The palpation of pulses

.Ah.strac~r.\

MAP 40 mm Hg for 60 min and nortnothermic fluid resuscitation: and group IV, HS at MAP 40 mm Hg for 60 min, PHCA for 60 min. and resuscitation. Controlled ventilation was maintained for at least ‘0 h and intensive care for 72 h. Results: In groups 1 and II, two of tive dogs in each group survived to 72 h. In groups III and IV, all ten dogs survived. All survivors were functionally normal, with neurologic deficit scores (OX= normal. 100%= brain dead) of < 10% Light microscopic scoring of 18 brain regions revealed no ischemic changes. All nonsurvivors had a severe metabolic acidemia after HS
haemorrhagic shock in mice: Allevia-

Rollwagen FM. Li Y-Y, Pdcheco ND, Nielsen TB Wound Repair Enhancement Progrutn, Natal Medical tute, 8901 Wisconsin Are.. Bethesda, MD 20889-5607.

Research USA

Insti-

Cytokine 1996; 8,2: 121 129 A murine model of haemorrhagic shock was used to 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 pressure of 35 mm Hg for one hour then resuscitated with shed blood and two-fold volume lactated Ringer’s solution. Upon awakening, they were given cytokineb or control media orally. Bacteriological cultures of livers. spleens and mesenteric lymph nodes from haemorrhaged mice given cytokine had significantly fewer bacteria;gm of tissue than those given media. Recombinant IL-6 mimicked the effects seen with crude cytokines. Reduction of proliferation among spleen cells from hdemorrha&ed mice was observed and could be partially returned to normal by cytokine feeding. Mixing experiments in which cells from haemorrbaged mice were added to those of normal mice in an MLR showed no suppressor activity. Flow cytometry analysis revealed a reduction in CD 3 t cells at 16 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 haemorrhaged mice fed cytokines or media revealed restoration of intestinal mucosal integrity by cytokine administration. These results suggest that oral administration of IL-6 may be an important treatment for the prevention of systemic sepsis following haemorrhage. Creatine kiilase and creatine kinase-MB cardiac arrest

release after nontraumatic

Mullner M. Sterz F, Binder M, Brunner M, Hirsch1 MM. Mustafa Cr. Schreiber W, Kurkciyan 1. Domanovits H. Laggner AN Medical School. Uniwrsi/~ qf’ Vienna, Vienno General Hospital. Woehringer

Guertel

18-20/6D.

1090 Viennct. AUT

Am J Cardiol 1096: 77:X: 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 laborator) blood investigations collected prospectively (on admission and after 6, 12, and 24 h) in I07 adult patients surviving a witnessed cardiac arrest for 24 h. CK and CK-MB were elevated in > 75% of the patients within 24 h. Release of CK and CK-MB was mainly
)I

infarction (AMI). cumulative energy administered during detihrillntion, and duration of chest trauma by compression. The OK-MB CK ratio was elevated in 32% of the patients. Of patients with electrocar(I/ had an elevated CK-MB <‘K diographic evidence of AMI, only 49,~) ratio. In conclusion, the elevation in serum CK and CK-MB fraction in patients after nontraumatic cardiac arrest is a trcqucnt finding, and is associated with ischemic myocardial injury. .IS well as physica! trauma to the chest. This should be considered \ahen mtcrpreting the course of CK and CK-MB fraction for the diap!!osIs <,I’,&MI. The palpation of pulses

Mather C, O’Kelty S

In 554 anaesthetised patients, the times taken I<)separately palpatr and identify each of the carotid, radial, hrachiai and femoral pulses were recorded. The patients were divided into three group+ based on the form of airway management chosen (tracheal tube, facemask ok laryngeal mask airway). Our results demonstrate thai in the operating theatre environment the identilication of the radial pulse IS tbc most rapid and reliable; by 5s. 98% and by 10s. more than 99” 0 of radial pulses were identilied. The carotid pulse was IIG: srt casrl> identified. requiring 10sto enable an identification rate ot g!‘rater than 95”ti) l-he presence of a laryngeal mask airway 01’;I ;rache:,i tri!w did no1 hirl~iel the identification of carotid pulse Tumor necrosis factor alpha and inter&kin lbeta are responsible for in vitro myocardial cell depression induced by human septic shock serum

Kumar A. Thota V. Dee L. Olson J. lJrct7 E. l’arrilio .I\: Seuion SL MC.

of C‘ritic,al 1653 West

Caw

Medicine.

C0npre.s.sPorkwav. J Exp Mctl 1996: 153 3: ‘14’) 93P

Jelke BIdg., K~tsi7-P~eshl~tc~rttrttChicqw. II hOhI?. I IS.4

Previous studies have demonstrated the prcbsencc01 myocardial depression in clinical and experimental septic shark This depression is associated with the presence of a circulatin: nry~\cnrdinldeprcssarlt substance with physlcal characteristics consisten! \vlth cytokines. ‘The present study utilized an in vitro myocardial cell assa! to cxaminc the role of various human recombinant cytokines. it&ding tumor necrclsis factor (TNF)alpha and interleukin (IL)1 beta. rn depression oi cardiac myocyte contractile function induced b! serum from lwnar~s with septic shock. The extent and velocity of -lbetd induced depres\crm dr m\ocardial cell contrdctihtl at substdmialtq lower concentratic!ni cc&~;tent with a synergistic effect. Using immunoabsorption, rentov.Ll ol‘ both TNI -
and safety in criti-

Perry JC. Fenrich Al.. Hulse JE. Triedma), .IK. t,nedm,m RA. Lamberti JJ C;ttdiolo,q St17 D&vi.

Dirt,ion. C‘/r!ltltw~ :r Hrorr ( ,A 92/l?.?, I ,C/f

lttstitrrrt

i!)?O ( 7ri/d~-c~tt:\ w;tr.