Effects of propofol on pulmonary inflammatory response and dysfunction induced by cardiopulmonary bypass*

Abstract

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,

Comparison of the myocardial protective effect of sevoflurane versus propofol in patients undergoing heart valve replacement surgery with cardiopulmonary bypass

“…Studies have reported that the cardioprotection mechanism of inhaled anesthetics such as, volatile anesthetics open intracellular K ATP channels, activate adenosine receptors, and inhibit Na + /K + pump [1, 8, 28, 29]. Studies have also reported that the cardioprotection mechanism of propofol is related to its anti-inflammatory, immunomodulatory and antioxidant properties [21, 30, 31]. Nevertheless, many studies, such as some prospective randomized controlled trials [10–13, 32] and observational study [14] in adult patients indicated some contradicting results on the cardioprotection between volatile and non volatile agents.…”

The Effects of Short-Term Propofol and Dexmedetomidine on Lung Mechanics, Histology, and Biological Markers in Experimental Obesity

“…[3][4][5] In lean animals, PRO decreases airway resistance and lung inflammation in experimental acute lung injury induced by endotoxin, 6,7 ischemia-reperfusion, 8 or oleic acid. 9 Similarly, in lean human subjects, PRO improves lung mechanics, 10 reduces inflammation, 11 and modulates oxidative stress. 12 Likewise, DEX has shown beneficial effects on lung mechanics, 13 inflammation, 14,15 and oxidative stress 16 in lean animals and humans.…”

Propofol Inhibits Superoxide Production, Elastase Release, and Chemotaxis in Formyl Peptide–Activated Human Neutrophils by Blocking Formyl Peptide Receptor 1

“…In animal studies, propofol has decreased cytokine release during sepsis (2,3) and reduced neutrophil-mediated inflammation in acute pulmonary injury (4,5). In human studies, propofol has attenuated myocardial reperfusion injury and pulmonary dysfunction following cardiopulmonary bypass by reducing free radical release and modulating the inflammatory process (6,7).…”

“…Similarly, in lung injury models, inappropriately activated neutrophils have resulted in acute respiratory distress syndrome or transfusion-related acute lung injury (19,20). Interestingly, it has been shown in animal and human studies that propofol may diminish the oxidative or inflammatory injury induced by neutrophils (2,4,7). These observations are interpreted to mean that propofol has an antioxidant capacity.…”