PURPOSE:Similar to the general population, parturients (and their fetuses) could benefit from the reduced manipulation associated with laparoscopy. The purpose of this article is to review the current state of knowledge (both clinical and experimental) with respect to the fetal effects of maternal laparoscopy for non-obstetric-related surgery during pregnancy.METHODS:Human and experimental animal results are examined, and we present preliminary data from our own laboratory.CONCLUSIONS:Future experiments are proposed to further develop and refine standards of care for general surgeons and obstetricians who are presented with gravid females in abdominal distress.

In most investigations, genetic and environmental factors have been shown to interact in altering the progression of ageing related disease including stroke and cognitive decline. The peri-operative period appears to be no different, with environmental (operative) and genetic factors interacting to determine the presence, absence or severity of neurological outcomes. In our initial work we confirmed that apolipoprotein E4 (apoE4) alters cognitive function after coronary artery bypass graft (CABG), the mechanism of this association apparently being related to atherosclerosis and inflammatory factors. These findings are consistent with multiple studies that have shown an important role of apoE in the modulation of neurological injury and recovery following a variety of acute ischaemic insults including intra-cerebral haemorrhage, closed head injury, acute stroke and dementia pugilistica. More recently we have found that polymorphism of the GPIIIa constituent of the platelet integrin receptor, GPIIb/IIIa (PLA2) polymorphism is also associated with early post-operative cognitive decline. The association of multiple genetic factors with the incidence or severity of neurological injury is not surprising, since the factors that alter cerebral injury and recovery are complex. Similarly, there are genetic factors that determine the occurrence of tissue injury and its recovery, including genes that modulate atherosclerosis, emboli, inflammation, thrombosis and vascular reactivity. We have only begun to scratch the surface in our understanding of functional genomics as it applies to peri-operative outcomes. Functional genomics, as applied to complex human disease, will require a unique combination of cutting-edge genetics and large, highly phenotyped patient populations in order to further our understanding of the complex genetic–environmental interactions. This chapter will concentrate initially on the broad classes of genetic factors that may play a role in neurological injury and recovery, and will conclude with our current data on those genetic factors that predict neurocognitive decline after cardiac surgery and the potential mechanisms driving these associations.

Sixty ASA physical status I and II, premedicated patients were administered propofol 2 mg.kg−1 and remifentanil 2 μg.kg−1 (group R), alfentanil 50 μg.kg−1 (group A) or suxamethonium 1 mg.kg−1 (group S) as a rapid bolus. One minute after study drug administration, tracheal intubation was performed. Intubation conditions were then scored. Excellent or good conditions were observed in only 35% in group R compared with groups S and A (100% and 85%, respectively; p < 0.001). The haemodynamic response to tracheal intubation was blunted in groups R and A compared with group S (p < 0.001). The mean heart rate in groups R and A was significantly lower than group S (p < 0.001). We conclude that remifentanil 2 μg.kg−1 given as a rapid bolus will not produce intubating conditions as good as those obtained with alfentanil 50 μg.kg−1 or suxamethonium 1 mg.kg−1 if administered after propofol 2 mg.kg−1.

Sixty ASA I and II patients, premedicated with midazolam, were administered propofol 2 mg.kg −1 and remifentanil 3 μg.kg −1 (group R3), remifentanil 4 μg.kg −1 (group R4) and remifentanil 5 μg.kg −1 (group R5). Laryngoscopy and intubation were performed 1 min after the administration of the study drugs and the intubating conditions were assessed. Good to excellent conditions were observed in 12 patients in group R3 compared with 19 patients each in groups R4 and R5 (p = 0.004). Significant reductions in mean arterial pressure (MAP) and heart rate (HR) after administration of the study drug were observed in each group, p < 0.01. There was, however, no difference in mean MAP and HR between the three groups at all time points. We conclude that remifentanil 4–5 μg.kg −1 may reliably provide good to excellent conditions for tracheal intubation when administered after propofol 2 mg.kg −1 .

Background: Previously the authors showed that myocardial beta-adrenergic (beta AR) function is reduced after cardiopulmonary bypass (CPB) in a canine model. Whether CPB results in similar effects on beta AR function in adult humans is not known. Therefore the current study tested two hypotheses: (1) That myocardial beta AR signaling is reduced in adult humans after CPB, and (2) that administration of long-term preoperative beta AR antagonists prevents this process. Methods: After they Save informed consent, 52 patients undergoing aortocoronary surgery were enrolled. Atrial biopsies were obtained before CPB and immediately before discontinuation of CPB. Plasma catecholamine concentrations, myocardial beta AR density, and functional responsiveness (basal, isoproterenol, zinterol, sodium fluoride, and manganese-stimulated adenylyl cyclase activity) were assessed. Results: Catecholamine levels increased significantly during CPB (P < 0.005). Myocardial beta AR adenylyl cyclase coupling decreased during CPB, as evidenced by a 21% decrease in isoproterenol-stimulated adenylyl cyclase activity (750 [430] pmol cyclic adenosine monophosphate per milligram total protein 15 min before CPB compared with 540 [390] at the end of CPB, P = 0.0062, medians [Interquartile range]) despite constant beta AR density. Differential activation along the beta AR signal transduction cascade localized the defect to the adenylyl cyclase moiety Administration of long-term preoperative beta AR antagonists did not prevent acute CPB-induced myocardial beta AR dysfunction. Conclusions: These data indicate that the myocardial adenylyl cyclase response to beta AR agonists decreases acutely in adults during aortocoronary surgery requiring CPB, regardless of whether long-term preoperative beta AR antagonists are administered. The mechanism underlying acute beta AR dysfunction appears to be direct impairment of the adenylyl cyclase moiety. Similar increases in manganese-stimulated activity before and at the end of CPB show preserved adenylyl cyclase catalytic activity, suggesting that other mechanisms (such as decreased protein levels or altered isoform expression or function) may be responsible for decreased adenylyl cyclase function.

Background Previously the authors showed that myocardial beta-adrenergic (betaAR) function is reduced after cardiopulmonary bypass (CPB) in a canine model Whether CPB results in similar effects on betaAR function in adult humans is not known. Therefore the current study tested two hypotheses: (1) That myocardial betaAR signaling is reduced in adult humans after CPB, and (2) that administration of long-term preoperative betaAR antagonists prevents this process. Methods After they gave informed consent, 52 patients undergoing aortocoronary surgery were enrolled. Atrial biopsies were obtained before CPB and immediately before discontinuation of CPB. Plasma catecholamine concentrations, myocardial betaAR density, and functional responsiveness (basal, isoproterenol, zinterol, sodium fluoride, and manganese-stimulated adenylyl cyclase activity) were assessed. Results Catecholamine levels increased significantly during CPB (P < 0.005). Myocardial betaAR adenylyl cyclase coupling decreased during CPB, as evidenced by a 21% decrease in isoproterenol-stimulated adenylyl cyclase activity (750 [430] pmol cyclic adenosine monophosphate per milligram total protein 15 min before CPB compared with 540 [390] at the end of CPB, P = 0.0062, medians [interquartile range]) despite constant betaAR density. Differential activation along the betaAR signal transduction cascade localized the defect to the adenylyl cyclase moiety. Administration of long-term preoperative betaAR antagonists did not prevent acute CPB-induced myocardial betaAR dysfunction. Conclusions These data indicate that the myocardial adenylyl cyclase response to betaAR agonists decreases acutely in adults during aortocoronary surgery requiring CPB, regardless of whether long-term preoperative betaAR antagonists are administered. The mechanism underlying acute betaAR dysfunction appears to be direct impairment of the adenylyl cyclase moiety. Similar increases in manganese-stimulated activity before and at the end of CPB show preserved adenylyl cyclase catalytic activity, suggesting that other mechanisms (such as decreased protein levels or altered isoform expression or function) may be responsible for decreased adenylyl cyclase function.