Vasoactive intestinal peptide and nitric oxide in the acute phase following burns and trauma.

VIP and NO co-localized in many of the same neurons, are co-released by some of the same physiological stimuli. In this study we seek the divergent roles in relation to tissue injury between the neurotransmitters within 24 h after burn injury. Forty-four subjects were examined. Fourteen were mechanical trauma patients with mean injury severity score (ISS) of 27, 15 burns patients with mean per cent total burn surface area (%TBSA) of 18%, and 15 healthy controls. Patients plasma were withdrawn immediately on admission (OA) and 24 h post-injury (PI). Controls fasted (>10 h) the night before morning sampling. Enzyme-linked immunosorbent assay (ELISA) technique suitable for the measurements of NO and VIP was used. For each comparison between the patients and control groups, NO(2)(-)/NO(3)(-) plasma levels were higher in burn (P<0.001) and trauma (P<0.0005) than controls. VIP was higher in trauma (P<0.05) but not in burns (P=NS). Trauma and human burn injuries are associated with increase levels of NO productions. While VIP rose in trauma, it remained unchanged in burns. The relationship between VIP and NO observed under physiological conditions in thermal and trauma injury may be of importance in wound healing.

Prediction of posttraumatic adult respiratory distress syndrome by albumin excretion rate eight hours after admission.

BACKGROUND: Adult respiratory distress syndrome (ARDS) in trauma victims carries a mortality on the order of 50%. An early feature is an increased capillary permeability causing an extravasation of plasma proteins and water, leading to interstitial edema. In the kidney, the increase in microvascular permeability is manifested as increased albumin excretion detectable by sensitive immunoassay. METHODS: Forty seven trauma victims were studied for 5 days; 32 of them had Injury Severity Scores > 18. A diagnosis of ARDS was made on the recommendations of the American-European Consensus Conference on ARDS (1994). Eight patients developed ARDS, five developed pulmonary dysfunction, and the remainder showed no significant pulmonary abnormality. RESULTS: Using the near patient urine albumin immunoassay, albumin excretion rate (AER) was measured after admission. For patients with Injury Severity Score > 18, the median (95% confidence interval) AER 8 hours after admission was 63 (range, 40-99) microg per minute for those without impaired lung function and 339 (range, 162-454) microg per minute for those in the combined ARDS and pulmonary dysfunction group (Mann-Whitney test, p = 0.0004). The median AER was 51 (range, 27-98) microg per minute for patients with Injury Severity Score < 18. The positive predictive value for the development of ARDS or pulmonary dysfunction of AER > 130 microg per minute was 85%, with a negative predictive value of 95%. CONCLUSIONS: These data indicate that the capillary leak associated with the subsequent development of pulmonary dysfunction and ARDS can be detected within 8 hours of admission at the patient's bedside, thus providing a means of early identification of patients at greatest risk and allowing for early intervention.

Immune response to Acinetobacter calcoaceticus infection in man.

After growth in an iron-depleted chemically-defined medium Acinetobacter calcoaceticus expressed four high mol. wt outer-membrane proteins (OMPs) which were repressed under iron supplementation or in a complex laboratory medium. Immunoblotting with serum from a septicaemic patient infected with A. calcoaceticus revealed antibody binding to these iron-repressible OMPs, indicating that they were expressed in vivo, and also to the 42- and 18-Kda OMPs. Although the antibody response to the OMPs did not vary significantly during convalescence, the response to the O-polysaccharide component of lipopolysaccharide decreased significantly. However, antibodies in serum from patients with A. calcoaceticus wound infections reacted with the iron repressible OMPs and a 54-Kda antigen suggesting a difference in immune recognition between local and systemic infection.