SummaryThe pulmonary inflammatory response and pulmonary dysfunction after cardiopulmonary bypass is a major problem in patients undergoing cardiac surgery. Propofol has anti-inflammatory and immunomodulatory properties which may attenuate this response. Thirty patients undergoing cardiopulmonary bypass were randomly assigned to receive saline (control group) or propofol (propofol group). Pulmonary thoracic compliance, respiratory index, malondialdehyde and interleukin-8 concentrations and intrapulmonary polymorphonucleocyte sequestration were measured at pre-bypass and 5, 30, 60, 90 and 120 min after unclamping the aorta. Plasma levels of interleukin-8, malondialdehyde and the respiratory index increased and reached peaks 30 min after unclamping in both groups. However, in the propofol group the increases were less than in the control group (p < 0.01). Intrapulmonary polymorphonucleocytes sequestration in the propofol group was less than in the control group 5 min after unclamping (p < 0.0001). Pulmonary thoracic compliance decreased significantly after unclamping in both groups, but the reduction was less in the propofol group (p < 0.01). These findings suggest that propofol administered during bypass could reduce the severity of pulmonary dysfunction. Pulmonary dysfunction is common after cardiopulmonary bypass (CPB). The clinical manifestations range from subclinical functional changes to full-blown adult respiratory distress syndrome (ARDS) seen in 2% of cases and which carries a 50% mortality rate [1]. System inflammatory response syndrome (SIRS) is the main cause of pulmonary dysfunction after CPB [2]. Although many strategies to attenuate SIRS have been developed [3], it has not been completely prevented and remains a significant contributor to pulmonary dysfunction after surgery [2,4,5].SIRS is mainly caused by the contact of blood with the non-endothelialised surface of CPB circuits activating multiple plasma protein cascades and blood cells, resulting in increased production of inflammatory mediators and activation of vascular endothelium [3,4]. Activated polymorphonucleocytes (PMNs) sequestered in the lung in response to chemotactic factor interleukin-8 (IL-8) may result in widespread pulmonary inflammatory response and injury through the release of harmful oxygen free radicals and specific enzymes [6,7]. Thus, inhibition of IL-8 release and PMNs sequestration in the lung is a key strategy to control the pulmonary inflammatory response.Propofol is structurally similar to endogenous antioxidant a-tocoferol (vitamin E) and possesses multiple anti-inflammatory [8][9][10] and immunomodulatory properties [11]. Experimental evidence suggests that propofol is a valuable pharmacological tool to treat pulmonary dysfunction related to CPB [12]. However, these studies are in vitro and may not be relevant to the clinical scenario. Hence, we undertook a prospective,
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