Ann Acad Med Singap
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The immune system is a powerful, complex entity composed of numerous cell types and regulated by autocrine, paracrine, and hormonal mechanisms. Trauma and haemorrhagic shock induce numerous changes within this system which are ultimately deleterious and contribute to the high incidence of organ dysfunction and infectious complications seen following injury. Regional hypoxia and depletion of intracellular energy stores occur in response to diminished microcirculatory blood flow, and these changes alter cellular signalling and result in the release of pro-inflammatory cytokines and prostanoids which mediate further suppression of immune function. ⋯ The resulting depression in cell mediated and humoral immunity renders the organism susceptible to microbial infection and contributes to the morbidity and mortality associated with nosocomial infections. Hormonal modulation of the immune response is highly evident following trauma and haemorrhage, and the preponderance of male morbidity associated with sepsis can be explained by the depression in immune function seen in males, but not females in the pro-oestrous state. Despite the multitude of changes induced by trauma and haemorrhage, experimental studies have revealed several promising pharmacologic interventions which may serve to blunt the effect of injury on the immune system, and render the host competent to withstand the bacterial and viral challenges responsible for so much of the late mortality following severe injury.
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Ann Acad Med Singap · Jan 1999
Efficacy of contraction uncoupling by 2,3-butanedione monoxime during initial reperfusion versus cardioplegic arrest for protection of isolated hearts.
The efficacy of 2,3-butanedione monoxime (BDM) as additive to St. Thomas Hospital II solution (STH) as compared to initial BDM reperfusion with regard to myocardial ischaemia/reperfusion injury was investigated in isolated guinea pig hearts. Isolated guinea pig hearts were perfused with Krebs-Henseleit buffer in the Langendorff technique at constant pressure of 55 mmHg. ⋯ Addition of BDM to the cardioplegic STH solution did not protect isolated hearts from cellular injury or depression of post-ischaemic function. In contrast, initial BDM reperfusion alone attenuated reperfusion contracture, prevented LDH release, and improved recovery of systolic and diastolic myocardial function. The combination of BDM treatment during cardioplegic arrest with initial BDM reperfusion provides no additional protection from reperfusion injury.