Lawrence Caruso | PubMed Health

PubMed2005

Oxidant injury occurs rapidly after cardiac arrest, cardiopulmonary resuscitation, and reperfusion.

OBJECTIVE: Investigations conducted in cellular models show that reperfusion of ischemic tissue is associated with a burst of reactive oxidant species within minutes after reperfusion. Oxidant injury may play a role in the poor outcome typical of people resuscitated from cardiac arrest. The objective of the present study was to determine the presence and timing of oxidant injury in an in vivo model of cardiac arrest. DESIGN: Randomized controlled. SETTING: University medical center laboratory. SUBJECTS: Domestic swine. INTERVENTIONS: We evaluated oxidant injury during and after 8 mins of cardiac arrest using a gas chromatography/mass spectrometry F2-isoprostane assay and compared these results with a matched control group. MEASUREMENTS AND MAIN RESULTS: Baseline mean arterial, venous, and brain tissue F2-isoprostane levels were not significantly different when the cardiac arrest group was compared with the control group. However, in the group subjected to cardiac arrest and cardiopulmonary resuscitation we found significant (p < .0006) two- to three-fold increases in venous and arterial F2-isoprostane levels, which peaked between 15 and 30 mins after reperfusion and returned to baseline within 90 mins (p < .0006). Overall mean (+/- SE) brain tissue F2-isoprostane levels increased significantly to 370 +/- 60 vs. 140 +/- 60 ng/g tissue in the cardiac arrest group compared with the control group (p = .026). CONCLUSION: This study shows that F2-isoprostane measurement could be used to assess oxidant injury in an animal model of cardiac arrest and that oxidant injury occurs rapidly after cardiac arrest and reperfusion.

Animals↗

PubMed2003

Burn injuries.

PURPOSE OF REVIEW: To summarize new advances and research findings that relate to the treatment of burn victims. RECENT FINDINGS: Recent advances in burn resuscitation and critical care reflect a better understanding of the acute phase pathophysiology of severe burns. Aggressive management of the unstable burn airway is always the most important clinical priority. Emphasis has been placed on the early identification of inhalation injury and its impact on fluid resuscitation, as well as on a protective lung strategy to reduce the development of pulmonary edema, acute lung injury and pneumonia, and to reduce the risk of barotrauma. New blood markers, such as serum cholinesterase and inflammatory cytokines, have been introduced to assist in the prognosis of morbidity and mortality, beyond the traditional vital signs. At this time, however, these are available only for research purposes. Finally, early burn wound excision and coverage with new biodegradable materials results in less pain and more rapid healing for the patient. SUMMARY: The combination of innovative approaches and a dedicated burn team is expected to continue to improve survival in the next few years even in the most severe cases.

Journal Article↗