Systemic bacteraemia following haemorrhagic shock in mice: Alleviation with oral interleukin 6

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Resuscitation 32 (1996) 165- 166

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Capone A, Safar P, Radovsky A, Wang Y-F, Peitzman A, Tisherman SA SCRR-Universify of Pittsburgh, 3434 5th Ave., Pittsburgh, PA 15260, L/SA J. Trauma Inj Infect Crit 1996;40/3: 388-395 Objective: We hypothesize that during severe normothennic hemorrhagic shock (HS), induction of profound hypothermic circulatory arrest (PHCA) of 60 min to allow repair of otherwise lethal injuries in a bloodless field, can be survived without brain damage. In previous dog studies, normothermic HS with meanarterial pressure(MAP) of 40 mmHg for 30 min, followed by PHCA of 2 h at brain (tympanic membrane) temperature of 5 to IOOCand core temperature of IO%, induced and reversed with cardiopulmonary bypass, resulted in survival with mild histop&mlogic brain damage. This study was designed to determinethe severity of HS that can safely allow I h of PHCA. In pilot studies with HS at MAP 30 mmHg for 90 min with or without su~wnt PHCA of 60 min there were no survivors. Methods: In the definitive study, outcomes in four groups of five dogs eachwerecompared: group I, HS at MAP 30 mmHg for 60 ttxin and normothermic fluid resuscitation; group II, H S at MAP 30 mmHg for 60 min. PHCA for 60 min, and resuscitation; group III, HS at MAP 40 mmHg for 60 min and normothermic fluid resuscitation; and group IV, HS at MAP 40 mmHg For 60 min, PHCA for 60 min. and resuscitation. Controlled ventilation was maintained for at least 20 h and intensive care for 72 h. Results: In groups I and II, two of five dogs in each group survived to 72 h. In groups III and IV, all ten dogs survived. All survivors were functionally normal, with neurolo.gicdeficit scores(oo/o= normal, 100%= brain dead) of < 10%.Light microscopic scoring of I8 brain regions revealed no ischemic changes.All nonsurvivors had a severe metabolic acidemio after HS and developed multiple organ failure, including pulmonary edema, pneumonia, and intestinal necrosis. Conclusions: The critical level of hypotension during 60 min normothermic HS that is compatible with survival in dogs is a MAP of bct~ecn 30 and 40 mmHg. After otherwise survivable severenormothemtic HS of 60 min, PHCA of 60 mitt does not add brain damage or mortality, and may atlow survival from injuries that would otherwise be irreparable. Systemk ketaneda fullewing Imcmarrhagic sbeck in mice: AlIevktkRwItkomIiIltcrIewkiIl6 Rollwagen FM, Li Y-Y, Pacheco ND, Nielsen TB

WoundRepair EnhancementProgram, Naval Medical Research Institute, 8901 WisconsinAve., Bethesda.MD 20889-5607.USA Cytokine 1996;812: 121-129 A murine model of haemorrhagic shock was usedto investigate bacterial translocation from the gut and subsequent systemic immunoreduction. Anaesthetized mice were bled from the femoral artery, and held at a mean arterial blood pressureof 35 mmHg for I h then resuscitatedwith shed blood and two-fold volume lactated Ringer’s solution. Upon awakening, they were given cytokines or control media orally. Bacteriological cultures of livers, spleens and mesenteric lymph nodes from haemorrhagedmice given cytokine had significantly fewer bacteria&m of tissue than those given media. Recombinant IL-6 mimicked the effects seen with crude cytokines. Reduction of proliferation among spleen cells from haemorrhaged mice was observedand cotrId be partially returned to normal by cytokine feeding. Mixing experiments in which cells from haetnorrhaged mice were added to those of normal mice in an MLR showed no suppressor activity. Flow cytometry analysis reveakd a reduction in CD 3+ cells at I6 h post-haemorrhage in mice fed control media or cytokines, suggesting that reduced proliferative capacity may be due to loss of function rather than active suppression. Histological examination of the intestines of haemorrhagedmice fed cytokines or media revealed restoration of intestinal mucosal integrity by cytokine administration. These results suggestthat oral administration of IL-6 may be an important treatment for the prevention of systemic sepsis following haemorrhage. Crcetioc kimse IUIII ereatInc kiiMI? nksse after nontmmaatieeudtaeerreat Mullner M, Stem F, Binder M, Bnmner M, Hirsch1 MM, Mustafa G, SchreiberW, Kurkciyan I, Domanovits H. Laggner AN Medical School, University of Vienna, ViennaGeneral Hospital, WaehringerGuertel 18-M&D. 1090 Vienna Austria Am. J. Cardiol 1996;7718:581-585 The aim of the study was to describe the course of serum creatine kinase (CK) and its MB fraction (CK-MB) in patients surviving cardiac arrest, and to identify factors influencing CK and CK-MB release. The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation, collected within a period of 33 months, were evaluated retrospectively and compared with laboratory blood investigations collected prospectively (on admission and after 6. 12,and

0300-9572/96/$15.00 0 1996Elsevier Science Ireland Ltd. All rights reserved