even without epinephrine, IAC-CPR produced mean rCCBF equal to 51% (0.27 +/- 0.17 ml/min/g) of normal. With epinephrine, IAC-CPR produced rCCBF (0.93 +/- 0.49 ml/min/g) statistically indistinguishable from normal. Both models of IAC-CPR were significantly superior to conventional CPR in perfusion of the cerebral cortex.