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Author(s): Niklas Nielsen [sup.1], Alain Cariou [sup.2] [sup.3], Christian Hassager [sup.4] Author Affiliations: (1) 0000 0001 0930 2361, grid.4514.4, Department of Clinical Sciences Lund, Anesthesia and Intensive Care, Lund University, [...]

Purpose Some of the neuroprotective effects of hydrogen sulfide (H.sub.2S) have been attributed to systemic hypometabolism and hypothermia. However, systemic metabolism may vary more dramatically than brain metabolism after cardiac arrest (CA). The authors investigated the effects of inhaled exogenous hydrogen sulfide on brain metabolism and neurological function in rabbits after CA and resuscitation. Methods Anesthetized rabbits were randomized into a sham group, a sham/H.sub.2S group, a CA group, and a CA/H.sub.2S group. Exogenous 80 ppm H.sub.2S was administered to the sham/H.sub.2S group and the CA/H.sub.2S group which suffered 3 min of untreated CA by asphyxia and resuscitation. Effects on brain metabolism (cerebral extraction of oxygen (CEO.sub.2), arterio-jugular venous difference of glucose [AJVD(glu)] and lactate clearance), S100B, viable neuron counts, neurological dysfunction score, and survival rate were evaluated. Results CEO.sub.2, AJVD(glu), and lactate increased significantly after CA. Inhalation of 80 ppm H.sub.2S significantly increased CEO.sub.2 (25.04 ± 7.11 vs. 16.72 ± 6.12 %) and decreased AJVD(glu) (0.77 ± 0.29 vs. 1.18 ± 0.38 mmol/L) and lactate (5.11 ± 0.43 vs. 6.01 ± 0.64 mmol/L) at 30 min after resuscitation when compared with the CA group (all P < 0.05). In addition, neurologic deficit scores, viable neuron counts, and survival rate were significantly better whereas S100B was decreased after H.sub.2S inhalation. Conclusions The present study reveals that inhalation of 80 ppm H.sub.2S reduced neurohistopathological damage and improves early neurological function after CA and resuscitation in rabbits. The increased CEO.sub.2 and decreased AJVD(glu) and enhanced lactate clearance may be involved in the protective effects., Author(s): Xia Wei [sup.1], Le Duan [sup.1], Liqun Bai [sup.1], Miaomiao Tian [sup.1], Wenzhi Li [sup.1], Bing Zhang [sup.1] Author Affiliations: (1) grid.412463.6, 0000000417626325, Department of Anesthesiology, Second Affiliated Hospital [...]

Byline: Alexandra Gendo (1), Ludwig Kramer (1), Michael Hafner (1), Georg-Christian Funk (1), Christian Zauner (1), Fritz Sterz (2), Michael Holzer (2), Edith Bauer (1), Christian Madl (1) Keywords: Sensory evoked potentials Cardiopulmonary resuscitation Postischemic metabolic and circulatory derangements Outcome prediction Abstract: Objective: To assess the validity of early sensory evoked potential (SEP) recording for reliable outcome prediction in comatose cardiac arrest survivors within 48 h after restoration of spontaneous circulation (ROSC). Design and setting: Prospective cohort study in a medical intensive care unit of a university hospital. Patients: Twenty-five comatose, mechanically ventilated patients following cardiopulmonary resuscitation Measurements and results: Median nerve short- and long-latency SEP were recorded 4, 12, 24, and 48 h after ROSC. Cortical N20 peak latency and cervicomedullary conduction time decreased (improved) significantly between 4, 12, and 24 h after resuscitation in 22 of the enrolled patients. There was no further change in short-latency SEP at 48 h. The cortical N70 peak was initially detectable in seven patients. The number of patients with increased N70 peak increased to 11 at 12 h and 14 at 24 h there was no further change at 48 h. Specificity of the N70 peak latency (critical cutoff 130 ms) increased from 0.43 at 4 h to 1.0 at 24 h after ROSC. Sensitivity decreased from 1.0 at 4 h to 0.83 at 24 h after ROSC. Conclusion: Within 24 h after ROSC there was a significant improvement in SEP. Therefore we recommend allowing a period of at least 24 h after cardiopulmonary resuscitation for obtaining a reliable prognosis based on SEP. Author Affiliation: (1) Department of Internal Medicine IV, Intensive Care Unit 13 H1, University of Vienna, Wahringer Gurtel 18-20, 1090 Vienna, Austria (2) Department of Emergency Medicine, University of Vienna, Wahringer Gurtel 18-20, 1090 Vienna, Austria Article History: Received Date: 01/11/2000 Accepted Date: 17/05/2001 Article note: Final revision received: 16 May 2001 Electronic Publication

Byline: S. Gando (1), S. Nanzaki (1), Y. Morimoto (1), S. Kobayashi (1), O. Kemmotsu (1) Keywords: Key words Cardiac arrest; Cardiopulmonary resuscitation; Selectin; Neutrophil; Endothelium Abstract: Objective: To investigate the relationship between cytokines and the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes of cytokines as well as alterations in the markers of neutrophil activation, platelet and endothelial activation, and endothelial injury. Design: Prospective, cohort study. Setting: General intensive care unit of a tertiary care center. Patients and participants: 26 out-of-hospital cardiac arrest patients were classified into two groups: those who achieved return of spontaneous circulation (ROSC) (n = 10) and those with no ROSC (n = 16). Eight normal healthy volunteers served as control subjects. Measurements and results: Serial levels of soluble L-selectin (sL-selectin), soluble P-selectin (sP-selectin), neutrophil elastase, and soluble thrombomodulin were measured during and after cardiopulmonary resuscitation (CPR). Serial levels of tumor necrosis factor [alpha] (TNF[alpha]) and interleukin-1[beta] (IL-1[beta]) were also measured. We could not find any elevations in either cytokine during the study period. In both groups, sP-selectin levels were significantly higher than those in control subjects from the time of arrival at the emergency department to 24 h after admission. sL-selectin levels in the two groups were markedly lower compared to those in control subjects at all sampling points. In patients with ROSC, cardiac arrest and CPR led to an increase in the levels of neutrophil elastase and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. No statistical differences in the levels of the two selectins, neutrophil elastase, and soluble thrombomodulin between the two groups were found during CPR. Conclusions: Out-of-hospital cardiac arrest and CPR induces platelet, neutrophil, and endothelial activation and is associated with endothelial injury. Inflammatory cytokines may not have an important role in human whole-body ischemia-reperfusion injury. Author Affiliation: (1) Department of Anesthesiology and Intensive Care, Hokkaido University School of Medicine, N15 W7, Kita-ku, Sapporo, 060 Japan e-mail: sgando@med.hokudai.ac.jp Tel. +81(11)716--1161 Fax +81(11)716--9666, JP Article note: Received: 2 November 1998 Final revision received: 3 March 1999 Accepted: 26 March 1999