The purpose of this presentation is to review our experience over a number of years regarding the chemical mediators of the pulmonary changes that occur during experimental shock induced by endotoxin derived from either Escherichia coli or Serratia marcescens organisms. Pulmonary dysfunction is a major complication of trauma and sepsis and the main features include interstitial and intra-alveolar oedema, reduced lung compliance and impaired pulmonary gas exchange. The main problem appears to be at the level of the pulmonary microcirculation and there is good evidence for a combination of mechanical obstruction (resulting from the presence of microthromboemboli) and of the active constriction of vascular smooth muscle, particularly in the post-capillary segment. One of the aims of the studies originating from the author's laboratory has been to determine which endogenously released vasoactive agents contribute to these pulmonary circulatory changes. This has been investigated in two main ways; firstly, by interfering with the synthesis or release of likely mediators or with their effects at receptor level. Secondly, by measuring circulating blood levels of these mediators and especially to determine their concentrations in pulmonary arterial and venous blood at different times during shock. This second approach has also been applied to studies involving patients during septic shock.
|Number of pages||17|
|Journal||Fernstrom Foundation Series|
|Publication status||Published - Jan 1 1983|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)